Nutrient chapter

Apigenin

Context-specific entity; species, compartment and exposure are stated on each claim.

116 recorded mechanisms · 6 availability situations · 3 preserved sources. Source recording and scientific verification are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

Recombinant human CYP1A2 supported apigenin 3′-hydroxylation to luteolin.
Human cytochrome P450 1A2 → Luteolin / 3′,4′,5,7-tetrahydroxyflavone Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human CYP expression and liver microsomes.
limitations
Not evidence that the two oral products give equivalent exposures.
nutrient_topic
Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
plain_language
A related flavone can be converted into luteolin.
primary_references
In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11955666/ · DOI 10.1016/s0278-6915(01)00125-9
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 140–146
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human CYP expression and liver microsomes. · Recorded from source · Recorded from source
## luteolin-cyp1a2-apigenin A related flavone can be converted into luteolin. Recombinant human CYP1A2 supported apigenin 3′-hydroxylation to luteolin. Model: Human CYP expression and liver microsomes. Limitations: Not evidence that the two oral products give equivalent exposures. Evidence access: Primary abstract In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11955666/ · DOI 10.1016/s0278-6915(01)00125-9
Complete structured claim and evidence
Recombinant human CYP3A4 supported apigenin 3′-hydroxylation to luteolin.
Human cytochrome P450 3A4 → Luteolin / 3′,4′,5,7-tetrahydroxyflavone Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human CYP expression and liver microsomes.
limitations
Not evidence that the two oral products give equivalent exposures.
nutrient_topic
Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
plain_language
A related flavone can be converted into luteolin.
primary_references
In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11955666/ · DOI 10.1016/s0278-6915(01)00125-9
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 148–154
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human CYP expression and liver microsomes. · Recorded from source · Recorded from source
## luteolin-cyp3a4-apigenin A related flavone can be converted into luteolin. Recombinant human CYP3A4 supported apigenin 3′-hydroxylation to luteolin. Model: Human CYP expression and liver microsomes. Limitations: Not evidence that the two oral products give equivalent exposures. Evidence access: Primary abstract In vitro investigation of cytochrome P450-mediated metabolism of dietary flavonoids. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11955666/ · DOI 10.1016/s0278-6915(01)00125-9
Complete structured claim and evidence
Aged mouse liver and white adipose tissue accumulated CD38-positive immune cells, including macrophages/monocytes, with increased expression per cell in several comparisons.
Inflammatory-cell accumulation during mouse aging → Mouse CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Young versus aged mice; flow cytometry, histology and macrophage experiments.
limitations
Cell abundance and expression observations do not alone quantify absolute tissue NAD flux.
nutrient_topic
NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
plain_language
More NAD-consuming immune cells can change a tissue metabolite pool.
primary_references
CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 100–106
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Young versus aged mice; flow cytometry, histology and macrophage experiments. · Recorded from source · Recorded from source
## nad-plus-aging-cd38 More NAD-consuming immune cells can change a tissue metabolite pool. Aged mouse liver and white adipose tissue accumulated CD38-positive immune cells, including macrophages/monocytes, with increased expression per cell in several comparisons. Model: Young versus aged mice; flow cytometry, histology and macrophage experiments. Limitations: Cell abundance and expression observations do not alone quantify absolute tissue NAD flux. Evidence access: Primary full text CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
Complete structured claim and evidence
The study linked extracellular CD38 enzymatic activity to NMN degradation and lower precursor availability; selective blockade of ecto-CD38 increased NAD+ in mouse experiments.
Mouse CD38 → NMN Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse biochemical, cellular and ecto-CD38 antibody experiments.
limitations
Not established clinical benefit from an over-the-counter CD38 inhibitor.
nutrient_topic
NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
plain_language
A precursor can be destroyed before a neighboring cell uses it.
primary_references
CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 116–122
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse biochemical, cellular and ecto-CD38 antibody experiments. · Recorded from source · Recorded from source
## nad-plus-ecto-cd38-nmn A precursor can be destroyed before a neighboring cell uses it. The study linked extracellular CD38 enzymatic activity to NMN degradation and lower precursor availability; selective blockade of ecto-CD38 increased NAD+ in mouse experiments. Model: Mouse biochemical, cellular and ecto-CD38 antibody experiments. Limitations: Not established clinical benefit from an over-the-counter CD38 inhibitor. Evidence access: Primary full text CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
Complete structured claim and evidence
Senescent-cell-associated inflammatory signals promoted CD38 expression; reducing senescent-cell burden partially restored NAD+ in the reported mouse experiments.
Secretory factors from senescent mouse-cell models → Mouse CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Senescent-cell conditioned media and mouse interventions.
limitations
Partial rescue supports a contributing mechanism, not a single cause of every age-associated NAD decline.
nutrient_topic
NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
plain_language
Signals from one cell population can change NAD availability in another.
primary_references
CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 108–114
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Senescent-cell conditioned media and mouse interventions. · Recorded from source · Recorded from source
## nad-plus-sasp-cd38 Signals from one cell population can change NAD availability in another. Senescent-cell-associated inflammatory signals promoted CD38 expression; reducing senescent-cell burden partially restored NAD+ in the reported mouse experiments. Model: Senescent-cell conditioned media and mouse interventions. Limitations: Partial rescue supports a contributing mechanism, not a single cause of every age-associated NAD decline. Evidence access: Primary full text CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
Complete structured claim and evidence
Apigenin is 4′,5,7-trihydroxyflavone, C15H10O5, molecular mass about 270.24 g/mol; it lacks the adjacent B-ring hydroxyls present in luteolin.
Apigenin → Apigenin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Official chemical identity record; not a clinical experiment.
experimental_model
Chemical identity; not an intervention.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin is 4′,5,7-trihydroxyflavone, C15H10O5, molecular mass about 270.24 g/mol; it lacks the adjacent B-ring hydroxyls present in luteolin.
primary_references
PubChem CID 5280443: Apigenin | https://pubchem.ncbi.nlm.nih.gov/compound/5280443
source_locator
Reviewed reference api-identity; Absence of a catechol does not mean all metal binding or downstream methylation is impossible. Existing human CYP1A2 and CYP3A4 conversion-to-luteolin records are reused.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 21–27
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Chemical identity; not an intervention. · Recorded from source · Recorded from source
### api-identity Apigenin is 4′,5,7-trihydroxyflavone, C15H10O5, molecular mass about 270.24 g/mol; it lacks the adjacent B-ring hydroxyls present in luteolin. Absence of a catechol does not mean all metal binding or downstream methylation is impossible. Existing human CYP1A2 and CYP3A4 conversion-to-luteolin records are reused. Model and exposure: Chemical identity; not an intervention. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: PubChem CID 5280443: Apigenin | accessed 2026-10-10 | https://pubchem.ncbi.nlm.nih.gov/compound/5280443 | Access: Official chemical identity record; not a clinical experiment.
Complete structured claim and evidence
After ingestion of 191 micromoles of apigenin, neither parent nor the targeted conjugates were detected in plasma at 0, 2, 4 or 6 hours.
Apigenin → Unconjugated apigenin measured in human plasma Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
experimental_contrast
{"intervention": "191 micromoles oral apigenin", "comparator": "Predose plasma", "endpoint": "After ingestion of 191 micromoles of apigenin, neither parent nor the targeted conjugates were detected in plasma at 0, 2, 4 or 6 hours.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Three healthy men; single aglycone capsule contents in hot water; about 51.6 mg calculated from molecular mass.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
After ingestion of 191 micromoles of apigenin, neither parent nor the targeted conjugates were detected in plasma at 0, 2, 4 or 6 hours.
primary_references
Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007
source_locator
Reviewed reference api-parent-pk-null; Table 3 and section 3.3.1. Detection was sampling- and assay-dependent, not proof of zero absorption.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 29–35
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Three healthy men; single aglycone capsule contents in hot water; about 51.6 mg calculated from molecular mass. · Recorded from source · Recorded from source
### api-parent-pk-null After ingestion of 191 micromoles of apigenin, neither parent nor the targeted conjugates were detected in plasma at 0, 2, 4 or 6 hours. Table 3 and section 3.3.1. Detection was sampling- and assay-dependent, not proof of zero absorption. Model and exposure: Three healthy men; single aglycone capsule contents in hot water; about 51.6 mg calculated from molecular mass. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
Complete structured claim and evidence
The same aglycone exposure yielded 0.9 ± 0.6 micromoles of measured urinary glucuronides over 24 hours, about 0.5% of intake.
Apigenin → Human urinary apigenin conjugate recovery Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
experimental_model
Three healthy men; authentic-standard HPLC-MS.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The same aglycone exposure yielded 0.9 ± 0.6 micromoles of measured urinary glucuronides over 24 hours, about 0.5% of intake.
primary_references
Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007
source_locator
Reviewed reference api-parent-urine; Recovery of selected metabolites is not an absolute bioavailability measurement.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 37–43
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Three healthy men; authentic-standard HPLC-MS. · Recorded from source · Recorded from source
### api-parent-urine The same aglycone exposure yielded 0.9 ± 0.6 micromoles of measured urinary glucuronides over 24 hours, about 0.5% of intake. Recovery of selected metabolites is not an absolute bioavailability measurement. Model and exposure: Three healthy men; authentic-standard HPLC-MS. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
Complete structured claim and evidence
A parsley drink containing 118 micromoles of apiin produced a plasma Apigenin 4′-O-glucuronide peak of 153 ± 61 nM at 4 hours.
Parsley drink in the 2022 apigenin metabolism study → Apigenin 4′-O-glucuronide Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
experimental_model
Four healthy men; 3.2 g parsley powder in 450 mL water.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
A parsley drink containing 118 micromoles of apiin produced a plasma Apigenin 4′-O-glucuronide peak of 153 ± 61 nM at 4 hours.
primary_references
Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007
source_locator
Reviewed reference api-parsley-glucuronide; Section 3.3.2, Figure 1. These concentrations are of intact conjugates, not free apigenin.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 45–51
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Four healthy men; 3.2 g parsley powder in 450 mL water. · Recorded from source · Recorded from source
### api-parsley-glucuronide A parsley drink containing 118 micromoles of apiin produced a plasma Apigenin 4′-O-glucuronide peak of 153 ± 61 nM at 4 hours. Section 3.3.2, Figure 1. These concentrations are of intact conjugates, not free apigenin. Model and exposure: Four healthy men; 3.2 g parsley powder in 450 mL water. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
Complete structured claim and evidence
A parsley drink containing 118 micromoles of apiin produced a plasma Apigenin 7-O-sulfate peak of 253 ± 202 nM at 4 hours.
Parsley drink in the 2022 apigenin metabolism study → Apigenin 7-O-sulfate Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
experimental_model
Four healthy men; 3.2 g parsley powder in 450 mL water.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
A parsley drink containing 118 micromoles of apiin produced a plasma Apigenin 7-O-sulfate peak of 253 ± 202 nM at 4 hours.
primary_references
Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007
source_locator
Reviewed reference api-parsley-sulfate; Section 3.3.2, Figure 1. These concentrations are of intact conjugates, not free apigenin.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 53–59
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Four healthy men; 3.2 g parsley powder in 450 mL water. · Recorded from source · Recorded from source
### api-parsley-sulfate A parsley drink containing 118 micromoles of apiin produced a plasma Apigenin 7-O-sulfate peak of 253 ± 202 nM at 4 hours. Section 3.3.2, Figure 1. These concentrations are of intact conjugates, not free apigenin. Model and exposure: Four healthy men; 3.2 g parsley powder in 450 mL water. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
Complete structured claim and evidence
Measured urinary apigenin metabolites after the initial parsley drink averaged 11.2% of ingested flavone equivalents.
Parsley drink in the 2022 apigenin metabolism study → Human urinary apigenin conjugate recovery Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
experimental_model
Four men; 0–24-hour urine.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Measured urinary apigenin metabolites after the initial parsley drink averaged 11.2% of ingested flavone equivalents.
primary_references
Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007
source_locator
Reviewed reference api-parsley-urine; The larger repeated-intake series gave 17.2 ± 9.8% recovery across 17 intakes, with greater inter-person than within-person variation. Neither figure is an intravenous-reference absolute bioavailability estimate.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 61–67
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Four men; 0–24-hour urine. · Recorded from source · Recorded from source
### api-parsley-urine Measured urinary apigenin metabolites after the initial parsley drink averaged 11.2% of ingested flavone equivalents. The larger repeated-intake series gave 17.2 ± 9.8% recovery across 17 intakes, with greater inter-person than within-person variation. Neither figure is an intravenous-reference absolute bioavailability estimate. Model and exposure: Four men; 0–24-hour urine. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
Complete structured claim and evidence
The yogurt/parsley preparation shifted observed conjugate peaks to the last sampled point at 6 hours or later, compared with 4 hours for the drink.
Parsley with yogurt in the 2022 apigenin metabolism study → Human apigenin-conjugate plasma timing Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
experimental_contrast
{"intervention": "Parsley with yogurt", "comparator": "Parsley drink", "endpoint": "The yogurt/parsley preparation shifted observed conjugate peaks to the last sampled point at 6 hours or later, compared with 4 hours for the drink.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Four men, 118 micromoles apiin with 100 g yogurt.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The yogurt/parsley preparation shifted observed conjugate peaks to the last sampled point at 6 hours or later, compared with 4 hours for the drink.
primary_references
Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007
source_locator
Reviewed reference api-yogurt-timing; Section 3.3.3; urinary recovery was not significantly different. Gastric emptying and matrix release were proposed explanations, not measured causal mediators.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 69–75
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Four men, 118 micromoles apiin with 100 g yogurt. · Recorded from source · Recorded from source
### api-yogurt-timing The yogurt/parsley preparation shifted observed conjugate peaks to the last sampled point at 6 hours or later, compared with 4 hours for the drink. Section 3.3.3; urinary recovery was not significantly different. Gastric emptying and matrix release were proposed explanations, not measured causal mediators. Model and exposure: Four men, 118 micromoles apiin with 100 g yogurt. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
Complete structured claim and evidence
Chamomile tea produced the same two plasma conjugates with observed peaks at 2 hours and approximately 34% urinary recovery of measured metabolites over 24 hours.
Chamomile tea in the 2022 apigenin metabolism study → Human urinary apigenin conjugate recovery Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
experimental_model
Four men; tea containing 13.4 micromoles apigenin 7-O-glucoside and 1.2 micromoles parent.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Chamomile tea produced the same two plasma conjugates with observed peaks at 2 hours and approximately 34% urinary recovery of measured metabolites over 24 hours.
primary_references
Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007
source_locator
Reviewed reference api-chamomile-pk; Section 3.3.4. The different glycoside and food matrix preclude equating this with a parent capsule.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 77–83
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Four men; tea containing 13.4 micromoles apigenin 7-O-glucoside and 1.2 micromoles parent. · Recorded from source · Recorded from source
### api-chamomile-pk Chamomile tea produced the same two plasma conjugates with observed peaks at 2 hours and approximately 34% urinary recovery of measured metabolites over 24 hours. Section 3.3.4. The different glycoside and food matrix preclude equating this with a parent capsule. Model and exposure: Four men; tea containing 13.4 micromoles apigenin 7-O-glucoside and 1.2 micromoles parent. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
Complete structured claim and evidence
The older parsley study reported a plasma peak of 127 ± 81 nM at 7.2 ± 1.3 hours and urinary recovery of 0.22 ± 0.16% of intake.
Blanched parsley meal in the 2006 apigenin study → Plasma apigenin equivalents after sample deconjugation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.; Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
experimental_model
Eleven volunteers; 2 g blanched parsley/kg body weight.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The older parsley study reported a plasma peak of 127 ± 81 nM at 7.2 ± 1.3 hours and urinary recovery of 0.22 ± 0.16% of intake.
primary_references
Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007
primary_references
Bioavailability of apigenin from apiin-rich parsley in humans. | https://pubmed.ncbi.nlm.nih.gov/16407641/ | https://doi.org/10.1159/000090736
source_locator
Reviewed reference api-older-parsley-pk; The 2022 primary paper identifies glucuronidase/sulfatase sample pretreatment in this earlier method. These results cannot be read as directly measured unbound parent. Food matrix and analytical methods differ between studies.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 85–92
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Eleven volunteers; 2 g blanched parsley/kg body weight. · Recorded from source · Recorded from source
### api-older-parsley-pk The older parsley study reported a plasma peak of 127 ± 81 nM at 7.2 ± 1.3 hours and urinary recovery of 0.22 ± 0.16% of intake. The 2022 primary paper identifies glucuronidase/sulfatase sample pretreatment in this earlier method. These results cannot be read as directly measured unbound parent. Food matrix and analytical methods differ between studies. Model and exposure: Eleven volunteers; 2 g blanched parsley/kg body weight. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Bioavailability of apigenin from apiin-rich parsley in humans. | 2006 | https://pubmed.ncbi.nlm.nih.gov/16407641/ | https://doi.org/10.1159/000090736 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown. Reference: Absorption, distribution, metabolism and excretion of apigenin and its glycosides in healthy male adults. | 2022 | https://pubmed.ncbi.nlm.nih.gov/35452808/ | https://doi.org/10.1016/j.freeradbiomed.2022.04.007 | Access: Full original primary-paper PDF, Methods, Results and Tables 1–7 reviewed; authentic-standard HPLC-MS analysis. PDF obtained from a public mirror; DOI and article identity verified.
Complete structured claim and evidence
Recombinant human CYP1B1 variants 1 and 3 hydroxylated apigenin at carbon 6 to scutellarein, with reported S50 values of 16 and 51 micromolar.
Human cytochrome P450 1B1 / CYP1B1 → Scutellarein / 6-hydroxyapigenin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract and publisher-indexed Results; recombinant-enzyme selectivity, not complete human metabolic mass balance.
experimental_model
Recombinant human enzymes; cooperative substrate-response curves.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Recombinant human CYP1B1 variants 1 and 3 hydroxylated apigenin at carbon 6 to scutellarein, with reported S50 values of 16 and 51 micromolar.
primary_references
Oxidation of Naringenin, Apigenin, and Genistein by Human Family 1 Cytochrome P450 Enzymes and Comparison of Interaction of Apigenin with Human P450 1B1.1 and Scutellaria P450 82D.1. | https://pubmed.ncbi.nlm.nih.gov/37783573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11497155/ | https://doi.org/10.1021/acs.chemrestox.3c00229
source_locator
Reviewed reference api-cyp1b1-scutellarein; S50 is not automatically a Michaelis constant. Rates and variant identity are assay-specific.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 98–104
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human enzymes; cooperative substrate-response curves. · Recorded from source · Recorded from source
### api-cyp1b1-scutellarein Recombinant human CYP1B1 variants 1 and 3 hydroxylated apigenin at carbon 6 to scutellarein, with reported S50 values of 16 and 51 micromolar. S50 is not automatically a Michaelis constant. Rates and variant identity are assay-specific. Model and exposure: Recombinant human enzymes; cooperative substrate-response curves. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Oxidation of Naringenin, Apigenin, and Genistein by Human Family 1 Cytochrome P450 Enzymes and Comparison of Interaction of Apigenin with Human P450 1B1.1 and Scutellaria P450 82D.1. | 2023 | https://pubmed.ncbi.nlm.nih.gov/37783573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11497155/ | https://doi.org/10.1021/acs.chemrestox.3c00229 | Access: Indexed primary abstract and publisher-indexed Results; recombinant-enzyme selectivity, not complete human metabolic mass balance.
Complete structured claim and evidence
Recombinant human CYP2A13 converted apigenin to luteolin, with reported substrate S50 of 14 micromolar.
