Human cytochrome P450 2C9

evidence_span

{"source_cache": "artifacts/thc-research/38583809.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "29593807ef463cf784578c2920ed864667e6ef46a0125ac14757a38c6b331bb1", "start_char": 0, "end_char": 1645, "text_sha256": "29593807ef463cf784578c2920ed864667e6ef46a0125ac14757a38c6b331bb1"}

experimental_model

Recombinant enzyme metabolism of THC with and without liver fatty acid binding protein

exposure

THC metabolism by CYP2C9, CYP3A and CYP2C19 with FABP1

limitations

Adds a binding protein that changes apparent metabolism, which matters because THC is extremely lipophilic. It is a recombinant system.

nutrient_topic

THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC

organism

Human enzymes

plain_language

Three enzymes share the job, and a fat-carrying protein changes how fast they do it.

primary_references

[thc-p38583809] CYP2C9, CYP3A and CYP2C19 metabolize Δ9-tetrahydrocannabinol to multiple metabolites but metabolism is affected by human liver fatty acid binding protein (FABP1). (2024). https://pubmed.ncbi.nlm.nih.gov/38583809/ DOI: 10.1016/j.bcp.2024.116191

tissue_or_cell_type

Recombinant system

THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 543–554

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant enzyme metabolism of THC with and without liver fatty acid binding protein · source_derived_draft · unverified_draft

### thc-multiple-cyps CYP2C9, CYP3A and CYP2C19 metabolised THC to multiple metabolites, but the metabolism was affected by human liver fatty acid binding protein. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: Three enzymes share the job, and a fat-carrying protein changes how fast they do it. organism: Human enzymes tissue_or_cell_type: Recombinant system experimental_model: Recombinant enzyme metabolism of THC with and without liver fatty acid binding protein limitations: Adds a binding protein that changes apparent metabolism, which matters because THC is extremely lipophilic. It is a recombinant system. exposure: THC metabolism by CYP2C9, CYP3A and CYP2C19 with FABP1 evidence_span: {"source_cache": "artifacts/thc-research/38583809.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "29593807ef463cf784578c2920ed864667e6ef46a0125ac14757a38c6b331bb1", "start_char": 0, "end_char": 1645, "text_sha256": "29593807ef463cf784578c2920ed864667e6ef46a0125ac14757a38c6b331bb1"} [thc-p38583809] CYP2C9, CYP3A and CYP2C19 metabolize Δ9-tetrahydrocannabinol to multiple metabolites but metabolism is affected by human liver fatty acid binding protein (FABP1). (2024). https://pubmed.ncbi.nlm.nih.gov/38583809/ DOI: 10.1016/j.bcp.2024.116191

evidence_span

{"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"}

experimental_model

Human receptor reporters and CYP inhibition assays

exposure

Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours

limitations

Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T.

nutrient_topic

Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations

organism

Human-derived reporter cells and human CYP assay systems

plain_language

The enzyme assay identifies an interaction to investigate, not a proven change in drug exposure.

primary_references

[ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

tissue_or_cell_type

HepG2, LS174T and AhR reporter cells

Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 870–881

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human receptor reporters and CYP inhibition assays · source_derived_draft · unverified_draft

### ceylon-ca-cyp2c9 Cinnamaldehyde inhibited CYP2C9 catalytic activity in the study enzyme assay. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: The enzyme assay identifies an interaction to investigate, not a proven change in drug exposure. organism: Human-derived reporter cells and human CYP assay systems tissue_or_cell_type: HepG2, LS174T and AhR reporter cells experimental_model: Human receptor reporters and CYP inhibition assays limitations: Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T. exposure: Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours evidence_span: {"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"} [ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

evidence_span

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experimental_model

Human receptor reporters and CYP inhibition assays

exposure

Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours

limitations

Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T.

nutrient_topic

Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations

organism

Human-derived reporter cells and human CYP assay systems

plain_language

This separate mixture result remains distinct from the pure chemical result.

primary_references

[ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

tissue_or_cell_type

HepG2, LS174T and AhR reporter cells

Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 896–907

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human receptor reporters and CYP inhibition assays · source_derived_draft · unverified_draft

### ceylon-oil-cyp2c9 The C. verum oil inhibited CYP2C9 catalytic activity in the study assay. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: This separate mixture result remains distinct from the pure chemical result. organism: Human-derived reporter cells and human CYP assay systems tissue_or_cell_type: HepG2, LS174T and AhR reporter cells experimental_model: Human receptor reporters and CYP inhibition assays limitations: Reporter activation is not demonstrated induction of clinical drug clearance. HepG2 is liver-derived; full results distinguish it from intestinal LS174T. exposure: Oil/parent/metabolite comparisons; PXR 0.62–20 micrograms/mL for 24 hours evidence_span: {"source_cache": "artifacts/ceylon-research/39845339.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118", "start_char": 0, "end_char": 1463, "text_sha256": "243c3bd561d9ff4d7dfe10fa748b1aacc0941a4ec9f712615f7dd7df4e98f118"} [ceylon-p39845339] Evaluation of bioaccessibility, metabolic clearance and interaction with xenobiotic receptors (PXR and AhR) of cinnamaldehyde. (2025). https://pubmed.ncbi.nlm.nih.gov/39845339/ DOI: 10.1016/j.fochms.2024.100237

evidence_span

{"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"}

experimental_model

Primary human hepatocyte exposure

exposure

Mangiferin 50-250 micrograms/mL for 48 hours

limitations

High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct.