Human cytochrome P450 2A13 / CYP2A13 → Luteolin / 3′,4′,5,7-tetrahydroxyflavone Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract and publisher-indexed Results; recombinant-enzyme selectivity, not complete human metabolic mass balance.
experimental_model
Recombinant human enzyme; not whole-body metabolic flux.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Recombinant human CYP2A13 converted apigenin to luteolin, with reported substrate S50 of 14 micromolar.
primary_references
Oxidation of Naringenin, Apigenin, and Genistein by Human Family 1 Cytochrome P450 Enzymes and Comparison of Interaction of Apigenin with Human P450 1B1.1 and Scutellaria P450 82D.1. | https://pubmed.ncbi.nlm.nih.gov/37783573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11497155/ | https://doi.org/10.1021/acs.chemrestox.3c00229
source_locator
Reviewed reference api-cyp2a13-luteolin;
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 106–112
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human enzyme; not whole-body metabolic flux. · Recorded from source · Recorded from source
### api-cyp2a13-luteolin Recombinant human CYP2A13 converted apigenin to luteolin, with reported substrate S50 of 14 micromolar. Model and exposure: Recombinant human enzyme; not whole-body metabolic flux. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Oxidation of Naringenin, Apigenin, and Genistein by Human Family 1 Cytochrome P450 Enzymes and Comparison of Interaction of Apigenin with Human P450 1B1.1 and Scutellaria P450 82D.1. | 2023 | https://pubmed.ncbi.nlm.nih.gov/37783573/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11497155/ | https://doi.org/10.1021/acs.chemrestox.3c00229 | Access: Indexed primary abstract and publisher-indexed Results; recombinant-enzyme selectivity, not complete human metabolic mass balance.
Complete structured claim and evidence
Rat microsomes formed luteolin, scutellarein and isoscutellarein from apigenin.
Apigenin → Isoscutellarein / 8-hydroxyapigenin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_model
Rat microsomal phase-I metabolism.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Rat microsomes formed luteolin, scutellarein and isoscutellarein from apigenin.
primary_references
Metabolism of apigenin by rat liver phase I and phase ii enzymes and by isolated perfused rat liver. | https://pubmed.ncbi.nlm.nih.gov/14709621/ | https://doi.org/10.1124/dmd.32.1.58
source_locator
Reviewed reference api-rat-hydroxylation; The intact perfused rat liver did not yield recovered phase-I products in the same report; it formed conjugates. Do not equate microsomal capability with exported in-vivo flux.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 114–120
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Rat microsomal phase-I metabolism. · Recorded from source · Recorded from source
### api-rat-hydroxylation Rat microsomes formed luteolin, scutellarein and isoscutellarein from apigenin. The intact perfused rat liver did not yield recovered phase-I products in the same report; it formed conjugates. Do not equate microsomal capability with exported in-vivo flux. Model and exposure: Rat microsomal phase-I metabolism. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Metabolism of apigenin by rat liver phase I and phase ii enzymes and by isolated perfused rat liver. | 2004 | https://pubmed.ncbi.nlm.nih.gov/14709621/ | https://doi.org/10.1124/dmd.32.1.58 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Luteolin formed downstream of apigenin could undergo methylation to diosmetin in the rat metabolic study.
Luteolin / 3′,4′,5,7-tetrahydroxyflavone → Diosmetin / 4′-O-methylluteolin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_model
Rat metabolism preparations; primary abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Luteolin formed downstream of apigenin could undergo methylation to diosmetin in the rat metabolic study.
primary_references
Metabolism of apigenin by rat liver phase I and phase ii enzymes and by isolated perfused rat liver. | https://pubmed.ncbi.nlm.nih.gov/14709621/ | https://doi.org/10.1124/dmd.32.1.58
source_locator
Reviewed reference api-rat-methylated-product; This does not show that parent apigenin depletes SAM, that one COMT genotype benefits, or that circulating human methyl-donor pools fall.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 122–128
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Rat metabolism preparations; primary abstract. · Recorded from source · Recorded from source
### api-rat-methylated-product Luteolin formed downstream of apigenin could undergo methylation to diosmetin in the rat metabolic study. This does not show that parent apigenin depletes SAM, that one COMT genotype benefits, or that circulating human methyl-donor pools fall. Model and exposure: Rat metabolism preparations; primary abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Metabolism of apigenin by rat liver phase I and phase ii enzymes and by isolated perfused rat liver. | 2004 | https://pubmed.ncbi.nlm.nih.gov/14709621/ | https://doi.org/10.1124/dmd.32.1.58 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin 7-O-glucuronide reduced LPS-induced NO, PGE2 and TNF production in RAW264.7 cells.
Apigenin 7-O-glucuronide → Inflammatory products in apigenin-glucuronide-treated RAW264.7 cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_condition
LPS alone Apigenin 7-O-glucuronide plus LPS · Apigenin 7-O-glucuronide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS alone LPS challenge · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin 7-O-glucuronide plus LPS", "comparator": "LPS alone", "endpoint": "Apigenin 7-O-glucuronide reduced LPS-induced NO, PGE2 and TNF production in RAW264.7 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin-7-glucuronide", "state": "Apigenin 7-O-glucuronide plus LPS"}, {"entity_slug": "lipopolysaccharide", "state": "LPS challenge"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse macrophage cell line; exposure details unavailable in the accessed abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin 7-O-glucuronide reduced LPS-induced NO, PGE2 and TNF production in RAW264.7 cells.
primary_references
Apigenin-7-O-β-D-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock. | https://pubmed.ncbi.nlm.nih.gov/26750400/ | https://doi.org/10.1039/c5fo01212k
source_locator
Reviewed reference api-glucuronide-activity; Do not assume conjugates are inert or assume intracellular parent regeneration; intracellular speciation was not established by this abstract.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 130–136
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse macrophage cell line; exposure details unavailable in the accessed abstract. · Recorded from source · Recorded from source
### api-glucuronide-activity Apigenin 7-O-glucuronide reduced LPS-induced NO, PGE2 and TNF production in RAW264.7 cells. Do not assume conjugates are inert or assume intracellular parent regeneration; intracellular speciation was not established by this abstract. Model and exposure: Mouse macrophage cell line; exposure details unavailable in the accessed abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin-7-O-β-D-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock. | 2016 | https://pubmed.ncbi.nlm.nih.gov/26750400/ | https://doi.org/10.1039/c5fo01212k | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
The glucuronide reduced AP-1/c-Jun activation, p38/ERK phosphorylation and iNOS/COX-2 expression in the reported macrophage model.
Apigenin 7-O-glucuronide → AP-1 signaling in the apigenin-glucuronide macrophage study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_condition
LPS alone Glucuronide plus LPS · Apigenin 7-O-glucuronide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS alone LPS challenge · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Glucuronide plus LPS", "comparator": "LPS alone", "endpoint": "The glucuronide reduced AP-1/c-Jun activation, p38/ERK phosphorylation and iNOS/COX-2 expression in the reported macrophage model.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin-7-glucuronide", "state": "Glucuronide plus LPS"}, {"entity_slug": "lipopolysaccharide", "state": "LPS challenge"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
LPS-stimulated mouse RAW264.7 cells; primary abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The glucuronide reduced AP-1/c-Jun activation, p38/ERK phosphorylation and iNOS/COX-2 expression in the reported macrophage model.
primary_references
Apigenin-7-O-β-D-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock. | https://pubmed.ncbi.nlm.nih.gov/26750400/ | https://doi.org/10.1039/c5fo01212k
source_locator
Reviewed reference api-glucuronide-ap1; Signaling and expression observations are not direct binding measurements.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 138–144
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · LPS-stimulated mouse RAW264.7 cells; primary abstract. · Recorded from source · Recorded from source
### api-glucuronide-ap1 The glucuronide reduced AP-1/c-Jun activation, p38/ERK phosphorylation and iNOS/COX-2 expression in the reported macrophage model. Signaling and expression observations are not direct binding measurements. Model and exposure: LPS-stimulated mouse RAW264.7 cells; primary abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin-7-O-β-D-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock. | 2016 | https://pubmed.ncbi.nlm.nih.gov/26750400/ | https://doi.org/10.1039/c5fo01212k | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin inhibited soluble human CD38 NADase activity with IC50 10.3 ± 2.4 micromolar.
Apigenin → Human CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.; Publisher erratum PDF read: Figures 3, 4 and 5 concentration axes should not be labelled Log[concentration]; the scale itself is logarithmic.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "Enzyme without inhibitor", "endpoint": "Apigenin inhibited soluble human CD38 NADase activity with IC50 10.3 ± 2.4 micromolar.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Recombinant soluble human CD38; fluorescent NAD substrate, 0.2 mM.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited soluble human CD38 NADase activity with IC50 10.3 ± 2.4 micromolar.
primary_references
Erratum: Apigenin inhibits the NADase CD38 | https://doi.org/10.2337/db14-er04
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-human-cd38-nadase; Figure 3. Corrected axis labels are concentrations on a logarithmic scale, not Log[concentration] values.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 150–157
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant soluble human CD38; fluorescent NAD substrate, 0.2 mM. · Recorded from source · Recorded from source
### api-human-cd38-nadase Apigenin inhibited soluble human CD38 NADase activity with IC50 10.3 ± 2.4 micromolar. Figure 3. Corrected axis labels are concentrations on a logarithmic scale, not Log[concentration] values. Model and exposure: Recombinant soluble human CD38; fluorescent NAD substrate, 0.2 mM. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated. Reference: Erratum: Apigenin inhibits the NADase CD38 | 2014 | https://doi.org/10.2337/db14-er04 | Access: Publisher erratum PDF read: Figures 3, 4 and 5 concentration axes should not be labelled Log[concentration]; the scale itself is logarithmic.
Complete structured claim and evidence
Apigenin inhibited human CD38 ADP-ribosyl cyclase activity with IC50 12.8 ± 1.6 micromolar.
Apigenin → Human CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.; Publisher erratum PDF read: Figures 3, 4 and 5 concentration axes should not be labelled Log[concentration]; the scale itself is logarithmic.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "Enzyme without inhibitor", "endpoint": "Apigenin inhibited human CD38 ADP-ribosyl cyclase activity with IC50 12.8 ± 1.6 micromolar.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Recombinant soluble enzyme; cyclase assay.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited human CD38 ADP-ribosyl cyclase activity with IC50 12.8 ± 1.6 micromolar.
primary_references
Erratum: Apigenin inhibits the NADase CD38 | https://doi.org/10.2337/db14-er04
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-human-cd38-cyclase; Separate assay from NAD hydrolysis.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 159–166
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant soluble enzyme; cyclase assay. · Recorded from source · Recorded from source
### api-human-cd38-cyclase Apigenin inhibited human CD38 ADP-ribosyl cyclase activity with IC50 12.8 ± 1.6 micromolar. Separate assay from NAD hydrolysis. Model and exposure: Recombinant soluble enzyme; cyclase assay. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated. Reference: Erratum: Apigenin inhibits the NADase CD38 | 2014 | https://doi.org/10.2337/db14-er04 | Access: Publisher erratum PDF read: Figures 3, 4 and 5 concentration axes should not be labelled Log[concentration]; the scale itself is logarithmic.
Complete structured claim and evidence
Apigenin inhibited cellular CD38 activity in A549 cells with IC50 14.8 ± 2.2 micromolar.
Apigenin → Human CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "Vehicle", "endpoint": "Apigenin inhibited cellular CD38 activity in A549 cells with IC50 14.8 ± 2.2 micromolar.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human A549 lung carcinoma cell line.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited cellular CD38 activity in A549 cells with IC50 14.8 ± 2.2 micromolar.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-a549-cd38; Cell assay potency is not proof of human oral target engagement.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 168–174
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human A549 lung carcinoma cell line. · Recorded from source · Recorded from source
### api-a549-cd38 Apigenin inhibited cellular CD38 activity in A549 cells with IC50 14.8 ± 2.2 micromolar. Cell assay potency is not proof of human oral target engagement. Model and exposure: Human A549 lung carcinoma cell line. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin at 25 micromolar for 6 hours increased measured cellular NAD+ in the reported human-cell experiments.
Apigenin → Whole-cell NAD+ content Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "25 micromolar apigenin for 6 hours", "comparator": "Vehicle", "endpoint": "Apigenin at 25 micromolar for 6 hours increased measured cellular NAD+ in the reported human-cell experiments.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
A549 and HepG2 cell experiments; Figure 4.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin at 25 micromolar for 6 hours increased measured cellular NAD+ in the reported human-cell experiments.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-cellular-nad;
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 176–182
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · A549 and HepG2 cell experiments; Figure 4. · Recorded from source · Recorded from source
### api-cellular-nad Apigenin at 25 micromolar for 6 hours increased measured cellular NAD+ in the reported human-cell experiments. Model and exposure: A549 and HepG2 cell experiments; Figure 4. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased NAD+ in wild-type mouse embryonic fibroblasts but produced no further NAD+ increase in CD38-knockout fibroblasts.
Apigenin → Whole-cell NAD+ content Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
Vehicle in Cd38-null cells Apigenin in Cd38-null cells · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Vehicle in Cd38-null cells genetically absent · Mouse CD38 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin in Cd38-null cells", "comparator": "Vehicle in Cd38-null cells", "endpoint": "Apigenin increased NAD+ in wild-type mouse embryonic fibroblasts but produced no further NAD+ increase in CD38-knockout fibroblasts.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin in Cd38-null cells"}, {"entity_slug": "mouse-cd38", "state": "genetically absent"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse wild-type and Cd38-null MEFs; 25 micromolar, 6 hours.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased NAD+ in wild-type mouse embryonic fibroblasts but produced no further NAD+ increase in CD38-knockout fibroblasts.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-cd38-knockout-nad; Figure 4 supports CD38 dependence of this NAD endpoint under these conditions, not of every apigenin phenotype.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 184–190
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse wild-type and Cd38-null MEFs; 25 micromolar, 6 hours. · Recorded from source · Recorded from source
### api-cd38-knockout-nad Apigenin increased NAD+ in wild-type mouse embryonic fibroblasts but produced no further NAD+ increase in CD38-knockout fibroblasts. Figure 4 supports CD38 dependence of this NAD endpoint under these conditions, not of every apigenin phenotype. Model and exposure: Mouse wild-type and Cd38-null MEFs; 25 micromolar, 6 hours. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin did not directly activate recombinant SIRT1 in the tested 0–100 micromolar series.
Apigenin → SIRT1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "Assay without apigenin", "endpoint": "Apigenin did not directly activate recombinant SIRT1 in the tested 0–100 micromolar series.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Cell-free SIRT1 assay.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin did not directly activate recombinant SIRT1 in the tested 0–100 micromolar series.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-direct-sirt1-null; The paper instead investigated NAD preservation upstream of cellular deacetylation.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 192–198
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Cell-free SIRT1 assay. · Recorded from source · Recorded from source
### api-direct-sirt1-null Apigenin did not directly activate recombinant SIRT1 in the tested 0–100 micromolar series. The paper instead investigated NAD preservation upstream of cellular deacetylation. Model and exposure: Cell-free SIRT1 assay. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin lowered protein acetylation in HepG2 cells, and EX-527 blocked this response.
Apigenin → Human cell protein acetylation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin lowered protein acetylation in HepG2 cells, and EX-527 blocked this response.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human HepG2 cells; 25 micromolar apigenin, 6 hours; 10 micromolar EX-527.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin lowered protein acetylation in HepG2 cells, and EX-527 blocked this response.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-cell-deacetylation; Inhibitor sensitivity supports a SIRT1-associated cellular response; it does not contradict the absence of direct SIRT1 activation.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 200–206
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human HepG2 cells; 25 micromolar apigenin, 6 hours; 10 micromolar EX-527. · Recorded from source · Recorded from source
### api-cell-deacetylation Apigenin lowered protein acetylation in HepG2 cells, and EX-527 blocked this response. Inhibitor sensitivity supports a SIRT1-associated cellular response; it does not contradict the absence of direct SIRT1 activation. Model and exposure: Human HepG2 cells; 25 micromolar apigenin, 6 hours; 10 micromolar EX-527. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin reduced triglyceride accumulation in lipid-loaded HepG2 cells; EX-527 suppressed the response.
Apigenin → HepG2 triglycerides in the apigenin lipid-loading experiment Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin during lipid loading", "comparator": "Same lipid loading without apigenin", "endpoint": "Apigenin reduced triglyceride accumulation in lipid-loaded HepG2 cells; EX-527 suppressed the response.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
0.5 mM oleate/palmitate, 2:1; 25 micromolar apigenin.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced triglyceride accumulation in lipid-loaded HepG2 cells; EX-527 suppressed the response.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-hepg2-lipids; Does not identify fatty-acid oxidation flux as the sole cause.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 208–214
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 0.5 mM oleate/palmitate, 2:1; 25 micromolar apigenin. · Recorded from source · Recorded from source
### api-hepg2-lipids Apigenin reduced triglyceride accumulation in lipid-loaded HepG2 cells; EX-527 suppressed the response. Does not identify fatty-acid oxidation flux as the sole cause. Model and exposure: 0.5 mM oleate/palmitate, 2:1; 25 micromolar apigenin. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin reduced hepatic CD38 activity in high-fat-fed mice.
Apigenin → Mouse CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin in high-fat-fed mice", "comparator": "High-fat-fed vehicle controls", "endpoint": "Apigenin reduced hepatic CD38 activity in high-fat-fed mice.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
100 mg/kg intraperitoneally daily for 7 days; n=6 per group.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced hepatic CD38 activity in high-fat-fed mice.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-mouse-cd38-activity; This pharmacological injection regimen is not a dietary human exposure.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 216–222
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 100 mg/kg intraperitoneally daily for 7 days; n=6 per group. · Recorded from source · Recorded from source
### api-mouse-cd38-activity Apigenin reduced hepatic CD38 activity in high-fat-fed mice. This pharmacological injection regimen is not a dietary human exposure. Model and exposure: 100 mg/kg intraperitoneally daily for 7 days; n=6 per group. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
The injected apigenin regimen increased mouse liver NAD+ and decreased global protein acetylation.
Apigenin → Whole-cell NAD+ content Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "The injected apigenin regimen increased mouse liver NAD+ and decreased global protein acetylation.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
High-fat-fed mice; 100 mg/kg intraperitoneally, 7 days.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The injected apigenin regimen increased mouse liver NAD+ and decreased global protein acetylation.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-mouse-liver-nad; NAD+ pool size and protein acetylation are distinct measured endpoints.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 224–230
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · High-fat-fed mice; 100 mg/kg intraperitoneally, 7 days. · Recorded from source · Recorded from source
### api-mouse-liver-nad The injected apigenin regimen increased mouse liver NAD+ and decreased global protein acetylation. NAD+ pool size and protein acetylation are distinct measured endpoints. Model and exposure: High-fat-fed mice; 100 mg/kg intraperitoneally, 7 days. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
The seven-day apigenin regimen did not change hepatic CD38, SIRT1 or NAMPT protein abundance.
Apigenin → Mouse CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "The seven-day apigenin regimen did not change hepatic CD38, SIRT1 or NAMPT protein abundance.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
High-fat-fed mice; western blots.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The seven-day apigenin regimen did not change hepatic CD38, SIRT1 or NAMPT protein abundance.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-mouse-protein-null; Activity inhibition must not be rewritten as protein depletion.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 232–238
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · High-fat-fed mice; western blots. · Recorded from source · Recorded from source
### api-mouse-protein-null The seven-day apigenin regimen did not change hepatic CD38, SIRT1 or NAMPT protein abundance. Activity inhibition must not be rewritten as protein depletion. Model and exposure: High-fat-fed mice; western blots. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Hepatic AMPK phosphorylation did not change detectably in this apigenin experiment.
Apigenin → Mouse AMPK complexes Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Hepatic AMPK phosphorylation did not change detectably in this apigenin experiment.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
High-fat-fed mice, 100 mg/kg intraperitoneally for 7 days.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Hepatic AMPK phosphorylation did not change detectably in this apigenin experiment.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-mouse-ampk-null; Do not label every metabolic effect AMPK-mediated.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 240–246
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · High-fat-fed mice, 100 mg/kg intraperitoneally for 7 days. · Recorded from source · Recorded from source
### api-mouse-ampk-null Hepatic AMPK phosphorylation did not change detectably in this apigenin experiment. Do not label every metabolic effect AMPK-mediated. Model and exposure: High-fat-fed mice, 100 mg/kg intraperitoneally for 7 days. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin lowered liver triglycerides in the high-fat-fed mouse experiment.
Apigenin → Hepatic triglycerides in apigenin-treated mice Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin lowered liver triglycerides in the high-fat-fed mouse experiment.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Seven-day intraperitoneal regimen.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin lowered liver triglycerides in the high-fat-fed mouse experiment.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-mouse-tg; Altered synthesis, export and oxidation remain alternatives.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 248–254
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Seven-day intraperitoneal regimen. · Recorded from source · Recorded from source
### api-mouse-tg Apigenin lowered liver triglycerides in the high-fat-fed mouse experiment. Altered synthesis, export and oxidation remain alternatives. Model and exposure: Seven-day intraperitoneal regimen. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased hepatic ACADM mRNA in the high-fat-fed mouse experiment.
Apigenin → Mouse medium-chain acyl-CoA dehydrogenase / Acadm Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin increased hepatic ACADM mRNA in the high-fat-fed mouse experiment.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
100 mg/kg intraperitoneally daily, 7 days.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased hepatic ACADM mRNA in the high-fat-fed mouse experiment.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-mouse-acadm; Transcript abundance is not enzyme activity or measured fatty-acid oxidation flux.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 256–262
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 100 mg/kg intraperitoneally daily, 7 days. · Recorded from source · Recorded from source
### api-mouse-acadm Apigenin increased hepatic ACADM mRNA in the high-fat-fed mouse experiment. Transcript abundance is not enzyme activity or measured fatty-acid oxidation flux. Model and exposure: 100 mg/kg intraperitoneally daily, 7 days. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased hepatic ACADL mRNA in the high-fat-fed mouse experiment.
Apigenin → Mouse long-chain acyl-CoA dehydrogenase / Acadl Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin increased hepatic ACADL mRNA in the high-fat-fed mouse experiment.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
100 mg/kg intraperitoneally daily, 7 days.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased hepatic ACADL mRNA in the high-fat-fed mouse experiment.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-mouse-acadl; Transcript abundance is not enzyme activity or measured fatty-acid oxidation flux.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 264–270
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 100 mg/kg intraperitoneally daily, 7 days. · Recorded from source · Recorded from source
### api-mouse-acadl Apigenin increased hepatic ACADL mRNA in the high-fat-fed mouse experiment. Transcript abundance is not enzyme activity or measured fatty-acid oxidation flux. Model and exposure: 100 mg/kg intraperitoneally daily, 7 days. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin improved glucose-tolerance readouts and lowered fasting glucose in high-fat-fed mice.
Apigenin → Mouse glucose tolerance in the 2013 apigenin study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin improved glucose-tolerance readouts and lowered fasting glucose in high-fat-fed mice.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Same seven-day injection regimen.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin improved glucose-tolerance readouts and lowered fasting glucose in high-fat-fed mice.
primary_references
Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139
source_locator
Reviewed reference api-mouse-glucose; No clinical diabetes efficacy follows from this experiment.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 272–278
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Same seven-day injection regimen. · Recorded from source · Recorded from source
### api-mouse-glucose Apigenin improved glucose-tolerance readouts and lowered fasting glucose in high-fat-fed mice. No clinical diabetes efficacy follows from this experiment. Model and exposure: Same seven-day injection regimen. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23172919/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ | https://doi.org/10.2337/db12-1139 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
CIB1 interacted with cytosol-facing type-III CD38 in the reported human-cell models.
Human calcium and integrin-binding protein 1 / CIB1 → Human CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_model
Human myeloma cells and topology-sensitive nanobody assays.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
CIB1 interacted with cytosol-facing type-III CD38 in the reported human-cell models.
primary_references
Cytosolic interaction of type III human CD38 with CIB1 modulates cellular cyclic ADP-ribose levels. | https://pubmed.ncbi.nlm.nih.gov/28720704/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5547619/ | https://doi.org/10.1073/pnas.1703718114
source_locator
Reviewed reference api-cib1-typeiii; This study did not test apigenin. Cytosolic and extracellular CD38 topology are not interchangeable.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 280–286
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human myeloma cells and topology-sensitive nanobody assays. · Recorded from source · Recorded from source
### api-cib1-typeiii CIB1 interacted with cytosol-facing type-III CD38 in the reported human-cell models. This study did not test apigenin. Cytosolic and extracellular CD38 topology are not interchangeable. Model and exposure: Human myeloma cells and topology-sensitive nanobody assays. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Cytosolic interaction of type III human CD38 with CIB1 modulates cellular cyclic ADP-ribose levels. | 2017 | https://pubmed.ncbi.nlm.nih.gov/28720704/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5547619/ | https://doi.org/10.1073/pnas.1703718114 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
CIB1 knockdown or knockout reduced cADPR production in the type-III CD38 study.
Human calcium and integrin-binding protein 1 / CIB1 → Cyclic ADP-ribose Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "CIB1 knockdown or knockout", "comparator": "Matched CIB1-intact controls", "endpoint": "CIB1 knockdown or knockout reduced cADPR production in the type-III CD38 study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human-cell perturbation experiments; primary abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
CIB1 knockdown or knockout reduced cADPR production in the type-III CD38 study.
primary_references
Cytosolic interaction of type III human CD38 with CIB1 modulates cellular cyclic ADP-ribose levels. | https://pubmed.ncbi.nlm.nih.gov/28720704/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5547619/ | https://doi.org/10.1073/pnas.1703718114
source_locator
Reviewed reference api-cib1-loss; No apigenin intervention. This is a requirement test for intracellular CD38 regulation, not evidence of impaired dietary calcium supply.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 288–294
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human-cell perturbation experiments; primary abstract. · Recorded from source · Recorded from source
### api-cib1-loss CIB1 knockdown or knockout reduced cADPR production in the type-III CD38 study. No apigenin intervention. This is a requirement test for intracellular CD38 regulation, not evidence of impaired dietary calcium supply. Model and exposure: Human-cell perturbation experiments; primary abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Cytosolic interaction of type III human CD38 with CIB1 modulates cellular cyclic ADP-ribose levels. | 2017 | https://pubmed.ncbi.nlm.nih.gov/28720704/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5547619/ | https://doi.org/10.1073/pnas.1703718114 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin reduced CD38 expression in monosodium-urate-stimulated mouse bone-marrow macrophages.
Apigenin → Mouse CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
MSU alone Apigenin plus MSU · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
MSU alone 0.2 mg/mL MSU challenge · Monosodium urate crystals Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin plus MSU", "comparator": "MSU alone", "endpoint": "Apigenin reduced CD38 expression in monosodium-urate-stimulated mouse bone-marrow macrophages.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin plus MSU"}, {"entity_slug": "monosodium-urate-crystals", "state": "0.2 mg/mL MSU challenge"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
25 micromolar apigenin; MSU 0.2 mg/mL; 6- and 24-hour readouts.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced CD38 expression in monosodium-urate-stimulated mouse bone-marrow macrophages.
primary_references
The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target. | https://pubmed.ncbi.nlm.nih.gov/38493256/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11058052/ | https://doi.org/10.1007/s00011-024-01863-y
source_locator
Reviewed reference api-gout-cd38;
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 300–306
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 25 micromolar apigenin; MSU 0.2 mg/mL; 6- and 24-hour readouts. · Recorded from source · Recorded from source
### api-gout-cd38 Apigenin reduced CD38 expression in monosodium-urate-stimulated mouse bone-marrow macrophages. Model and exposure: 25 micromolar apigenin; MSU 0.2 mg/mL; 6- and 24-hour readouts. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target. | 2024 | https://pubmed.ncbi.nlm.nih.gov/38493256/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11058052/ | https://doi.org/10.1007/s00011-024-01863-y | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased the NAD+/NADH ratio in the MSU experiment mainly by reducing the MSU-associated NADH increase.
Apigenin → Cellular NAD+/NADH ratio Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
MSU alone Apigenin plus MSU · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
MSU alone 0.2 mg/mL MSU challenge · Monosodium urate crystals Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin plus MSU", "comparator": "MSU alone", "endpoint": "Apigenin increased the NAD+/NADH ratio in the MSU experiment mainly by reducing the MSU-associated NADH increase.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin plus MSU"}, {"entity_slug": "monosodium-urate-crystals", "state": "0.2 mg/mL MSU challenge"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse BMDMs; separate NAD+ and NADH assay readouts.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased the NAD+/NADH ratio in the MSU experiment mainly by reducing the MSU-associated NADH increase.
primary_references
The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target. | https://pubmed.ncbi.nlm.nih.gov/38493256/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11058052/ | https://doi.org/10.1007/s00011-024-01863-y
source_locator
Reviewed reference api-gout-nad-ratio; A higher ratio does not itself demonstrate more NAD+ molecules.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 308–314
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse BMDMs; separate NAD+ and NADH assay readouts. · Recorded from source · Recorded from source
### api-gout-nad-ratio Apigenin increased the NAD+/NADH ratio in the MSU experiment mainly by reducing the MSU-associated NADH increase. A higher ratio does not itself demonstrate more NAD+ molecules. Model and exposure: Mouse BMDMs; separate NAD+ and NADH assay readouts. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target. | 2024 | https://pubmed.ncbi.nlm.nih.gov/38493256/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11058052/ | https://doi.org/10.1007/s00011-024-01863-y | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin restored SIRT3 protein abundance and decreased acetylated SOD2 in MSU-challenged mouse macrophages.
Apigenin → Mouse mitochondrial sirtuin 3 / Sirt3 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
MSU alone Apigenin plus MSU · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
MSU alone 0.2 mg/mL MSU challenge · Monosodium urate crystals Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin plus MSU", "comparator": "MSU alone", "endpoint": "Apigenin restored SIRT3 protein abundance and decreased acetylated SOD2 in MSU-challenged mouse macrophages.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin plus MSU"}, {"entity_slug": "monosodium-urate-crystals", "state": "0.2 mg/mL MSU challenge"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse BMDMs; 25 micromolar apigenin.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin restored SIRT3 protein abundance and decreased acetylated SOD2 in MSU-challenged mouse macrophages.
primary_references
The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target. | https://pubmed.ncbi.nlm.nih.gov/38493256/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11058052/ | https://doi.org/10.1007/s00011-024-01863-y
source_locator
Reviewed reference api-gout-sirt3; Restored SIRT3 protein is not a direct binding or activity assay.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 316–322
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse BMDMs; 25 micromolar apigenin. · Recorded from source · Recorded from source
### api-gout-sirt3 Apigenin restored SIRT3 protein abundance and decreased acetylated SOD2 in MSU-challenged mouse macrophages. Restored SIRT3 protein is not a direct binding or activity assay. Model and exposure: Mouse BMDMs; 25 micromolar apigenin. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target. | 2024 | https://pubmed.ncbi.nlm.nih.gov/38493256/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11058052/ | https://doi.org/10.1007/s00011-024-01863-y | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin reduced NLRP3 expression and accompanying caspase-1 activation and IL-1β release in the urate-crystal macrophage model.
Apigenin → Mouse NLRP3 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
MSU alone Apigenin plus MSU · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
MSU alone 0.2 mg/mL MSU challenge · Monosodium urate crystals Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin plus MSU", "comparator": "MSU alone", "endpoint": "Apigenin reduced NLRP3 expression and accompanying caspase-1 activation and IL-1β release in the urate-crystal macrophage model.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin plus MSU"}, {"entity_slug": "monosodium-urate-crystals", "state": "0.2 mg/mL MSU challenge"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
MSU-stimulated mouse BMDMs; longer exposure than the 2025 post-priming experiments.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced NLRP3 expression and accompanying caspase-1 activation and IL-1β release in the urate-crystal macrophage model.
primary_references
The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target. | https://pubmed.ncbi.nlm.nih.gov/38493256/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11058052/ | https://doi.org/10.1007/s00011-024-01863-y
source_locator
Reviewed reference api-gout-nlrp3; CD38 knockout/inhibitor comparisons in this study support a contribution in this model, not unique mediation across all stimuli.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 324–330
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · MSU-stimulated mouse BMDMs; longer exposure than the 2025 post-priming experiments. · Recorded from source · Recorded from source
### api-gout-nlrp3 Apigenin reduced NLRP3 expression and accompanying caspase-1 activation and IL-1β release in the urate-crystal macrophage model. CD38 knockout/inhibitor comparisons in this study support a contribution in this model, not unique mediation across all stimuli. Model and exposure: MSU-stimulated mouse BMDMs; longer exposure than the 2025 post-priming experiments. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target. | 2024 | https://pubmed.ncbi.nlm.nih.gov/38493256/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11058052/ | https://doi.org/10.1007/s00011-024-01863-y | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin reduced ATP-, MSU- and nigericin-triggered IL-1β release from LPS-primed human monocytes and macrophages.
Apigenin → Interleukin-1 beta / IL1B Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin before the second activation signal", "comparator": "Same priming and activator without apigenin", "endpoint": "Apigenin reduced ATP-, MSU- and nigericin-triggered IL-1β release from LPS-primed human monocytes and macrophages.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
100 micromolar apigenin after LPS priming; 30-min pretreatment; ATP 3 mM, MSU 200 micrograms/mL or nigericin 10 micromolar.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced ATP-, MSU- and nigericin-triggered IL-1β release from LPS-primed human monocytes and macrophages.
primary_references
Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984
source_locator
Reviewed reference api-human-inflammasome; Figures 1 and 3. Pharmacological exposure; not demonstrated at oral human parent concentrations.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 332–338
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 100 micromolar apigenin after LPS priming; 30-min pretreatment; ATP 3 mM, MSU 200 micrograms/mL or nigericin 10 micromolar. · Recorded from source · Recorded from source
### api-human-inflammasome Apigenin reduced ATP-, MSU- and nigericin-triggered IL-1β release from LPS-primed human monocytes and macrophages. Figures 1 and 3. Pharmacological exposure; not demonstrated at oral human parent concentrations. Model and exposure: 100 micromolar apigenin after LPS priming; 30-min pretreatment; ATP 3 mM, MSU 200 micrograms/mL or nigericin 10 micromolar. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | 2024 | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin strongly reduced ATP-triggered cytosolic calcium mobilization in LPS-primed human macrophages.
Apigenin → Human macrophage cytosolic calcium response Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
ATP without apigenin Apigenin before ATP · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
ATP without apigenin extracellular activation signal · ATP Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
ATP without apigenin prior priming · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin before ATP", "comparator": "ATP without apigenin", "endpoint": "Apigenin strongly reduced ATP-triggered cytosolic calcium mobilization in LPS-primed human macrophages.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin before ATP"}, {"entity_slug": "lipopolysaccharide", "state": "prior priming"}, {"entity_slug": "atp", "state": "extracellular activation signal"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Fluo-4 imaging; 100 micromolar apigenin, 30 minutes, then ATP 3 mM.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin strongly reduced ATP-triggered cytosolic calcium mobilization in LPS-primed human macrophages.
primary_references
Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984
source_locator
Reviewed reference api-human-calcium; The responsible direct target was not established; do not assume a P2X7-only mechanism.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 340–346
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Fluo-4 imaging; 100 micromolar apigenin, 30 minutes, then ATP 3 mM. · Recorded from source · Recorded from source
### api-human-calcium Apigenin strongly reduced ATP-triggered cytosolic calcium mobilization in LPS-primed human macrophages. The responsible direct target was not established; do not assume a P2X7-only mechanism. Model and exposure: Fluo-4 imaging; 100 micromolar apigenin, 30 minutes, then ATP 3 mM. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | 2024 | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Thirty-minute apigenin exposure did not detectably raise NAD+ in the human primary-macrophage assay.
Apigenin → Whole-cell NAD+ content Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin for 30 minutes", "comparator": "Untreated macrophages", "endpoint": "Thirty-minute apigenin exposure did not detectably raise NAD+ in the human primary-macrophage assay.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Figure 2G; increasing apigenin doses, short exposure.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Thirty-minute apigenin exposure did not detectably raise NAD+ in the human primary-macrophage assay.
primary_references
Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984
source_locator
Reviewed reference api-human-nad-short-null; This does not refute the six-hour NAD response in other cell types; time and cell identity matter.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 348–354
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Figure 2G; increasing apigenin doses, short exposure. · Recorded from source · Recorded from source
### api-human-nad-short-null Thirty-minute apigenin exposure did not detectably raise NAD+ in the human primary-macrophage assay. This does not refute the six-hour NAD response in other cell types; time and cell identity matter. Model and exposure: Figure 2G; increasing apigenin doses, short exposure. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | 2024 | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Short apigenin treatment after LPS priming did not decrease pro-IL-1β protein in the initial human-cell experiment.
Apigenin → Interleukin-1 beta / IL1B Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
LPS priming alone Apigenin after completed priming · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS priming alone prior priming · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin after completed priming", "comparator": "LPS priming alone", "endpoint": "Short apigenin treatment after LPS priming did not decrease pro-IL-1β protein in the initial human-cell experiment.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin after completed priming"}, {"entity_slug": "lipopolysaccharide", "state": "prior priming"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Figure 1E–G; 100 micromolar, 30 minutes; immunoblot pro-protein.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Short apigenin treatment after LPS priming did not decrease pro-IL-1β protein in the initial human-cell experiment.
primary_references
Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984
source_locator
Reviewed reference api-human-proil1b-null; Reduced release can occur without reduced precursor synthesis. TNF was unchanged in the initial experiment, although some later comparisons showed reductions.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 356–362
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Figure 1E–G; 100 micromolar, 30 minutes; immunoblot pro-protein. · Recorded from source · Recorded from source
### api-human-proil1b-null Short apigenin treatment after LPS priming did not decrease pro-IL-1β protein in the initial human-cell experiment. Reduced release can occur without reduced precursor synthesis. TNF was unchanged in the initial experiment, although some later comparisons showed reductions. Model and exposure: Figure 1E–G; 100 micromolar, 30 minutes; immunoblot pro-protein. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | 2024 | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin reduced ATP-induced N-terminal gasdermin-D formation in LPS-primed human monocytes.
Apigenin → GSDMD Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
LPS/ATP alone Apigenin plus LPS/ATP · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS/ATP alone extracellular activation signal · ATP Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS/ATP alone prior priming · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin plus LPS/ATP", "comparator": "LPS/ATP alone", "endpoint": "Apigenin reduced ATP-induced N-terminal gasdermin-D formation in LPS-primed human monocytes.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin plus LPS/ATP"}, {"entity_slug": "lipopolysaccharide", "state": "prior priming"}, {"entity_slug": "atp", "state": "extracellular activation signal"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Figure 3M–N; 100 micromolar apigenin; ATP 3 mM for 15 minutes.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced ATP-induced N-terminal gasdermin-D formation in LPS-primed human monocytes.
primary_references
Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984
source_locator
Reviewed reference api-human-gsdmd; This cleavage readout does not establish direct binding to gasdermin D.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 364–370
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Figure 3M–N; 100 micromolar apigenin; ATP 3 mM for 15 minutes. · Recorded from source · Recorded from source
### api-human-gsdmd Apigenin reduced ATP-induced N-terminal gasdermin-D formation in LPS-primed human monocytes. This cleavage readout does not establish direct binding to gasdermin D. Model and exposure: Figure 3M–N; 100 micromolar apigenin; ATP 3 mM for 15 minutes. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | 2024 | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin still suppressed nigericin-induced IL-1β release in CD38-knockout mouse macrophages, with a similar pattern to wild-type cells.
Apigenin → Mouse IL-1 beta Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
Activated Cd38-null cells without apigenin Apigenin in Cd38-null cells during activation · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Activated Cd38-null cells without apigenin genetically absent · Mouse CD38 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Activated Cd38-null cells without apigenin prior priming · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Activated Cd38-null cells without apigenin activation challenge · Nigericin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin in Cd38-null cells during activation", "comparator": "Activated Cd38-null cells without apigenin", "endpoint": "Apigenin still suppressed nigericin-induced IL-1β release in CD38-knockout mouse macrophages, with a similar pattern to wild-type cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin in Cd38-null cells during activation"}, {"entity_slug": "mouse-cd38", "state": "genetically absent"}, {"entity_slug": "nigericin", "state": "activation challenge"}, {"entity_slug": "lipopolysaccharide", "state": "prior priming"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse BMDMs, n=3; 100 micromolar apigenin; LPS priming and nigericin.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin still suppressed nigericin-induced IL-1β release in CD38-knockout mouse macrophages, with a similar pattern to wild-type cells.
primary_references
Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984
source_locator
Reviewed reference api-mouse-cd38-independent; Figure 5. Small n and genetic adaptation are limitations. This demonstrates that CD38 is not necessary for this apigenin response.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 372–378
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse BMDMs, n=3; 100 micromolar apigenin; LPS priming and nigericin. · Recorded from source · Recorded from source
### api-mouse-cd38-independent Apigenin still suppressed nigericin-induced IL-1β release in CD38-knockout mouse macrophages, with a similar pattern to wild-type cells. Figure 5. Small n and genetic adaptation are limitations. This demonstrates that CD38 is not necessary for this apigenin response. Model and exposure: Mouse BMDMs, n=3; 100 micromolar apigenin; LPS priming and nigericin. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | 2024 | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
CD38-knockout BMDMs retained inflammasome-associated IL-1β responses to the tested activation signals.
Mouse CD38 → Mouse IL-1 beta Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Cd38 knockout", "comparator": "Matched wild-type cells", "endpoint": "CD38-knockout BMDMs retained inflammasome-associated IL-1β responses to the tested activation signals.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
LPS-primed mouse macrophages; ATP, MSU and nigericin; n=3.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
CD38-knockout BMDMs retained inflammasome-associated IL-1β responses to the tested activation signals.
primary_references
Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984
source_locator
Reviewed reference api-mouse-cd38-activation-null; No required CD38 contribution was demonstrated in these comparisons; not a universal statement about all cell types or inflammatory pathways.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 380–386
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · LPS-primed mouse macrophages; ATP, MSU and nigericin; n=3. · Recorded from source · Recorded from source
### api-mouse-cd38-activation-null CD38-knockout BMDMs retained inflammasome-associated IL-1β responses to the tested activation signals. No required CD38 contribution was demonstrated in these comparisons; not a universal statement about all cell types or inflammatory pathways. Model and exposure: LPS-primed mouse macrophages; ATP, MSU and nigericin; n=3. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38. | 2024 | https://pubmed.ncbi.nlm.nih.gov/39840045/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11746122/ | https://doi.org/10.3389/fimmu.2024.1497984 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin bound immobilized recombinant human FGR in a concentration-dependent surface-plasmon-resonance assay.
Apigenin → Human tyrosine-protein kinase FGR Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_model
Recombinant human FGR, 0.5–80 micromolar apigenin; Figure 5I and Methods.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin bound immobilized recombinant human FGR in a concentration-dependent surface-plasmon-resonance assay.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-fgr-binding; DARTS/CETSA in mouse and human macrophage preparations supplied additional association evidence. Docking alone was not treated as binding proof; no unverified numeric KD assigned.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 392–398
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human FGR, 0.5–80 micromolar apigenin; Figure 5I and Methods. · Recorded from source · Recorded from source
### api-fgr-binding Apigenin bound immobilized recombinant human FGR in a concentration-dependent surface-plasmon-resonance assay. DARTS/CETSA in mouse and human macrophage preparations supplied additional association evidence. Docking alone was not treated as binding proof; no unverified numeric KD assigned. Model and exposure: Recombinant human FGR, 0.5–80 micromolar apigenin; Figure 5I and Methods. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin decreased the association of Fgr with Syk in mouse macrophages.
Apigenin → Mouse tyrosine-protein kinase Fgr Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin decreased the association of Fgr with Syk in mouse macrophages.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse BMDMs; co-immunoprecipitation; 20 micromolar apigenin in the cell experiments.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin decreased the association of Fgr with Syk in mouse macrophages.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-mouse-fgr-syk; Association disruption is not equivalent to pan-inhibition of every Fgr kinase function.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 400–406
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse BMDMs; co-immunoprecipitation; 20 micromolar apigenin in the cell experiments. · Recorded from source · Recorded from source
### api-mouse-fgr-syk Apigenin decreased the association of Fgr with Syk in mouse macrophages. Association disruption is not equivalent to pan-inhibition of every Fgr kinase function. Model and exposure: Mouse BMDMs; co-immunoprecipitation; 20 micromolar apigenin in the cell experiments. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased Vav1 phosphorylation in the macrophage phagocytosis experiments.
Apigenin → Mouse Vav1 guanine nucleotide exchange factor Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased Vav1 phosphorylation in the macrophage phagocytosis experiments.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse BMDMs; signaling downstream of the Fgr/Syk interaction.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased Vav1 phosphorylation in the macrophage phagocytosis experiments.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-vav1; These measured readouts are not all direct binding targets.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 408–414
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse BMDMs; signaling downstream of the Fgr/Syk interaction. · Recorded from source · Recorded from source
### api-vav1 Apigenin increased Vav1 phosphorylation in the macrophage phagocytosis experiments. These measured readouts are not all direct binding targets. Model and exposure: Mouse BMDMs; signaling downstream of the Fgr/Syk interaction. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased GTP-loaded Rac1 in the macrophage phagocytosis experiments.
Apigenin → Mouse Rac1 small GTPase Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased GTP-loaded Rac1 in the macrophage phagocytosis experiments.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse BMDMs; signaling downstream of the Fgr/Syk interaction.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased GTP-loaded Rac1 in the macrophage phagocytosis experiments.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-rac1; These measured readouts are not all direct binding targets.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 416–422
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse BMDMs; signaling downstream of the Fgr/Syk interaction. · Recorded from source · Recorded from source
### api-rac1 Apigenin increased GTP-loaded Rac1 in the macrophage phagocytosis experiments. These measured readouts are not all direct binding targets. Model and exposure: Mouse BMDMs; signaling downstream of the Fgr/Syk interaction. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased GTP-loaded Cdc42 in the macrophage phagocytosis experiments.
Apigenin → Mouse Cdc42 small GTPase Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased GTP-loaded Cdc42 in the macrophage phagocytosis experiments.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse BMDMs; signaling downstream of the Fgr/Syk interaction.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased GTP-loaded Cdc42 in the macrophage phagocytosis experiments.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-cdc42; These measured readouts are not all direct binding targets.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 424–430
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse BMDMs; signaling downstream of the Fgr/Syk interaction. · Recorded from source · Recorded from source
### api-cdc42 Apigenin increased GTP-loaded Cdc42 in the macrophage phagocytosis experiments. These measured readouts are not all direct binding targets. Model and exposure: Mouse BMDMs; signaling downstream of the Fgr/Syk interaction. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased Arp2/3 expression in the macrophage phagocytosis experiments.
Apigenin → Mouse Arp2/3 complex Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased Arp2/3 expression in the macrophage phagocytosis experiments.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse BMDMs; signaling downstream of the Fgr/Syk interaction.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased Arp2/3 expression in the macrophage phagocytosis experiments.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-arp23; These measured readouts are not all direct binding targets.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 432–438
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse BMDMs; signaling downstream of the Fgr/Syk interaction. · Recorded from source · Recorded from source
### api-arp23 Apigenin increased Arp2/3 expression in the macrophage phagocytosis experiments. These measured readouts are not all direct binding targets. Model and exposure: Mouse BMDMs; signaling downstream of the Fgr/Syk interaction. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased E. coli bioparticle uptake and bacterial phagocytosis in mouse macrophage experiments.
Apigenin → Mouse macrophage bacterial phagocytosis in the apigenin study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin before bacterial challenge", "comparator": "DMSO before the same challenge", "endpoint": "Apigenin increased E. coli bioparticle uptake and bacterial phagocytosis in mouse macrophage experiments.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse peritoneal macrophages and BMDMs; typical cell exposure 20 micromolar, 3 hours.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased E. coli bioparticle uptake and bacterial phagocytosis in mouse macrophage experiments.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-mouse-phagocytosis; Neutrophil phagocytosis and direct E. coli growth did not show the same response.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 440–446
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse peritoneal macrophages and BMDMs; typical cell exposure 20 micromolar, 3 hours. · Recorded from source · Recorded from source
### api-mouse-phagocytosis Apigenin increased E. coli bioparticle uptake and bacterial phagocytosis in mouse macrophage experiments. Neutrophil phagocytosis and direct E. coli growth did not show the same response. Model and exposure: Mouse peritoneal macrophages and BMDMs; typical cell exposure 20 micromolar, 3 hours. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased bacterial phagocytosis in differentiated human THP-1 macrophages.
Apigenin → Human macrophage bacterial phagocytosis in the apigenin study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin before bacterial challenge", "comparator": "DMSO control", "endpoint": "Apigenin increased bacterial phagocytosis in differentiated human THP-1 macrophages.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
THP1-derived macrophages; apigenin treatment followed by E. coli stimulation.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased bacterial phagocytosis in differentiated human THP-1 macrophages.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-human-phagocytosis; Human cell-line evidence is not a human infection-outcome trial.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 448–454
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · THP1-derived macrophages; apigenin treatment followed by E. coli stimulation. · Recorded from source · Recorded from source
### api-human-phagocytosis Apigenin increased bacterial phagocytosis in differentiated human THP-1 macrophages. Human cell-line evidence is not a human infection-outcome trial. Model and exposure: THP1-derived macrophages; apigenin treatment followed by E. coli stimulation. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Fgr knockdown raised baseline macrophage phagocytosis and blunted the additional response to apigenin.
Apigenin → Mouse macrophage bacterial phagocytosis in the apigenin study Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
Apigenin response with control knockdown Apigenin with Fgr knockdown · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Apigenin response with control knockdown knocked down · Mouse tyrosine-protein kinase Fgr Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin with Fgr knockdown", "comparator": "Apigenin response with control knockdown", "endpoint": "Fgr knockdown raised baseline macrophage phagocytosis and blunted the additional response to apigenin.", "effect_direction": "mixed", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin with Fgr knockdown"}, {"entity_slug": "mouse-fgr", "state": "knocked down"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse macrophage knockdown; Fgr overexpression also weakened the apigenin response.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Fgr knockdown raised baseline macrophage phagocytosis and blunted the additional response to apigenin.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-fgr-knockdown; Baseline and incremental effects must be separated. Epistasis supports involvement without proving a single exclusive target.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 456–462
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse macrophage knockdown; Fgr overexpression also weakened the apigenin response. · Recorded from source · Recorded from source
### api-fgr-knockdown Fgr knockdown raised baseline macrophage phagocytosis and blunted the additional response to apigenin. Baseline and incremental effects must be separated. Epistasis supports involvement without proving a single exclusive target. Model and exposure: Mouse macrophage knockdown; Fgr overexpression also weakened the apigenin response. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin pretreatment improved bacterial-clearance and survival outcomes in aged-mouse CLP and E. coli infection experiments.
Apigenin → Infection outcomes in apigenin-pretreated aged mice Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Prophylactic apigenin before challenge", "comparator": "Vehicle before challenge", "endpoint": "Apigenin pretreatment improved bacterial-clearance and survival outcomes in aged-mouse CLP and E. coli infection experiments.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Oral 10 mg/kg at 27, 15 and 3 hours before challenge.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin pretreatment improved bacterial-clearance and survival outcomes in aged-mouse CLP and E. coli infection experiments.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-mouse-sepsis; This is pretreatment in mice, not established treatment for ongoing human sepsis.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 464–470
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Oral 10 mg/kg at 27, 15 and 3 hours before challenge. · Recorded from source · Recorded from source
### api-mouse-sepsis Apigenin pretreatment improved bacterial-clearance and survival outcomes in aged-mouse CLP and E. coli infection experiments. This is pretreatment in mice, not established treatment for ongoing human sepsis. Model and exposure: Oral 10 mg/kg at 27, 15 and 3 hours before challenge. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
The investigators detected apigenin in P. goldsteinii culture preparations by LC-MS and linked bacterial administration to host apigenin measurements.
Parabacteroides goldsteinii → Apigenin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_model
Cultured bacterium, germ-free/aged mouse experiments and metabolite measurements.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The investigators detected apigenin in P. goldsteinii culture preparations by LC-MS and linked bacterial administration to host apigenin measurements.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-bacterial-production; Human abundance/metabolite associations are observational. The plant-like biosynthetic pathway was not completely reconstituted.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 472–478
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Cultured bacterium, germ-free/aged mouse experiments and metabolite measurements. · Recorded from source · Recorded from source
### api-bacterial-production The investigators detected apigenin in P. goldsteinii culture preparations by LC-MS and linked bacterial administration to host apigenin measurements. Human abundance/metabolite associations are observational. The plant-like biosynthetic pathway was not completely reconstituted. Model and exposure: Cultured bacterium, germ-free/aged mouse experiments and metabolite measurements. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Deleting bacterial ampB eliminated the reported apigenin signal without the same loss of growth or colonization in the tested P. goldsteinii model.
Parabacteroides goldsteinii AmpB candidate biosynthetic protein → Apigenin Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "ampB knockout", "comparator": "Wild-type bacterium", "endpoint": "Deleting bacterial ampB eliminated the reported apigenin signal without the same loss of growth or colonization in the tested P. goldsteinii model.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Bacterial knockout and mouse colonization experiments.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Deleting bacterial ampB eliminated the reported apigenin signal without the same loss of growth or colonization in the tested P. goldsteinii model.
primary_references
Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008
source_locator
Reviewed reference api-ampb-loss; Supports a genetic requirement in this model; docking and structural similarity do not by themselves prove AmpB is a purified chalcone synthase.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 480–486
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Bacterial knockout and mouse colonization experiments. · Recorded from source · Recorded from source
### api-ampb-loss Deleting bacterial ampB eliminated the reported apigenin signal without the same loss of growth or colonization in the tested P. goldsteinii model. Supports a genetic requirement in this model; docking and structural similarity do not by themselves prove AmpB is a purified chalcone synthase. Model and exposure: Bacterial knockout and mouse colonization experiments. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Aging-induced Alternation in the Gut Microbiota Impairs Host Antibacterial Defense. | 2025 | https://pubmed.ncbi.nlm.nih.gov/39792643/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC11948050/ | https://doi.org/10.1002/advs.202411008 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
The 2024 multicomponent trial reported a 26.5% increase from baseline at day 28 in its main whole-blood NAD assay.
Nuchido TIME+ multicomponent preparation in the 2024 trial → Whole-blood NAD+ plus NADH assay signal Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Nuchido TIME+ for 28 days", "comparator": "The active-arm baseline", "endpoint": "The 2024 multicomponent trial reported a 26.5% increase from baseline at day 28 in its main whole-blood NAD assay.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Randomized double-blind crossover; 26 completed, 23 in the main assay analysis.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The 2024 multicomponent trial reported a 26.5% increase from baseline at day 28 in its main whole-blood NAD assay.
primary_references
The use of a systems approach to increase NAD+ in human participants. | https://pubmed.ncbi.nlm.nih.gov/38302501/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10834541/ | https://doi.org/10.1038/s41514-023-00134-0
source_locator
Reviewed reference api-human-combined-nad; The Methods describe total NAD+ plus NADH, despite NAD+ terminology elsewhere. Main P=0.007. This is not an isolated-apigenin trial or demonstrated slowing of aging.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 492–498
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Randomized double-blind crossover; 26 completed, 23 in the main assay analysis. · Recorded from source · Recorded from source
### api-human-combined-nad The 2024 multicomponent trial reported a 26.5% increase from baseline at day 28 in its main whole-blood NAD assay. The Methods describe total NAD+ plus NADH, despite NAD+ terminology elsewhere. Main P=0.007. This is not an isolated-apigenin trial or demonstrated slowing of aging. Model and exposure: Randomized double-blind crossover; 26 completed, 23 in the main assay analysis. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The use of a systems approach to increase NAD+ in human participants. | 2024 | https://pubmed.ncbi.nlm.nih.gov/38302501/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10834541/ | https://doi.org/10.1038/s41514-023-00134-0 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
The smaller LC-MS subset did not show a statistically significant NAD+ treatment effect in the same human trial.
Nuchido TIME+ multicomponent preparation in the 2024 trial → Circulating NAD content Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Multicomponent preparation", "comparator": "Baseline and placebo comparisons reported by the study", "endpoint": "The smaller LC-MS subset did not show a statistically significant NAD+ treatment effect in the same human trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Seventeen-person subset; stored samples and missing participants.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The smaller LC-MS subset did not show a statistically significant NAD+ treatment effect in the same human trial.
primary_references
The use of a systems approach to increase NAD+ in human participants. | https://pubmed.ncbi.nlm.nih.gov/38302501/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10834541/ | https://doi.org/10.1038/s41514-023-00134-0
source_locator
Reviewed reference api-human-combined-lcms-null; Matched reduction of the main assay sample also lost significance. Sample size, selection, storage and assay identity limit comparison.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 500–506
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Seventeen-person subset; stored samples and missing participants. · Recorded from source · Recorded from source
### api-human-combined-lcms-null The smaller LC-MS subset did not show a statistically significant NAD+ treatment effect in the same human trial. Matched reduction of the main assay sample also lost significance. Sample size, selection, storage and assay identity limit comparison. Model and exposure: Seventeen-person subset; stored samples and missing participants. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The use of a systems approach to increase NAD+ in human participants. | 2024 | https://pubmed.ncbi.nlm.nih.gov/38302501/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10834541/ | https://doi.org/10.1038/s41514-023-00134-0 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
PBMC CD38 protein abundance did not change detectably during the 2024 combined-product trial.
Nuchido TIME+ multicomponent preparation in the 2024 trial → Human CD38 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Multicomponent preparation", "comparator": "Study baseline/placebo comparisons", "endpoint": "PBMC CD38 protein abundance did not change detectably during the 2024 combined-product trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
PBMC protein assays; 28-day intervention.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
PBMC CD38 protein abundance did not change detectably during the 2024 combined-product trial.
primary_references
The use of a systems approach to increase NAD+ in human participants. | https://pubmed.ncbi.nlm.nih.gov/38302501/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10834541/ | https://doi.org/10.1038/s41514-023-00134-0
source_locator
Reviewed reference api-human-combined-cd38-null; Protein amount is not enzyme activity; this does not measure direct apigenin occupancy or CD38 inhibition.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 508–514
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · PBMC protein assays; 28-day intervention. · Recorded from source · Recorded from source
### api-human-combined-cd38-null PBMC CD38 protein abundance did not change detectably during the 2024 combined-product trial. Protein amount is not enzyme activity; this does not measure direct apigenin occupancy or CD38 inhibition. Model and exposure: PBMC protein assays; 28-day intervention. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The use of a systems approach to increase NAD+ in human participants. | 2024 | https://pubmed.ncbi.nlm.nih.gov/38302501/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10834541/ | https://doi.org/10.1038/s41514-023-00134-0 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
The combined-product study reported increased PBMC NAMPT and SIRT1 protein abundance.
Nuchido TIME+ multicomponent preparation in the 2024 trial → Human nicotinamide phosphoribosyltransferase / NAMPT Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Multicomponent preparation", "comparator": "Study baseline comparison", "endpoint": "The combined-product study reported increased PBMC NAMPT and SIRT1 protein abundance.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human crossover trial; multicomponent preparation.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The combined-product study reported increased PBMC NAMPT and SIRT1 protein abundance.
primary_references
The use of a systems approach to increase NAD+ in human participants. | https://pubmed.ncbi.nlm.nih.gov/38302501/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10834541/ | https://doi.org/10.1038/s41514-023-00134-0
source_locator
Reviewed reference api-human-combined-nampt; Individual ingredient causality and enzyme flux were not isolated.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 516–522
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human crossover trial; multicomponent preparation. · Recorded from source · Recorded from source
### api-human-combined-nampt The combined-product study reported increased PBMC NAMPT and SIRT1 protein abundance. Individual ingredient causality and enzyme flux were not isolated. Model and exposure: Human crossover trial; multicomponent preparation. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: The use of a systems approach to increase NAD+ in human participants. | 2024 | https://pubmed.ncbi.nlm.nih.gov/38302501/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10834541/ | https://doi.org/10.1038/s41514-023-00134-0 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
NMN plus apigenin increased NAD+ and the NAD+/NADH ratio in the 2026 oxidative-stress musculoskeletal-cell experiments.
NMN plus apigenin preparation in the 2026 musculoskeletal study → Cellular NAD+/NADH ratio Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
experimental_condition
Stressed controls; monotherapy comparisons also reported co-administered · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Stressed controls; monotherapy comparisons also reported NMN plus apigenin during the stress model · NMN plus apigenin preparation in the 2026 musculoskeletal study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Stressed controls; monotherapy comparisons also reported co-administered · NMN Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "NMN plus apigenin during the stress model", "comparator": "Stressed controls; monotherapy comparisons also reported", "endpoint": "NMN plus apigenin increased NAD+ and the NAD+/NADH ratio in the 2026 oxidative-stress musculoskeletal-cell experiments.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "nmn-apigenin-combination-2026", "state": "NMN plus apigenin during the stress model"}, {"entity_slug": "nmn", "state": "co-administered"}, {"entity_slug": "apigenin", "state": "co-administered"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Three precursor-cell models under tert-butyl hydroperoxide stress; combined and single-component comparisons.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
NMN plus apigenin increased NAD+ and the NAD+/NADH ratio in the 2026 oxidative-stress musculoskeletal-cell experiments.
primary_references
Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468
source_locator
Reviewed reference api-nmn-cell-nad; Main-text figures reviewed; exact supplementary doses not verified. A combination outperforming each component is not by itself a formal interaction test.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 524–530
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Three precursor-cell models under tert-butyl hydroperoxide stress; combined and single-component comparisons. · Recorded from source · Recorded from source
### api-nmn-cell-nad NMN plus apigenin increased NAD+ and the NAD+/NADH ratio in the 2026 oxidative-stress musculoskeletal-cell experiments. Main-text figures reviewed; exact supplementary doses not verified. A combination outperforming each component is not by itself a formal interaction test. Model and exposure: Three precursor-cell models under tert-butyl hydroperoxide stress; combined and single-component comparisons. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | 2026 | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468 | Access: Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
Complete structured claim and evidence
The combined preparation improved ATP content, membrane-potential readouts and basal/maximal respiration in the stressed precursor-cell models.
NMN plus apigenin preparation in the 2026 musculoskeletal study → Mitochondrial readouts in the 2026 NMN/apigenin cell study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
experimental_condition
Stressed controls co-administered · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Stressed controls NMN plus apigenin during stress · NMN plus apigenin preparation in the 2026 musculoskeletal study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Stressed controls co-administered · NMN Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "NMN plus apigenin during stress", "comparator": "Stressed controls", "endpoint": "The combined preparation improved ATP content, membrane-potential readouts and basal/maximal respiration in the stressed precursor-cell models.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "nmn-apigenin-combination-2026", "state": "NMN plus apigenin during stress"}, {"entity_slug": "nmn", "state": "co-administered"}, {"entity_slug": "apigenin", "state": "co-administered"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Main-text Results; three musculoskeletal precursor models.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The combined preparation improved ATP content, membrane-potential readouts and basal/maximal respiration in the stressed precursor-cell models.
primary_references
Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468
source_locator
Reviewed reference api-nmn-cell-energy; Neither whole-cell NAD nor bulk respiration localizes drug-target occupancy.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 532–538
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Main-text Results; three musculoskeletal precursor models. · Recorded from source · Recorded from source
### api-nmn-cell-energy The combined preparation improved ATP content, membrane-potential readouts and basal/maximal respiration in the stressed precursor-cell models. Neither whole-cell NAD nor bulk respiration localizes drug-target occupancy. Model and exposure: Main-text Results; three musculoskeletal precursor models. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | 2026 | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468 | Access: Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
Complete structured claim and evidence
The combined preparation improved chondrogenic matrix, osteogenic mineralization and myogenic differentiation readouts in the reported stress models.
NMN plus apigenin preparation in the 2026 musculoskeletal study → Chondrogenic, osteogenic and myogenic readouts in the 2026 combination study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
experimental_condition
Stressed differentiation controls co-administered · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Stressed differentiation controls NMN plus apigenin · NMN plus apigenin preparation in the 2026 musculoskeletal study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Stressed differentiation controls co-administered · NMN Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "NMN plus apigenin", "comparator": "Stressed differentiation controls", "endpoint": "The combined preparation improved chondrogenic matrix, osteogenic mineralization and myogenic differentiation readouts in the reported stress models.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "nmn-apigenin-combination-2026", "state": "NMN plus apigenin"}, {"entity_slug": "nmn", "state": "co-administered"}, {"entity_slug": "apigenin", "state": "co-administered"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
SOX9/COL2A1, ALP/calcium nodules/RUNX2/SP7/OCN, and MyoD1/MYOG/myotube endpoints.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The combined preparation improved chondrogenic matrix, osteogenic mineralization and myogenic differentiation readouts in the reported stress models.
primary_references
Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468
source_locator
Reviewed reference api-nmn-differentiation; These are model-specific readouts, not proof that apigenin increases systemic calcium or cures human musculoskeletal disease.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 540–546
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · SOX9/COL2A1, ALP/calcium nodules/RUNX2/SP7/OCN, and MyoD1/MYOG/myotube endpoints. · Recorded from source · Recorded from source
### api-nmn-differentiation The combined preparation improved chondrogenic matrix, osteogenic mineralization and myogenic differentiation readouts in the reported stress models. These are model-specific readouts, not proof that apigenin increases systemic calcium or cures human musculoskeletal disease. Model and exposure: SOX9/COL2A1, ALP/calcium nodules/RUNX2/SP7/OCN, and MyoD1/MYOG/myotube endpoints. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | 2026 | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468 | Access: Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
Complete structured claim and evidence
Oral NMN plus apigenin improved cartilage, bone, muscle and motor readouts in the 20-month-old mouse study.
NMN plus apigenin preparation in the 2026 musculoskeletal study → Musculoskeletal outcomes in aged NMN/apigenin-treated mice Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
experimental_condition
Aged untreated/control mice co-administered · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Aged untreated/control mice Oral combined preparation · NMN plus apigenin preparation in the 2026 musculoskeletal study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Aged untreated/control mice co-administered · NMN Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Oral combined preparation", "comparator": "Aged untreated/control mice", "endpoint": "Oral NMN plus apigenin improved cartilage, bone, muscle and motor readouts in the 20-month-old mouse study.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "nmn-apigenin-combination-2026", "state": "Oral combined preparation"}, {"entity_slug": "nmn", "state": "co-administered"}, {"entity_slug": "apigenin", "state": "co-administered"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Aged mice; detailed supplement Methods not obtained.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Oral NMN plus apigenin improved cartilage, bone, muscle and motor readouts in the 20-month-old mouse study.
primary_references
Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468
source_locator
Reviewed reference api-nmn-aged-mice; No human combination efficacy is demonstrated.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 548–554
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Aged mice; detailed supplement Methods not obtained. · Recorded from source · Recorded from source
### api-nmn-aged-mice Oral NMN plus apigenin improved cartilage, bone, muscle and motor readouts in the 20-month-old mouse study. No human combination efficacy is demonstrated. Model and exposure: Aged mice; detailed supplement Methods not obtained. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | 2026 | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468 | Access: Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
Complete structured claim and evidence
The NMN/apigenin-associated blood NAD+ and NAD+/NADH increases persisted in Sirt3-knockout mice.
NMN plus apigenin preparation in the 2026 musculoskeletal study → Circulating NAD content Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
experimental_condition
Sirt3-null control mice co-administered · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Sirt3-null control mice Combined preparation in Sirt3-null mice · NMN plus apigenin preparation in the 2026 musculoskeletal study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Sirt3-null control mice genetically absent · Mouse mitochondrial sirtuin 3 / Sirt3 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Sirt3-null control mice co-administered · NMN Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Combined preparation in Sirt3-null mice", "comparator": "Sirt3-null control mice", "endpoint": "The NMN/apigenin-associated blood NAD+ and NAD+/NADH increases persisted in Sirt3-knockout mice.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "nmn-apigenin-combination-2026", "state": "Combined preparation in Sirt3-null mice"}, {"entity_slug": "nmn", "state": "co-administered"}, {"entity_slug": "apigenin", "state": "co-administered"}, {"entity_slug": "mouse-sirt3", "state": "genetically absent"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Aged Sirt3-null mice; main Figure 7.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The NMN/apigenin-associated blood NAD+ and NAD+/NADH increases persisted in Sirt3-knockout mice.
primary_references
Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468
source_locator
Reviewed reference api-nmn-sirt3-nad-retained; Precursor supply and downstream response are different steps.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 556–562
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Aged Sirt3-null mice; main Figure 7. · Recorded from source · Recorded from source
### api-nmn-sirt3-nad-retained The NMN/apigenin-associated blood NAD+ and NAD+/NADH increases persisted in Sirt3-knockout mice. Precursor supply and downstream response are different steps. Model and exposure: Aged Sirt3-null mice; main Figure 7. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | 2026 | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468 | Access: Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
Complete structured claim and evidence
Sirt3 deletion partially attenuated the structural and functional benefits of NMN plus apigenin.
NMN plus apigenin preparation in the 2026 musculoskeletal study → Musculoskeletal outcomes in aged NMN/apigenin-treated mice Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
experimental_condition
Combined-preparation response in wild-type mice co-administered · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Combined-preparation response in wild-type mice Combined preparation in Sirt3-knockout mice · NMN plus apigenin preparation in the 2026 musculoskeletal study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Combined-preparation response in wild-type mice genetically absent · Mouse mitochondrial sirtuin 3 / Sirt3 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Combined-preparation response in wild-type mice co-administered · NMN Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Combined preparation in Sirt3-knockout mice", "comparator": "Combined-preparation response in wild-type mice", "endpoint": "Sirt3 deletion partially attenuated the structural and functional benefits of NMN plus apigenin.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "nmn-apigenin-combination-2026", "state": "Combined preparation in Sirt3-knockout mice"}, {"entity_slug": "nmn", "state": "co-administered"}, {"entity_slug": "apigenin", "state": "co-administered"}, {"entity_slug": "mouse-sirt3", "state": "genetically absent"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Aged-mouse genotype comparison.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Sirt3 deletion partially attenuated the structural and functional benefits of NMN plus apigenin.
primary_references
Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468
source_locator
Reviewed reference api-nmn-sirt3-benefit-attenuated; Partial attenuation supports a contributing requirement; it is not complete elimination or direct apigenin binding to SIRT3.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 564–570
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Aged-mouse genotype comparison. · Recorded from source · Recorded from source
### api-nmn-sirt3-benefit-attenuated Sirt3 deletion partially attenuated the structural and functional benefits of NMN plus apigenin. Partial attenuation supports a contributing requirement; it is not complete elimination or direct apigenin binding to SIRT3. Model and exposure: Aged-mouse genotype comparison. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | 2026 | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468 | Access: Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
Complete structured claim and evidence
The combined-treatment group had higher fecal phytosphingosine; its abundance correlated with selected microbial taxa.
NMN plus apigenin preparation in the 2026 musculoskeletal study → Phytosphingosine Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
experimental_condition
Aged controls co-administered · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Aged controls NMN plus apigenin · NMN plus apigenin preparation in the 2026 musculoskeletal study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Aged controls co-administered · NMN Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "NMN plus apigenin", "comparator": "Aged controls", "endpoint": "The combined-treatment group had higher fecal phytosphingosine; its abundance correlated with selected microbial taxa.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "nmn-apigenin-combination-2026", "state": "NMN plus apigenin"}, {"entity_slug": "nmn", "state": "co-administered"}, {"entity_slug": "apigenin", "state": "co-administered"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Aged mice, fecal metabolomics and microbiome correlations.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The combined-treatment group had higher fecal phytosphingosine; its abundance correlated with selected microbial taxa.
primary_references
Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468
source_locator
Reviewed reference api-nmn-phytosphingosine; Taxon correlations do not prove that those organisms synthesized phytosphingosine. FMT and separate phytosphingosine supplementation supported follow-up routes but did not isolate an apigenin-only mechanism.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 572–578
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Aged mice, fecal metabolomics and microbiome correlations. · Recorded from source · Recorded from source
### api-nmn-phytosphingosine The combined-treatment group had higher fecal phytosphingosine; its abundance correlated with selected microbial taxa. Taxon correlations do not prove that those organisms synthesized phytosphingosine. FMT and separate phytosphingosine supplementation supported follow-up routes but did not isolate an apigenin-only mechanism. Model and exposure: Aged mice, fecal metabolomics and microbiome correlations. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration. | 2026 | https://pubmed.ncbi.nlm.nih.gov/41944220/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13054677/ | https://doi.org/10.1111/acel.70468 | Access: Primary main-text Results and figure descriptions reviewed. Detailed supporting Methods/supplements inaccessible; exact doses and preparation details not independently extracted.
Complete structured claim and evidence
Crystallography placed apigenin in the catalytic pocket of Zea mays CK2, with ATP-competitive inhibition reported in the study.
Apigenin → Zea mays CK2 catalytic subunit Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_model
Primary abstract plus PDB 4DGM, 1.65 Å; maize catalytic subunit.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Crystallography placed apigenin in the catalytic pocket of Zea mays CK2, with ATP-competitive inhibition reported in the study.
primary_references
Inhibition of protein kinase CK2 by flavonoids and tyrphostins. A structural insight. | https://pubmed.ncbi.nlm.nih.gov/22794353/ | https://doi.org/10.1021/bi300531c
source_locator
Reviewed reference api-ck2-crystal; The structure is not human CK2. The low-micromolar/submicromolar kinase results are not a measured oral tissue exposure.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 584–590
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Primary abstract plus PDB 4DGM, 1.65 Å; maize catalytic subunit. · Recorded from source · Recorded from source
### api-ck2-crystal Crystallography placed apigenin in the catalytic pocket of Zea mays CK2, with ATP-competitive inhibition reported in the study. The structure is not human CK2. The low-micromolar/submicromolar kinase results are not a measured oral tissue exposure. Model and exposure: Primary abstract plus PDB 4DGM, 1.65 Å; maize catalytic subunit. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Inhibition of protein kinase CK2 by flavonoids and tyrphostins. A structural insight. | 2012 | https://pubmed.ncbi.nlm.nih.gov/22794353/ | https://doi.org/10.1021/bi300531c | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin inhibited reconstituted human CK2 alpha-prime/beta with IC50 1.72 micromolar in the earlier assay.
Apigenin → Human CK2 alpha-prime/beta reconstituted holoenzyme Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "No inhibitor", "endpoint": "Apigenin inhibited reconstituted human CK2 alpha-prime/beta with IC50 1.72 micromolar in the earlier assay.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human recombinant alpha-prime and beta subunits; ATP-incorporation assay.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited reconstituted human CK2 alpha-prime/beta with IC50 1.72 micromolar in the earlier assay.
primary_references
Structure-activity relationship of 7 flavonoids on recombinant human protein kinase CK2 holoenzyme. | https://pubmed.ncbi.nlm.nih.gov/19197122/
source_locator
Reviewed reference api-ck2-earlier;
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 592–598
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human recombinant alpha-prime and beta subunits; ATP-incorporation assay. · Recorded from source · Recorded from source
### api-ck2-earlier Apigenin inhibited reconstituted human CK2 alpha-prime/beta with IC50 1.72 micromolar in the earlier assay. Model and exposure: Human recombinant alpha-prime and beta subunits; ATP-incorporation assay. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Structure-activity relationship of 7 flavonoids on recombinant human protein kinase CK2 holoenzyme. | 2009 | https://pubmed.ncbi.nlm.nih.gov/19197122/ | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin inhibited this human CK2 preparation with IC50 9.8 micromolar using P2B substrate and 3.9 micromolar using the peptide substrate.
Apigenin → Human CK2 alpha / CSNK2A1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "No inhibitor", "endpoint": "Apigenin inhibited this human CK2 preparation with IC50 9.8 micromolar using P2B substrate and 3.9 micromolar using the peptide substrate.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Recombinant human CK2; ATP 20 micromolar; Table 1.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited this human CK2 preparation with IC50 9.8 micromolar using P2B substrate and 3.9 micromolar using the peptide substrate.
primary_references
Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1
source_locator
Reviewed reference api-ck2-alpha; Subunit identity and assay substrate are part of the potency result; no universal IC50 or physiological ATP correction is implied.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 600–606
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human CK2; ATP 20 micromolar; Table 1. · Recorded from source · Recorded from source
### api-ck2-alpha Apigenin inhibited this human CK2 preparation with IC50 9.8 micromolar using P2B substrate and 3.9 micromolar using the peptide substrate. Subunit identity and assay substrate are part of the potency result; no universal IC50 or physiological ATP correction is implied. Model and exposure: Recombinant human CK2; ATP 20 micromolar; Table 1. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | 2018 | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin inhibited this human CK2 preparation with IC50 2.3 micromolar using P2B substrate and 1.5 micromolar using the peptide substrate.
Apigenin → Human CK2 alpha-prime / CSNK2A2 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "No inhibitor", "endpoint": "Apigenin inhibited this human CK2 preparation with IC50 2.3 micromolar using P2B substrate and 1.5 micromolar using the peptide substrate.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Recombinant human CK2; ATP 20 micromolar; Table 1.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited this human CK2 preparation with IC50 2.3 micromolar using P2B substrate and 1.5 micromolar using the peptide substrate.
primary_references
Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1
source_locator
Reviewed reference api-ck2-alpha-prime; Subunit identity and assay substrate are part of the potency result; no universal IC50 or physiological ATP correction is implied.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 608–614
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human CK2; ATP 20 micromolar; Table 1. · Recorded from source · Recorded from source
### api-ck2-alpha-prime Apigenin inhibited this human CK2 preparation with IC50 2.3 micromolar using P2B substrate and 1.5 micromolar using the peptide substrate. Subunit identity and assay substrate are part of the potency result; no universal IC50 or physiological ATP correction is implied. Model and exposure: Recombinant human CK2; ATP 20 micromolar; Table 1. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | 2018 | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin inhibited this human CK2 preparation with IC50 1.5 micromolar using P2B substrate and 0.8 micromolar using the peptide substrate.
Apigenin → Human CK2 alpha/beta reconstituted holoenzyme Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "No inhibitor", "endpoint": "Apigenin inhibited this human CK2 preparation with IC50 1.5 micromolar using P2B substrate and 0.8 micromolar using the peptide substrate.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Recombinant human CK2; ATP 20 micromolar; Table 1.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited this human CK2 preparation with IC50 1.5 micromolar using P2B substrate and 0.8 micromolar using the peptide substrate.
primary_references
Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1
source_locator
Reviewed reference api-ck2-alpha-holo; Subunit identity and assay substrate are part of the potency result; no universal IC50 or physiological ATP correction is implied.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 616–622
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human CK2; ATP 20 micromolar; Table 1. · Recorded from source · Recorded from source
### api-ck2-alpha-holo Apigenin inhibited this human CK2 preparation with IC50 1.5 micromolar using P2B substrate and 0.8 micromolar using the peptide substrate. Subunit identity and assay substrate are part of the potency result; no universal IC50 or physiological ATP correction is implied. Model and exposure: Recombinant human CK2; ATP 20 micromolar; Table 1. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | 2018 | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin inhibited this human CK2 preparation with IC50 2.5 micromolar using P2B substrate and 2.4 micromolar using the peptide substrate.
Apigenin → Human CK2 alpha-prime/beta reconstituted holoenzyme Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "No inhibitor", "endpoint": "Apigenin inhibited this human CK2 preparation with IC50 2.5 micromolar using P2B substrate and 2.4 micromolar using the peptide substrate.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Recombinant human CK2; ATP 20 micromolar; Table 1.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited this human CK2 preparation with IC50 2.5 micromolar using P2B substrate and 2.4 micromolar using the peptide substrate.
primary_references
Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1
source_locator
Reviewed reference api-ck2-alpha-prime-holo; Subunit identity and assay substrate are part of the potency result; no universal IC50 or physiological ATP correction is implied.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 624–630
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human CK2; ATP 20 micromolar; Table 1. · Recorded from source · Recorded from source
### api-ck2-alpha-prime-holo Apigenin inhibited this human CK2 preparation with IC50 2.5 micromolar using P2B substrate and 2.4 micromolar using the peptide substrate. Subunit identity and assay substrate are part of the potency result; no universal IC50 or physiological ATP correction is implied. Model and exposure: Recombinant human CK2; ATP 20 micromolar; Table 1. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | 2018 | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin 7-O-glucuronide inhibited isolated human CK2 alpha-prime with IC50 0.4 micromolar using P2B but 5.4 micromolar using the peptide substrate.
Apigenin 7-O-glucuronide → Human CK2 alpha-prime / CSNK2A2 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Glucuronide concentration series", "comparator": "No inhibitor", "endpoint": "Apigenin 7-O-glucuronide inhibited isolated human CK2 alpha-prime with IC50 0.4 micromolar using P2B but 5.4 micromolar using the peptide substrate.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Table 1; ATP 20 micromolar; isolated catalytic subunit, not holoenzyme.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin 7-O-glucuronide inhibited isolated human CK2 alpha-prime with IC50 0.4 micromolar using P2B but 5.4 micromolar using the peptide substrate.
primary_references
Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1
source_locator
Reviewed reference api-glucuronide-ck2; A conjugate can retain assay activity; this does not establish its cellular uptake or direct in-vivo effect.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 632–638
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Table 1; ATP 20 micromolar; isolated catalytic subunit, not holoenzyme. · Recorded from source · Recorded from source
### api-glucuronide-ck2 Apigenin 7-O-glucuronide inhibited isolated human CK2 alpha-prime with IC50 0.4 micromolar using P2B but 5.4 micromolar using the peptide substrate. A conjugate can retain assay activity; this does not establish its cellular uptake or direct in-vivo effect. Model and exposure: Table 1; ATP 20 micromolar; isolated catalytic subunit, not holoenzyme. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Inhibitory influence of natural flavonoids on human protein kinase CK2 isoforms: effect of the regulatory subunit. | 2018 | https://pubmed.ncbi.nlm.nih.gov/29188536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6002439/ | https://doi.org/10.1007/s11010-017-3228-1 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin bound the glycine-rich C-terminal region of hnRNPA2 and inhibited its homodimerization in the reported biochemical experiments.
Apigenin → Human heterogeneous nuclear ribonucleoprotein A2/B1 / HNRNPA2B1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract plus PMC full-text Results retrieved through web; no claim that every screening hit is functionally validated.
experimental_model
Human protein fragments, affinity pull-down and follow-up assays.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin bound the glycine-rich C-terminal region of hnRNPA2 and inhibited its homodimerization in the reported biochemical experiments.
primary_references
Molecular basis for the action of a dietary flavonoid revealed by the comprehensive identification of apigenin human targets. | https://pubmed.ncbi.nlm.nih.gov/23697369/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3683737/ | https://doi.org/10.1073/pnas.1303726110
source_locator
Reviewed reference api-hnrnpa2-binding; The screen nominated 160 candidate proteins; only selected targets received functional follow-up. Do not label all 160 validated causal targets or dietary target engagement.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 644–650
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human protein fragments, affinity pull-down and follow-up assays. · Recorded from source · Recorded from source
### api-hnrnpa2-binding Apigenin bound the glycine-rich C-terminal region of hnRNPA2 and inhibited its homodimerization in the reported biochemical experiments. The screen nominated 160 candidate proteins; only selected targets received functional follow-up. Do not label all 160 validated causal targets or dietary target engagement. Model and exposure: Human protein fragments, affinity pull-down and follow-up assays. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Molecular basis for the action of a dietary flavonoid revealed by the comprehensive identification of apigenin human targets. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23697369/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3683737/ | https://doi.org/10.1073/pnas.1303726110 | Access: Primary indexed abstract plus PMC full-text Results retrieved through web; no claim that every screening hit is functionally validated.
Complete structured claim and evidence
Apigenin decreased the relative abundance of Human CFLAR short transcript / CFLAR-S in MDA-MB-231 breast-cancer cells.
Apigenin → Human CFLAR short transcript / CFLAR-S Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin decreased the relative abundance of Human CFLAR short transcript / CFLAR-S in MDA-MB-231 breast-cancer cells.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin decreased the relative abundance of Human CFLAR short transcript / CFLAR-S in MDA-MB-231 breast-cancer cells.
primary_references
Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
source_locator
Reviewed reference api-splice-cflar; Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 652–658
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. · Recorded from source · Recorded from source
### api-splice-cflar Apigenin decreased the relative abundance of Human CFLAR short transcript / CFLAR-S in MDA-MB-231 breast-cancer cells. Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis. Model and exposure: 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin decreased the relative abundance of Human MAP3K7-A transcript lacking exon 12 in MDA-MB-231 breast-cancer cells.
Apigenin → Human MAP3K7-A transcript lacking exon 12 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin decreased the relative abundance of Human MAP3K7-A transcript lacking exon 12 in MDA-MB-231 breast-cancer cells.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin decreased the relative abundance of Human MAP3K7-A transcript lacking exon 12 in MDA-MB-231 breast-cancer cells.
primary_references
Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
source_locator
Reviewed reference api-splice-map3k7a; Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 660–666
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. · Recorded from source · Recorded from source
### api-splice-map3k7a Apigenin decreased the relative abundance of Human MAP3K7-A transcript lacking exon 12 in MDA-MB-231 breast-cancer cells. Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis. Model and exposure: 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased the relative abundance of Human BAXL transcript in MDA-MB-231 breast-cancer cells.
Apigenin → Human BAXL transcript Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased the relative abundance of Human BAXL transcript in MDA-MB-231 breast-cancer cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased the relative abundance of Human BAXL transcript in MDA-MB-231 breast-cancer cells.
primary_references
Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
source_locator
Reviewed reference api-splice-baxl; Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 668–674
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. · Recorded from source · Recorded from source
### api-splice-baxl Apigenin increased the relative abundance of Human BAXL transcript in MDA-MB-231 breast-cancer cells. Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis. Model and exposure: 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased the relative abundance of Human translation-competent CCNL2 transcripts in MDA-MB-231 breast-cancer cells.
Apigenin → Human translation-competent CCNL2 transcripts Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased the relative abundance of Human translation-competent CCNL2 transcripts in MDA-MB-231 breast-cancer cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased the relative abundance of Human translation-competent CCNL2 transcripts in MDA-MB-231 breast-cancer cells.
primary_references
Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
source_locator
Reviewed reference api-splice-ccnl2; Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 676–682
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. · Recorded from source · Recorded from source
### api-splice-ccnl2 Apigenin increased the relative abundance of Human translation-competent CCNL2 transcripts in MDA-MB-231 breast-cancer cells. Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis. Model and exposure: 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin did not detectably alter the selected CFLAR, MAP3K7, BAX and CCNL2 splice events in non-tumor MCF10A cells under the same exposure.
Apigenin → Selected splice events in apigenin-treated MCF10A cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin did not detectably alter the selected CFLAR, MAP3K7, BAX and CCNL2 splice events in non-tumor MCF10A cells under the same exposure.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
50 micromolar, 48 hours; Figure 4.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin did not detectably alter the selected CFLAR, MAP3K7, BAX and CCNL2 splice events in non-tumor MCF10A cells under the same exposure.
primary_references
Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
source_locator
Reviewed reference api-splice-nontumor-null; One non-tumor cell line does not establish universal tumor selectivity or safety.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 684–690
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar, 48 hours; Figure 4. · Recorded from source · Recorded from source
### api-splice-nontumor-null Apigenin did not detectably alter the selected CFLAR, MAP3K7, BAX and CCNL2 splice events in non-tumor MCF10A cells under the same exposure. One non-tumor cell line does not establish universal tumor selectivity or safety. Model and exposure: 50 micromolar, 48 hours; Figure 4. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased apoptosis/caspase-3 readouts and reduced proliferation in MDA-MB-231 cells.
Apigenin → Apoptosis in apigenin-treated MDA-MB-231 cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased apoptosis/caspase-3 readouts and reduced proliferation in MDA-MB-231 cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
50 micromolar, 48 hours; Figure 1.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased apoptosis/caspase-3 readouts and reduced proliferation in MDA-MB-231 cells.
primary_references
Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
source_locator
Reviewed reference api-tnbc-apoptosis; No clinical cancer efficacy or recommended combination follows from this cell exposure.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 692–698
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar, 48 hours; Figure 1. · Recorded from source · Recorded from source
### api-tnbc-apoptosis Apigenin increased apoptosis/caspase-3 readouts and reduced proliferation in MDA-MB-231 cells. No clinical cancer efficacy or recommended combination follows from this cell exposure. Model and exposure: 50 micromolar, 48 hours; Figure 1. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin reduced MDA-MB-231 xenograft growth and shifted selected tumor splice patterns in the reported mouse experiment.
Apigenin → Growth of apigenin-treated human-cell xenografts in mice Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin regimen", "comparator": "Vehicle", "endpoint": "Apigenin reduced MDA-MB-231 xenograft growth and shifted selected tumor splice patterns in the reported mouse experiment.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
25 mg/kg for 28 days; Figure 6, n=12; route not extracted here.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced MDA-MB-231 xenograft growth and shifted selected tumor splice patterns in the reported mouse experiment.
primary_references
Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
source_locator
Reviewed reference api-tnbc-xenograft; Xenografts contain human tumor cells in mice. Patient-transcriptome comparisons were observational datasets, not treated patients.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 700–706
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 25 mg/kg for 28 days; Figure 6, n=12; route not extracted here. · Recorded from source · Recorded from source
### api-tnbc-xenograft Apigenin reduced MDA-MB-231 xenograft growth and shifted selected tumor splice patterns in the reported mouse experiment. Xenografts contain human tumor cells in mice. Patient-transcriptome comparisons were observational datasets, not treated patients. Model and exposure: 25 mg/kg for 28 days; Figure 6, n=12; route not extracted here. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin reduced recombinant human topoisomerase-I DNA relaxation: over 30% inhibition at 10 micromolar and over 80% at 100 micromolar.
Apigenin → Human DNA topoisomerase I / TOP1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "Vehicle", "endpoint": "Apigenin reduced recombinant human topoisomerase-I DNA relaxation: over 30% inhibition at 10 micromolar and over 80% at 100 micromolar.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Cell-free DNA-unwinding/relaxation assay.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced recombinant human topoisomerase-I DNA relaxation: over 30% inhibition at 10 micromolar and over 80% at 100 micromolar.
primary_references
Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894
source_locator
Reviewed reference api-top1-enzyme; Functional inhibition plus modeling does not supply an independently measured binding affinity.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 708–714
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Cell-free DNA-unwinding/relaxation assay. · Recorded from source · Recorded from source
### api-top1-enzyme Apigenin reduced recombinant human topoisomerase-I DNA relaxation: over 30% inhibition at 10 micromolar and over 80% at 100 micromolar. Functional inhibition plus modeling does not supply an independently measured binding affinity. Model and exposure: Cell-free DNA-unwinding/relaxation assay. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | 2022 | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin did not detectably change TOP1 mRNA or protein in HT-29 cells despite the functional enzyme-assay effect.
Apigenin → Human DNA topoisomerase I / TOP1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin did not detectably change TOP1 mRNA or protein in HT-29 cells despite the functional enzyme-assay effect.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human HT-29 cells; 30–60 micromolar apigenin, 48 hours.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin did not detectably change TOP1 mRNA or protein in HT-29 cells despite the functional enzyme-assay effect.
primary_references
Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894
source_locator
Reviewed reference api-top1-expression-null; Abundance and enzyme activity are distinct endpoints.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 716–722
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human HT-29 cells; 30–60 micromolar apigenin, 48 hours. · Recorded from source · Recorded from source
### api-top1-expression-null Apigenin did not detectably change TOP1 mRNA or protein in HT-29 cells despite the functional enzyme-assay effect. Abundance and enzyme activity are distinct endpoints. Model and exposure: Human HT-29 cells; 30–60 micromolar apigenin, 48 hours. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | 2022 | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin increased cell-surface CD26/DPP4 expression in HT-29 cells.
Apigenin → Human dipeptidyl peptidase 4 / DPP4 / CD26 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin increased cell-surface CD26/DPP4 expression in HT-29 cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human colorectal cancer cell line; 30–60 micromolar, 48 hours.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin increased cell-surface CD26/DPP4 expression in HT-29 cells.
primary_references
Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894
source_locator
Reviewed reference api-cd26; Surface expression is not necessarily catalytic activity, glucose control or an anti-tumor endpoint.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 724–730
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human colorectal cancer cell line; 30–60 micromolar, 48 hours. · Recorded from source · Recorded from source
### api-cd26 Apigenin increased cell-surface CD26/DPP4 expression in HT-29 cells. Surface expression is not necessarily catalytic activity, glucose control or an anti-tumor endpoint. Model and exposure: Human colorectal cancer cell line; 30–60 micromolar, 48 hours. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | 2022 | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
TOP1 knockdown raised basal CD26 expression and occluded the additional CD26 response to apigenin.
Apigenin → Human dipeptidyl peptidase 4 / DPP4 / CD26 Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
TOP1-knockdown cells without apigenin siRNA knockdown · Human DNA topoisomerase I / TOP1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
TOP1-knockdown cells without apigenin Apigenin after TOP1 knockdown · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin after TOP1 knockdown", "comparator": "TOP1-knockdown cells without apigenin", "endpoint": "TOP1 knockdown raised basal CD26 expression and occluded the additional CD26 response to apigenin.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin after TOP1 knockdown"}, {"entity_slug": "human-top1", "state": "siRNA knockdown"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
HT-29 cells; over 75% TOP1 knockdown.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
TOP1 knockdown raised basal CD26 expression and occluded the additional CD26 response to apigenin.
primary_references
Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894
source_locator
Reviewed reference api-top1-knockdown; Supports pathway involvement for this expression endpoint without identifying a clinical therapeutic interaction.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 732–738
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · HT-29 cells; over 75% TOP1 knockdown. · Recorded from source · Recorded from source
### api-top1-knockdown TOP1 knockdown raised basal CD26 expression and occluded the additional CD26 response to apigenin. Supports pathway involvement for this expression endpoint without identifying a clinical therapeutic interaction. Model and exposure: HT-29 cells; over 75% TOP1 knockdown. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | 2022 | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin plus irinotecan increased CD26 expression in the reported HT-29 combination assay.
Apigenin → Human dipeptidyl peptidase 4 / DPP4 / CD26 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
Single-agent comparison reported by the study co-administered · Irinotecan Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Single-agent comparison reported by the study Apigenin plus irinotecan · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin plus irinotecan", "comparator": "Single-agent comparison reported by the study", "endpoint": "Apigenin plus irinotecan increased CD26 expression in the reported HT-29 combination assay.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin plus irinotecan"}, {"entity_slug": "irinotecan", "state": "co-administered"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Cell-surface CD26 endpoint; the paper also tested other topoisomerase drugs.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin plus irinotecan increased CD26 expression in the reported HT-29 combination assay.
primary_references
Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894
source_locator
Reviewed reference api-irinotecan-cd26; Do not translate this expression interaction into proven synergistic tumor killing or a clinical co-treatment recommendation.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 740–746
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Cell-surface CD26 endpoint; the paper also tested other topoisomerase drugs. · Recorded from source · Recorded from source
### api-irinotecan-cd26 Apigenin plus irinotecan increased CD26 expression in the reported HT-29 combination assay. Do not translate this expression interaction into proven synergistic tumor killing or a clinical co-treatment recommendation. Model and exposure: Cell-surface CD26 endpoint; the paper also tested other topoisomerase drugs. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | 2022 | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.
Apigenin → Senescence-associated secretory phenotype in apigenin-treated human fibroblasts Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Apigenin in senescent fibroblasts", "comparator": "Senescent vehicle controls", "endpoint": "Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers.
primary_references
Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1
source_locator
Reviewed reference api-sasp; Primary abstract scope. Suppression was linked to IL-1/IRAK/p38/NF-kappaB signaling; this does not prove senolysis.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 752–758
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments. · Recorded from source · Recorded from source
### api-sasp Apigenin suppressed multiple SASP outputs in human fibroblasts made senescent by several experimental triggers. Primary abstract scope. Suppression was linked to IL-1/IRAK/p38/NF-kappaB signaling; this does not prove senolysis. Model and exposure: Three human fibroblast strains; irradiation, replicative and oncogene-related senescence experiments. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | 2017 | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Conditioned medium from apigenin-treated senescent fibroblasts showed less pro-aggressive activity toward the breast-cancer cells in the study.
Apigenin → Breast-cancer-cell response to medium from apigenin-treated senescent fibroblasts Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Medium conditioned by apigenin-treated senescent fibroblasts", "comparator": "Medium from untreated senescent fibroblasts", "endpoint": "Conditioned medium from apigenin-treated senescent fibroblasts showed less pro-aggressive activity toward the breast-cancer cells in the study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human fibroblast-to-cancer-cell conditioned-medium comparison.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Conditioned medium from apigenin-treated senescent fibroblasts showed less pro-aggressive activity toward the breast-cancer cells in the study.
primary_references
Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1
source_locator
Reviewed reference api-sasp-conditioned-medium; Indirect conditioned-medium effects must not be relabelled direct cancer-cell apigenin exposure.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 760–766
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human fibroblast-to-cancer-cell conditioned-medium comparison. · Recorded from source · Recorded from source
### api-sasp-conditioned-medium Conditioned medium from apigenin-treated senescent fibroblasts showed less pro-aggressive activity toward the breast-cancer cells in the study. Indirect conditioned-medium effects must not be relabelled direct cancer-cell apigenin exposure. Model and exposure: Human fibroblast-to-cancer-cell conditioned-medium comparison. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin suppresses the senescence-associated secretory phenotype and paracrine effects on breast cancer cells. | 2017 | https://pubmed.ncbi.nlm.nih.gov/28378188/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5411372/ | https://doi.org/10.1007/s11357-017-9970-1 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin reduced LPS-associated TLR4/Akt/mTOR/NF-kappaB and stress-kinase signaling readouts in human keratinocyte experiments.
Apigenin → Inflammatory signaling in apigenin-treated human keratinocytes Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_condition
LPS alone Apigenin during LPS challenge · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS alone LPS challenge · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin during LPS challenge", "comparator": "LPS alone", "endpoint": "Apigenin reduced LPS-associated TLR4/Akt/mTOR/NF-kappaB and stress-kinase signaling readouts in human keratinocyte experiments.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin during LPS challenge"}, {"entity_slug": "lipopolysaccharide", "state": "LPS challenge"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
HEK001 and primary human keratinocytes; accessed primary abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin reduced LPS-associated TLR4/Akt/mTOR/NF-kappaB and stress-kinase signaling readouts in human keratinocyte experiments.
primary_references
Apigenin reduces the Toll-like receptor-4-dependent activation of NF-κB by suppressing the Akt, mTOR, JNK, and p38-MAPK. | https://pubmed.ncbi.nlm.nih.gov/29264665/ | https://doi.org/10.1007/s00210-017-1454-4
source_locator
Reviewed reference api-keratinocyte-inflammation; Pathway readouts are not evidence that each listed protein directly binds apigenin.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 768–774
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · HEK001 and primary human keratinocytes; accessed primary abstract. · Recorded from source · Recorded from source
### api-keratinocyte-inflammation Apigenin reduced LPS-associated TLR4/Akt/mTOR/NF-kappaB and stress-kinase signaling readouts in human keratinocyte experiments. Pathway readouts are not evidence that each listed protein directly binds apigenin. Model and exposure: HEK001 and primary human keratinocytes; accessed primary abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin reduces the Toll-like receptor-4-dependent activation of NF-κB by suppressing the Akt, mTOR, JNK, and p38-MAPK. | 2018 | https://pubmed.ncbi.nlm.nih.gov/29264665/ | https://doi.org/10.1007/s00210-017-1454-4 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin displaced flunitrazepam binding with reported Ki 4 micromolar in the 1995 receptor-binding study.
Apigenin → The modulatory benzodiazepine-binding site of the GABA-A receptor Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "Binding assay without competitor", "endpoint": "Apigenin displaced flunitrazepam binding with reported Ki 4 micromolar in the 1995 receptor-binding study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Central benzodiazepine-site binding assay; primary abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin displaced flunitrazepam binding with reported Ki 4 micromolar in the 1995 receptor-binding study.
primary_references
Apigenin, a component of Matricaria recutita flowers, is a central benzodiazepine receptors-ligand with anxiolytic effects. | https://pubmed.ncbi.nlm.nih.gov/7617761/ | https://doi.org/10.1055/s-2006-958058
source_locator
Reviewed reference api-gaba-binding; No muscimol-binding, muscarinic or alpha-1-adrenergic binding effects were reported in the tested assays. No proven alpha-1-sparing clinical receptor profile follows.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 780–786
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Central benzodiazepine-site binding assay; primary abstract. · Recorded from source · Recorded from source
### api-gaba-binding Apigenin displaced flunitrazepam binding with reported Ki 4 micromolar in the 1995 receptor-binding study. No muscimol-binding, muscarinic or alpha-1-adrenergic binding effects were reported in the tested assays. No proven alpha-1-sparing clinical receptor profile follows. Model and exposure: Central benzodiazepine-site binding assay; primary abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin, a component of Matricaria recutita flowers, is a central benzodiazepine receptors-ligand with anxiolytic effects. | 1995 | https://pubmed.ncbi.nlm.nih.gov/7617761/ | https://doi.org/10.1055/s-2006-958058 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin decreased GABA-activated chloride currents in cultured cerebellar granule cells; flumazenil antagonized that effect.
Apigenin → GABA-activated chloride current in the apigenin cerebellar-cell assay Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_condition
GABA response without apigenin Apigenin during GABA application · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
GABA response without apigenin agonist applied during electrophysiology · Gamma-aminobutyric acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin during GABA application", "comparator": "GABA response without apigenin", "endpoint": "Apigenin decreased GABA-activated chloride currents in cultured cerebellar granule cells; flumazenil antagonized that effect.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin during GABA application"}, {"entity_slug": "gaba", "state": "agonist applied during electrophysiology"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Electrophysiology; cell species not specified in the accessed abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin decreased GABA-activated chloride currents in cultured cerebellar granule cells; flumazenil antagonized that effect.
primary_references
Pharmacological profile of apigenin, a flavonoid isolated from Matricaria chamomilla. | https://pubmed.ncbi.nlm.nih.gov/10751547/ | https://doi.org/10.1016/s0006-2952(00)00264-1
source_locator
Reviewed reference api-gaba-current; This is not evidence of a conventional positive allosteric modulator. Chloride-current direction is not a blood chloride depletion claim.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 788–794
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Electrophysiology; cell species not specified in the accessed abstract. · Recorded from source · Recorded from source
### api-gaba-current Apigenin decreased GABA-activated chloride currents in cultured cerebellar granule cells; flumazenil antagonized that effect. This is not evidence of a conventional positive allosteric modulator. Chloride-current direction is not a blood chloride depletion claim. Model and exposure: Electrophysiology; cell species not specified in the accessed abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Pharmacological profile of apigenin, a flavonoid isolated from Matricaria chamomilla. | 2000 | https://pubmed.ncbi.nlm.nih.gov/10751547/ | https://doi.org/10.1016/s0006-2952(00)00264-1 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Intraperitoneal apigenin reduced rat locomotion but did not produce an anxiolytic effect in that study.
Apigenin → Rat anxiety behavior in the 2000 apigenin study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle anxiety-assay controls", "endpoint": "Intraperitoneal apigenin reduced rat locomotion but did not produce an anxiolytic effect in that study.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Rat behavioral experiments; dose not independently extracted from abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Intraperitoneal apigenin reduced rat locomotion but did not produce an anxiolytic effect in that study.
primary_references
Pharmacological profile of apigenin, a flavonoid isolated from Matricaria chamomilla. | https://pubmed.ncbi.nlm.nih.gov/10751547/ | https://doi.org/10.1016/s0006-2952(00)00264-1
source_locator
Reviewed reference api-rat-anxiety-null; The locomotor effect was not blocked by flumazenil. Earlier mouse plus-maze findings used a different experimental setting.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 796–802
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Rat behavioral experiments; dose not independently extracted from abstract. · Recorded from source · Recorded from source
### api-rat-anxiety-null Intraperitoneal apigenin reduced rat locomotion but did not produce an anxiolytic effect in that study. The locomotor effect was not blocked by flumazenil. Earlier mouse plus-maze findings used a different experimental setting. Model and exposure: Rat behavioral experiments; dose not independently extracted from abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Pharmacological profile of apigenin, a flavonoid isolated from Matricaria chamomilla. | 2000 | https://pubmed.ncbi.nlm.nih.gov/10751547/ | https://doi.org/10.1016/s0006-2952(00)00264-1 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
The earlier mouse experiment reported anxiolytic-like plus-maze behavior without the tested anticonvulsant or muscle-relaxant effects; a tenfold larger dose caused mild sedation.
Apigenin → Mouse elevated-plus-maze behavior with apigenin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "The earlier mouse experiment reported anxiolytic-like plus-maze behavior without the tested anticonvulsant or muscle-relaxant effects; a tenfold larger dose caused mild sedation.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Mouse behavior accompanying the 1995 binding study.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The earlier mouse experiment reported anxiolytic-like plus-maze behavior without the tested anticonvulsant or muscle-relaxant effects; a tenfold larger dose caused mild sedation.
primary_references
Apigenin, a component of Matricaria recutita flowers, is a central benzodiazepine receptors-ligand with anxiolytic effects. | https://pubmed.ncbi.nlm.nih.gov/7617761/ | https://doi.org/10.1055/s-2006-958058
source_locator
Reviewed reference api-mouse-plus-maze; Behavioral assay labels do not establish a human anxiety indication or subtype-selective GABA pharmacology.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 804–810
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Mouse behavior accompanying the 1995 binding study. · Recorded from source · Recorded from source
### api-mouse-plus-maze The earlier mouse experiment reported anxiolytic-like plus-maze behavior without the tested anticonvulsant or muscle-relaxant effects; a tenfold larger dose caused mild sedation. Behavioral assay labels do not establish a human anxiety indication or subtype-selective GABA pharmacology. Model and exposure: Mouse behavior accompanying the 1995 binding study. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin, a component of Matricaria recutita flowers, is a central benzodiazepine receptors-ligand with anxiolytic effects. | 1995 | https://pubmed.ncbi.nlm.nih.gov/7617761/ | https://doi.org/10.1055/s-2006-958058 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
The eight-week chamomile trial found greater reduction of HAM-A scores than placebo, with primary comparison P=0.047.
Chamomile extract in the 2009 generalized-anxiety trial → Human HAM-A score in the 2009 chamomile trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Chamomile extract", "comparator": "Placebo", "endpoint": "The eight-week chamomile trial found greater reduction of HAM-A scores than placebo, with primary comparison P=0.047.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
57 randomized participants, 28 extract and 29 placebo; mild-to-moderate generalized anxiety.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The eight-week chamomile trial found greater reduction of HAM-A scores than placebo, with primary comparison P=0.047.
primary_references
A randomized, double-blind, placebo-controlled trial of oral Matricaria recutita (chamomile) extract therapy for generalized anxiety disorder. | https://pubmed.ncbi.nlm.nih.gov/19593179/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3600416/ | https://doi.org/10.1097/jcp.0b013e3181ac935c
source_locator
Reviewed reference api-chamomile-gad2009; The active constituent was not isolated; this does not establish apigenin monotherapy efficacy.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 812–818
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 57 randomized participants, 28 extract and 29 placebo; mild-to-moderate generalized anxiety. · Recorded from source · Recorded from source
### api-chamomile-gad2009 The eight-week chamomile trial found greater reduction of HAM-A scores than placebo, with primary comparison P=0.047. The active constituent was not isolated; this does not establish apigenin monotherapy efficacy. Model and exposure: 57 randomized participants, 28 extract and 29 placebo; mild-to-moderate generalized anxiety. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: A randomized, double-blind, placebo-controlled trial of oral Matricaria recutita (chamomile) extract therapy for generalized anxiety disorder. | 2009 | https://pubmed.ncbi.nlm.nih.gov/19593179/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3600416/ | https://doi.org/10.1097/jcp.0b013e3181ac935c | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Chamomile continuation did not significantly reduce the primary relapse outcome: 7/46 versus 12/47, hazard ratio 0.52, 95% CI 0.20–1.33, P=0.16.
Chamomile extract in the 2016 anxiety-relapse trial → Anxiety relapse in the 2016 chamomile continuation trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Continued chamomile extract", "comparator": "Placebo after initial response", "endpoint": "Chamomile continuation did not significantly reduce the primary relapse outcome: 7/46 versus 12/47, hazard ratio 0.52, 95% CI 0.20–1.33, P=0.16.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
93 responders randomized after a 12-week open-label phase; 1500 mg extract/day, 26-week continuation.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Chamomile continuation did not significantly reduce the primary relapse outcome: 7/46 versus 12/47, hazard ratio 0.52, 95% CI 0.20–1.33, P=0.16.
primary_references
Long-term chamomile (Matricaria chamomilla L.) treatment for generalized anxiety disorder: A randomized clinical trial. | https://pubmed.ncbi.nlm.nih.gov/27912875/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5646235/ | https://doi.org/10.1016/j.phymed.2016.10.012
source_locator
Reviewed reference api-chamomile-relapse-null; Responder-enriched design and imprecision limit inference. Secondary symptom scores improved, but they do not replace the null primary outcome.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 820–826
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 93 responders randomized after a 12-week open-label phase; 1500 mg extract/day, 26-week continuation. · Recorded from source · Recorded from source
### api-chamomile-relapse-null Chamomile continuation did not significantly reduce the primary relapse outcome: 7/46 versus 12/47, hazard ratio 0.52, 95% CI 0.20–1.33, P=0.16. Responder-enriched design and imprecision limit inference. Secondary symptom scores improved, but they do not replace the null primary outcome. Model and exposure: 93 responders randomized after a 12-week open-label phase; 1500 mg extract/day, 26-week continuation. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Long-term chamomile (Matricaria chamomilla L.) treatment for generalized anxiety disorder: A randomized clinical trial. | 2016 | https://pubmed.ncbi.nlm.nih.gov/27912875/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5646235/ | https://doi.org/10.1016/j.phymed.2016.10.012 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
The continuation trial reported better secondary anxiety-symptom scores with chamomile, P=0.0032.
Chamomile extract in the 2016 anxiety-relapse trial → Secondary anxiety symptoms in the 2016 chamomile trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Continued extract", "comparator": "Placebo", "endpoint": "The continuation trial reported better secondary anxiety-symptom scores with chamomile, P=0.0032.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Same responder-enriched study.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The continuation trial reported better secondary anxiety-symptom scores with chamomile, P=0.0032.
primary_references
Long-term chamomile (Matricaria chamomilla L.) treatment for generalized anxiety disorder: A randomized clinical trial. | https://pubmed.ncbi.nlm.nih.gov/27912875/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5646235/ | https://doi.org/10.1016/j.phymed.2016.10.012
source_locator
Reviewed reference api-chamomile-symptoms; Kept alongside the nonsignificant primary relapse result, not substituted for it.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 828–834
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Same responder-enriched study. · Recorded from source · Recorded from source
### api-chamomile-symptoms The continuation trial reported better secondary anxiety-symptom scores with chamomile, P=0.0032. Kept alongside the nonsignificant primary relapse result, not substituted for it. Model and exposure: Same responder-enriched study. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Long-term chamomile (Matricaria chamomilla L.) treatment for generalized anxiety disorder: A randomized clinical trial. | 2016 | https://pubmed.ncbi.nlm.nih.gov/27912875/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5646235/ | https://doi.org/10.1016/j.phymed.2016.10.012 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Chamomile did not significantly improve total sleep time, sleep efficiency or the other reported sleep-diary outcomes.
Chamomile extract in the 2011 insomnia trial → Sleep-diary outcomes in the 2011 chamomile trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract reviewed; full text located but not used to extract additional methods. The exact tested preparation remains the actor.
experimental_contrast
{"intervention": "Chamomile extract", "comparator": "Placebo", "endpoint": "Chamomile did not significantly improve total sleep time, sleep efficiency or the other reported sleep-diary outcomes.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
34 adults; 270 mg extract twice daily, 28 days.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Chamomile did not significantly improve total sleep time, sleep efficiency or the other reported sleep-diary outcomes.
primary_references
Preliminary examination of the efficacy and safety of a standardized chamomile extract for chronic primary insomnia: a randomized placebo-controlled pilot study. | https://pubmed.ncbi.nlm.nih.gov/21939549/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3198755/ | https://doi.org/10.1186/1472-6882-11-78
source_locator
Reviewed reference api-chamomile-insomnia-null; A small extract trial cannot establish that purified apigenin is an effective hypnotic.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 836–842
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 34 adults; 270 mg extract twice daily, 28 days. · Recorded from source · Recorded from source
### api-chamomile-insomnia-null Chamomile did not significantly improve total sleep time, sleep efficiency or the other reported sleep-diary outcomes. A small extract trial cannot establish that purified apigenin is an effective hypnotic. Model and exposure: 34 adults; 270 mg extract twice daily, 28 days. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Preliminary examination of the efficacy and safety of a standardized chamomile extract for chronic primary insomnia: a randomized placebo-controlled pilot study. | 2011 | https://pubmed.ncbi.nlm.nih.gov/21939549/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3198755/ | https://doi.org/10.1186/1472-6882-11-78 | Access: Indexed primary abstract reviewed; full text located but not used to extract additional methods. The exact tested preparation remains the actor.
Complete structured claim and evidence
Apigenin inhibited recombinant human CYP3A4-dependent nifedipine oxidation with IC50 8.4 ± 1.1 micromolar.
Apigenin → Human cytochrome P450 3A4 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin concentration series", "comparator": "Enzyme without inhibitor", "endpoint": "Apigenin inhibited recombinant human CYP3A4-dependent nifedipine oxidation with IC50 8.4 ± 1.1 micromolar.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Baculosomal human CYP3A4 with reductase/cytochrome b5 and NADPH regeneration.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin inhibited recombinant human CYP3A4-dependent nifedipine oxidation with IC50 8.4 ± 1.1 micromolar.
primary_references
Characterization of the CYP3A4 Enzyme Inhibition Potential of Selected Flavonoids. | https://pubmed.ncbi.nlm.nih.gov/34069400/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC8158701/ | https://doi.org/10.3390/molecules26103018
source_locator
Reviewed reference api-cyp3a4-inhibition; Assay substrate and preincubation conditions determine potency; no universal supplement-dose threshold follows.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 848–854
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Baculosomal human CYP3A4 with reductase/cytochrome b5 and NADPH regeneration. · Recorded from source · Recorded from source
### api-cyp3a4-inhibition Apigenin inhibited recombinant human CYP3A4-dependent nifedipine oxidation with IC50 8.4 ± 1.1 micromolar. Assay substrate and preincubation conditions determine potency; no universal supplement-dose threshold follows. Model and exposure: Baculosomal human CYP3A4 with reductase/cytochrome b5 and NADPH regeneration. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Characterization of the CYP3A4 Enzyme Inhibition Potential of Selected Flavonoids. | 2021 | https://pubmed.ncbi.nlm.nih.gov/34069400/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC8158701/ | https://doi.org/10.3390/molecules26103018 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin produced time-dependent CYP3A4 inactivation with reported KI 20.2 ± 12.7 micromolar and kinact 0.11 ± 0.04 per minute.
Apigenin → Human cytochrome P450 3A4 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin preincubation", "comparator": "Matched no-apigenin incubation", "endpoint": "Apigenin produced time-dependent CYP3A4 inactivation with reported KI 20.2 ± 12.7 micromolar and kinact 0.11 ± 0.04 per minute.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Recombinant human CYP3A4; persistence after dialysis/oxidant challenge was investigated.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin produced time-dependent CYP3A4 inactivation with reported KI 20.2 ± 12.7 micromolar and kinact 0.11 ± 0.04 per minute.
primary_references
Characterization of the CYP3A4 Enzyme Inhibition Potential of Selected Flavonoids. | https://pubmed.ncbi.nlm.nih.gov/34069400/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC8158701/ | https://doi.org/10.3390/molecules26103018
source_locator
Reviewed reference api-cyp3a4-inactivation; The proposed heme-adduct mechanism was not a directly identified covalent adduct structure.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 856–862
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant human CYP3A4; persistence after dialysis/oxidant challenge was investigated. · Recorded from source · Recorded from source
### api-cyp3a4-inactivation Apigenin produced time-dependent CYP3A4 inactivation with reported KI 20.2 ± 12.7 micromolar and kinact 0.11 ± 0.04 per minute. The proposed heme-adduct mechanism was not a directly identified covalent adduct structure. Model and exposure: Recombinant human CYP3A4; persistence after dialysis/oxidant challenge was investigated. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Characterization of the CYP3A4 Enzyme Inhibition Potential of Selected Flavonoids. | 2021 | https://pubmed.ncbi.nlm.nih.gov/34069400/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC8158701/ | https://doi.org/10.3390/molecules26103018 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
With 25 micromolar apigenin for 30 minutes, residual heme signal was approximately 45% of control in the enzyme preparation.
Apigenin → Spectrally measured heme in the apigenin CYP3A4 preparation Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin preincubation", "comparator": "No-apigenin preparation", "endpoint": "With 25 micromolar apigenin for 30 minutes, residual heme signal was approximately 45% of control in the enzyme preparation.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Recombinant CYP3A4 heme assay; SOD/catalase condition retained about 55%.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
With 25 micromolar apigenin for 30 minutes, residual heme signal was approximately 45% of control in the enzyme preparation.
primary_references
Characterization of the CYP3A4 Enzyme Inhibition Potential of Selected Flavonoids. | https://pubmed.ncbi.nlm.nih.gov/34069400/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC8158701/ | https://doi.org/10.3390/molecules26103018
source_locator
Reviewed reference api-cyp3a4-heme; This is not evidence that oral apigenin causes systemic iron deficiency.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 864–870
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Recombinant CYP3A4 heme assay; SOD/catalase condition retained about 55%. · Recorded from source · Recorded from source
### api-cyp3a4-heme With 25 micromolar apigenin for 30 minutes, residual heme signal was approximately 45% of control in the enzyme preparation. This is not evidence that oral apigenin causes systemic iron deficiency. Model and exposure: Recombinant CYP3A4 heme assay; SOD/catalase condition retained about 55%. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Characterization of the CYP3A4 Enzyme Inhibition Potential of Selected Flavonoids. | 2021 | https://pubmed.ncbi.nlm.nih.gov/34069400/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC8158701/ | https://doi.org/10.3390/molecules26103018 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin pretreatment increased oral dasatinib Cmax by about 94.6% and AUC0–t by about 80.2% in rats.
Apigenin → Dasatinib Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_condition
Dasatinib alone Apigenin pretreatment plus dasatinib · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Dasatinib alone oral partner drug · Dasatinib Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin pretreatment plus dasatinib", "comparator": "Dasatinib alone", "endpoint": "Apigenin pretreatment increased oral dasatinib Cmax by about 94.6% and AUC0–t by about 80.2% in rats.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin pretreatment plus dasatinib"}, {"entity_slug": "dasatinib", "state": "oral partner drug"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
n=6/group; reported 40 mg/kg/day oral apigenin pretreatment for 7 days; dasatinib 25 mg/kg on day 7.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin pretreatment increased oral dasatinib Cmax by about 94.6% and AUC0–t by about 80.2% in rats.
primary_references
Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism. | https://pubmed.ncbi.nlm.nih.gov/36838589/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9964503/ | https://doi.org/10.3390/molecules28041602
source_locator
Reviewed reference api-rat-dasatinib; The abstract and Results describe pretreatment; regimen wording is imperfect in one Methods sentence. Rat exposure does not determine the human interaction magnitude.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 872–878
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · n=6/group; reported 40 mg/kg/day oral apigenin pretreatment for 7 days; dasatinib 25 mg/kg on day 7. · Recorded from source · Recorded from source
### api-rat-dasatinib Apigenin pretreatment increased oral dasatinib Cmax by about 94.6% and AUC0–t by about 80.2% in rats. The abstract and Results describe pretreatment; regimen wording is imperfect in one Methods sentence. Rat exposure does not determine the human interaction magnitude. Model and exposure: n=6/group; reported 40 mg/kg/day oral apigenin pretreatment for 7 days; dasatinib 25 mg/kg on day 7. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism. | 2023 | https://pubmed.ncbi.nlm.nih.gov/36838589/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9964503/ | https://doi.org/10.3390/molecules28041602 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin decreased measured hepatic/intestinal Rat cytochrome P450 3A2 / Cyp3a2 expression in the rat dasatinib study.
Apigenin → Rat cytochrome P450 3A2 / Cyp3a2 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin pretreatment in the drug experiment", "comparator": "Drug-only controls", "endpoint": "Apigenin decreased measured hepatic/intestinal Rat cytochrome P450 3A2 / Cyp3a2 expression in the rat dasatinib study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Seven-day oral apigenin regimen with subsequent dasatinib exposure.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin decreased measured hepatic/intestinal Rat cytochrome P450 3A2 / Cyp3a2 expression in the rat dasatinib study.
primary_references
Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism. | https://pubmed.ncbi.nlm.nih.gov/36838589/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9964503/ | https://doi.org/10.3390/molecules28041602
source_locator
Reviewed reference api-rat-cyp3a2; Protein/mRNA expression is not a transport-flux or human clinical drug-clearance measurement.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 880–886
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Seven-day oral apigenin regimen with subsequent dasatinib exposure. · Recorded from source · Recorded from source
### api-rat-cyp3a2 Apigenin decreased measured hepatic/intestinal Rat cytochrome P450 3A2 / Cyp3a2 expression in the rat dasatinib study. Protein/mRNA expression is not a transport-flux or human clinical drug-clearance measurement. Model and exposure: Seven-day oral apigenin regimen with subsequent dasatinib exposure. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism. | 2023 | https://pubmed.ncbi.nlm.nih.gov/36838589/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9964503/ | https://doi.org/10.3390/molecules28041602 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin decreased measured hepatic/intestinal Rat P-glycoprotein / Abcb1 transporters expression in the rat dasatinib study.
Apigenin → Rat P-glycoprotein / Abcb1 transporters Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin pretreatment in the drug experiment", "comparator": "Drug-only controls", "endpoint": "Apigenin decreased measured hepatic/intestinal Rat P-glycoprotein / Abcb1 transporters expression in the rat dasatinib study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Seven-day oral apigenin regimen with subsequent dasatinib exposure.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin decreased measured hepatic/intestinal Rat P-glycoprotein / Abcb1 transporters expression in the rat dasatinib study.
primary_references
Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism. | https://pubmed.ncbi.nlm.nih.gov/36838589/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9964503/ | https://doi.org/10.3390/molecules28041602
source_locator
Reviewed reference api-rat-pgp; Protein/mRNA expression is not a transport-flux or human clinical drug-clearance measurement.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 888–894
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Seven-day oral apigenin regimen with subsequent dasatinib exposure. · Recorded from source · Recorded from source
### api-rat-pgp Apigenin decreased measured hepatic/intestinal Rat P-glycoprotein / Abcb1 transporters expression in the rat dasatinib study. Protein/mRNA expression is not a transport-flux or human clinical drug-clearance measurement. Model and exposure: Seven-day oral apigenin regimen with subsequent dasatinib exposure. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism. | 2023 | https://pubmed.ncbi.nlm.nih.gov/36838589/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9964503/ | https://doi.org/10.3390/molecules28041602 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin decreased measured hepatic/intestinal Rat breast cancer resistance protein / Abcg2 expression in the rat dasatinib study.
Apigenin → Rat breast cancer resistance protein / Abcg2 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
experimental_contrast
{"intervention": "Apigenin pretreatment in the drug experiment", "comparator": "Drug-only controls", "endpoint": "Apigenin decreased measured hepatic/intestinal Rat breast cancer resistance protein / Abcg2 expression in the rat dasatinib study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Seven-day oral apigenin regimen with subsequent dasatinib exposure.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin decreased measured hepatic/intestinal Rat breast cancer resistance protein / Abcg2 expression in the rat dasatinib study.
primary_references
Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism. | https://pubmed.ncbi.nlm.nih.gov/36838589/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9964503/ | https://doi.org/10.3390/molecules28041602
source_locator
Reviewed reference api-rat-bcrp; Protein/mRNA expression is not a transport-flux or human clinical drug-clearance measurement.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 896–902
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Seven-day oral apigenin regimen with subsequent dasatinib exposure. · Recorded from source · Recorded from source
### api-rat-bcrp Apigenin decreased measured hepatic/intestinal Rat breast cancer resistance protein / Abcg2 expression in the rat dasatinib study. Protein/mRNA expression is not a transport-flux or human clinical drug-clearance measurement. Model and exposure: Seven-day oral apigenin regimen with subsequent dasatinib exposure. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Effects of Apigenin on Pharmacokinetics of Dasatinib and Probable Interaction Mechanism. | 2023 | https://pubmed.ncbi.nlm.nih.gov/36838589/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9964503/ | https://doi.org/10.3390/molecules28041602 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidence
Apigenin at 25 micromolar for 24 hours decreased intracellular glutathione in PC-3 cells; the reported apigenin/chrysin reductions were approximately 50–70%.
Apigenin → GSH Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_contrast
{"intervention": "Apigenin exposure", "comparator": "Vehicle", "endpoint": "Apigenin at 25 micromolar for 24 hours decreased intracellular glutathione in PC-3 cells; the reported apigenin/chrysin reductions were approximately 50–70%.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
Human prostate-cancer PC-3 cells; primary abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin at 25 micromolar for 24 hours decreased intracellular glutathione in PC-3 cells; the reported apigenin/chrysin reductions were approximately 50–70%.
primary_references
Flavonoid-induced glutathione depletion: potential implications for cancer treatment. | https://pubmed.ncbi.nlm.nih.gov/16781454/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3983951/ | https://doi.org/10.1016/j.freeradbiomed.2006.03.002
source_locator
Reviewed reference api-pc3-gsh; Later drug-potentiation comparisons in the abstract used chrysin/chalcone and must not be reassigned to apigenin. This is not a demonstrated nutritional GSH depletion syndrome.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 904–910
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human prostate-cancer PC-3 cells; primary abstract. · Recorded from source · Recorded from source
### api-pc3-gsh Apigenin at 25 micromolar for 24 hours decreased intracellular glutathione in PC-3 cells; the reported apigenin/chrysin reductions were approximately 50–70%. Later drug-potentiation comparisons in the abstract used chrysin/chalcone and must not be reassigned to apigenin. This is not a demonstrated nutritional GSH depletion syndrome. Model and exposure: Human prostate-cancer PC-3 cells; primary abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Flavonoid-induced glutathione depletion: potential implications for cancer treatment. | 2006 | https://pubmed.ncbi.nlm.nih.gov/16781454/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3983951/ | https://doi.org/10.1016/j.freeradbiomed.2006.03.002 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin formed Cu(II) complexes in the cell-free metal-binding study despite lacking a catechol group.
Apigenin → Copper(II) ion Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_model
UV spectroscopy and electrospray mass spectrometry; pH 5.5 and 7.4.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin formed Cu(II) complexes in the cell-free metal-binding study despite lacking a catechol group.
primary_references
Interactions of flavonoids with iron and copper ions: a mechanism for their antioxidant activity. | https://pubmed.ncbi.nlm.nih.gov/12592672/ | https://doi.org/10.1080/1071576021000016463
source_locator
Reviewed reference api-copper-complex; Coordination involving the 5-hydroxyl/4-oxo region was proposed. Complex formation does not establish therapeutic chelation, copper depletion or net antioxidant benefit.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 912–918
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · UV spectroscopy and electrospray mass spectrometry; pH 5.5 and 7.4. · Recorded from source · Recorded from source
### api-copper-complex Apigenin formed Cu(II) complexes in the cell-free metal-binding study despite lacking a catechol group. Coordination involving the 5-hydroxyl/4-oxo region was proposed. Complex formation does not establish therapeutic chelation, copper depletion or net antioxidant benefit. Model and exposure: UV spectroscopy and electrospray mass spectrometry; pH 5.5 and 7.4. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Interactions of flavonoids with iron and copper ions: a mechanism for their antioxidant activity. | 2002 | https://pubmed.ncbi.nlm.nih.gov/12592672/ | https://doi.org/10.1080/1071576021000016463 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
Apigenin had antioxidant effects at lower iron exposure but pro-oxidant effects at higher iron exposure in the tested hepatocyte system.
Apigenin → Lipid peroxidation in metal-challenged, linolenate-loaded hepatocytes Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_condition
Matched metal-exposed cells without flavonoid Apigenin with varying iron exposure · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Matched metal-exposed cells without flavonoid varying exposure; matched metal-exposed comparison · Iron Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Apigenin with varying iron exposure", "comparator": "Matched metal-exposed cells without flavonoid", "endpoint": "Apigenin had antioxidant effects at lower iron exposure but pro-oxidant effects at higher iron exposure in the tested hepatocyte system.", "effect_direction": "mixed", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin with varying iron exposure"}, {"entity_slug": "iron", "state": "varying exposure; matched metal-exposed comparison"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
Hepatocytes loaded with linolenic acid; metals 20–500 micromolar, flavonoids 10–500 micromolar; species unresolved in accessed abstract.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
Apigenin had antioxidant effects at lower iron exposure but pro-oxidant effects at higher iron exposure in the tested hepatocyte system.
primary_references
Anti- and pro-oxidative effects of flavonoids on metal-induced lipid hydroperoxide-dependent lipid peroxidation in cultured hepatocytes loaded with alpha-linolenic acid. | https://pubmed.ncbi.nlm.nih.gov/10641726/ | https://doi.org/10.1016/s0891-5849(99)00167-7
source_locator
Reviewed reference api-iron-context; This is an exposure-dependent cell result, not a prediction of dietary iron interactions.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 920–926
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Hepatocytes loaded with linolenic acid; metals 20–500 micromolar, flavonoids 10–500 micromolar; species unresolved in accessed abstract. · Recorded from source · Recorded from source
### api-iron-context Apigenin had antioxidant effects at lower iron exposure but pro-oxidant effects at higher iron exposure in the tested hepatocyte system. This is an exposure-dependent cell result, not a prediction of dietary iron interactions. Model and exposure: Hepatocytes loaded with linolenic acid; metals 20–500 micromolar, flavonoids 10–500 micromolar; species unresolved in accessed abstract. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Anti- and pro-oxidative effects of flavonoids on metal-induced lipid hydroperoxide-dependent lipid peroxidation in cultured hepatocytes loaded with alpha-linolenic acid. | 1999 | https://pubmed.ncbi.nlm.nih.gov/10641726/ | https://doi.org/10.1016/s0891-5849(99)00167-7 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
A case report described serious bleeding during combined warfarin and chamomile tea/lotion exposure.
Chamomile tea and lotion exposure in the 2006 warfarin case → Anticoagulant response to warfarin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_condition
The patient’s prior reported clinical state Reported chamomile exposure during warfarin use · Chamomile tea and lotion exposure in the 2006 warfarin case Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
The patient’s prior reported clinical state concurrent treatment · Warfarin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Reported chamomile exposure during warfarin use", "comparator": "The patient’s prior reported clinical state", "endpoint": "A case report described serious bleeding during combined warfarin and chamomile tea/lotion exposure.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "chamomile-warfarin-case-2006", "state": "Reported chamomile exposure during warfarin use"}, {"entity_slug": "warfarin", "state": "concurrent treatment"}]} Explicit extracted experimental comparison; recorded from source.
experimental_model
70-year-old woman; single uncontrolled case.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
A case report described serious bleeding during combined warfarin and chamomile tea/lotion exposure.
primary_references
Warfarin interaction with Matricaria chamomilla. | https://pubmed.ncbi.nlm.nih.gov/16636327/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC1435958/ | https://doi.org/10.1503/cmaj.051191
source_locator
Reviewed reference api-chamomile-warfarin-case; Temporal association is not proof of causality or identification of apigenin as the interacting constituent.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 928–934
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 70-year-old woman; single uncontrolled case. · Recorded from source · Recorded from source
### api-chamomile-warfarin-case A case report described serious bleeding during combined warfarin and chamomile tea/lotion exposure. Temporal association is not proof of causality or identification of apigenin as the interacting constituent. Model and exposure: 70-year-old woman; single uncontrolled case. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Warfarin interaction with Matricaria chamomilla. | 2006 | https://pubmed.ncbi.nlm.nih.gov/16636327/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC1435958/ | https://doi.org/10.1503/cmaj.051191 | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence
The small crossover study found no significant change in its coagulation endpoints after chamomile tea or extract.
Chamomile tea or extract in the 2023 healthy-volunteer crossover study → Coagulation tests in the healthy-volunteer chamomile study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract reviewed; full text located but not used to extract additional methods. The exact tested preparation remains the actor.
experimental_contrast
{"intervention": "Chamomile tea or extract", "comparator": "Placebo/control arm", "endpoint": "The small crossover study found no significant change in its coagulation endpoints after chamomile tea or extract.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
experimental_model
12 healthy volunteers; seven-day arms including nine tea bags/day or extract three times daily.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The small crossover study found no significant change in its coagulation endpoints after chamomile tea or extract.
primary_references
Effect of chamomile intake on blood coagulation tests in healthy volunteers: a randomized, placebo-controlled, crossover trial. | https://pubmed.ncbi.nlm.nih.gov/37730613/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10510223/ | https://doi.org/10.1186/s13741-023-00339-7
source_locator
Reviewed reference api-chamomile-coagulation-null; No warfarin coadministration: this cannot exclude a warfarin interaction. It is not evidence about isolated apigenin.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 936–942
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 12 healthy volunteers; seven-day arms including nine tea bags/day or extract three times daily. · Recorded from source · Recorded from source
### api-chamomile-coagulation-null The small crossover study found no significant change in its coagulation endpoints after chamomile tea or extract. No warfarin coadministration: this cannot exclude a warfarin interaction. It is not evidence about isolated apigenin. Model and exposure: 12 healthy volunteers; seven-day arms including nine tea bags/day or extract three times daily. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Effect of chamomile intake on blood coagulation tests in healthy volunteers: a randomized, placebo-controlled, crossover trial. | 2023 | https://pubmed.ncbi.nlm.nih.gov/37730613/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10510223/ | https://doi.org/10.1186/s13741-023-00339-7 | Access: Indexed primary abstract reviewed; full text located but not used to extract additional methods. The exact tested preparation remains the actor.
Complete structured claim and evidence
The report described anaphylaxis after chamomile tea in an atopic child, with IgE cross-reactivity involving plant/pollen preparations.
Chamomile tea in the 1989 allergy case → IgE-associated reaction to chamomile in the 1989 case Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
experimental_model
Eight-year-old boy; case report and allergy testing.
interpretation_status
Recorded from source with stated access limits; ungraded, not independent replication.
limitations
Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
nutrient_topic
Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
plain_language
The report described anaphylaxis after chamomile tea in an atopic child, with IgE cross-reactivity involving plant/pollen preparations.
primary_references
Anaphylactic reaction after the ingestion of chamomile tea: a study of cross-reactivity with other composite pollens. | https://pubmed.ncbi.nlm.nih.gov/2674263/ | https://doi.org/10.1016/0091-6749(89)90420-x
source_locator
Reviewed reference api-chamomile-allergy; This does not identify purified apigenin as the allergen; the preparation remains the actor.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 944–950
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Eight-year-old boy; case report and allergy testing. · Recorded from source · Recorded from source
### api-chamomile-allergy The report described anaphylaxis after chamomile tea in an atopic child, with IgE cross-reactivity involving plant/pollen preparations. This does not identify purified apigenin as the allergen; the preparation remains the actor. Model and exposure: Eight-year-old boy; case report and allergy testing. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Anaphylactic reaction after the ingestion of chamomile tea: a study of cross-reactivity with other composite pollens. | 1989 | https://pubmed.ncbi.nlm.nih.gov/2674263/ | https://doi.org/10.1016/0091-6749(89)90420-x | Access: Indexed primary abstract/metadata only; unextracted doses, figures and methods remain unknown.
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

CD38 loss separates NAD and inflammasome responses

Condition: machinery_impairment · Cd38 deletion in mouse cells