nutrient_topic

Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin

organism

Homo sapiens

plain_language

A drug-metabolizing enzyme was inhibited under the tested exposure.

primary_references

[mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782

tissue_or_cell_type

Cultured hepatocytes

Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 796–807

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocyte exposure · source_derived_draft · unverified_draft

### mangiferin-cyp2c9-activity Mangiferin reduced measured CYP2C9 activity in the hepatocyte experiment. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A drug-metabolizing enzyme was inhibited under the tested exposure. organism: Homo sapiens tissue_or_cell_type: Cultured hepatocytes experimental_model: Primary human hepatocyte exposure limitations: High in vitro concentrations; decreased enzyme activity is not proof of human drug-level changes. Extract and isolated mangiferin are distinct. exposure: Mangiferin 50-250 micrograms/mL for 48 hours evidence_span: {"source_cache": "artifacts/mangiferin-research/22815239.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0", "start_char": 0, "end_char": 1728, "text_sha256": "e85ebd0af89f030dbeda45ed922e93a8a616c51f5ce1b64badc44d90791716c0"} [mangiferin-p22815239] Mangifera indica L. extract and mangiferin modulate cytochrome P450 and UDP-glucuronosyltransferase enzymes in primary cultures of human hepatocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/22815239/ DOI: 10.1002/ptr.4782

evidence_access

Primary full text

experimental_model

42 initiated; enzyme activities assessed in 40; before/after pharmacological-dose study.

limitations

Probe indices are not proof of transcriptional induction or a quantified interaction with every substrate; no medication adjustment follows.

nutrient_topic

Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol

plain_language

A human drug-metabolism interaction was measured with a specific probe.

primary_references

Resveratrol modulates drug- and carcinogen-metabolizing enzymes in a healthy volunteer study. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20716633/ · DOI 10.1158/1940-6207.CAPR-09-0155

Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 430–436

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 42 initiated; enzyme activities assessed in 40; before/after pharmacological-dose study. · source_derived_draft · unverified_draft

## resveratrol-human-cyp2c9 A human drug-metabolism interaction was measured with a specific probe. After 1 g/day resveratrol for four weeks, the healthy-volunteer study found decreased CYP2C9 phenotypic activity using losartan as the probe. Model: 42 initiated; enzyme activities assessed in 40; before/after pharmacological-dose study. Limitations: Probe indices are not proof of transcriptional induction or a quantified interaction with every substrate; no medication adjustment follows. Evidence access: Primary full text Resveratrol modulates drug- and carcinogen-metabolizing enzymes in a healthy volunteer study. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20716633/ · DOI 10.1158/1940-6207.CAPR-09-0155

evidence_span

{"source_cache": "artifacts/curcumin-research/18480186.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1155ca38a767b3c3fa7bd494d0ad5590eed70a47812b7a6f3d977b43aa8a922", "start_char": 0, "end_char": 1788, "text_sha256": "c1155ca38a767b3c3fa7bd494d0ad5590eed70a47812b7a6f3d977b43aa8a922"}

experimental_model

Human microsomal/cytosolic and recombinant enzyme inhibition assays

exposure

Curcuminoid mixture, purified curcuminoids and piperine; micromolar concentrations

limitations

In-vitro inhibition does not automatically predict human drug levels. Extract, isolated curcumin and piperine are separate interventions.

nutrient_topic

Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin

organism

Human enzyme systems

plain_language

Related curcuminoids did not have identical effects.

primary_references

[curcumin-p18480186] Curcuminoids inhibit multiple human cytochromes P450, UDP-glucuronosyltransferase, and sulfotransferase enzymes, whereas piperine is a relatively selective CYP3A4 inhibitor. (2008). https://pubmed.ncbi.nlm.nih.gov/18480186/ DOI: 10.1124/dmd.108.020552

tissue_or_cell_type

Drug metabolism assays

Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 866–877

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human microsomal/cytosolic and recombinant enzyme inhibition assays · source_derived_draft · unverified_draft

### curcumin-extract-cyp2c9 The mixture inhibited CYP2C9; purified curcumin was less potent than demethoxycurcumin against this activity. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Related curcuminoids did not have identical effects. organism: Human enzyme systems tissue_or_cell_type: Drug metabolism assays experimental_model: Human microsomal/cytosolic and recombinant enzyme inhibition assays limitations: In-vitro inhibition does not automatically predict human drug levels. Extract, isolated curcumin and piperine are separate interventions. exposure: Curcuminoid mixture, purified curcuminoids and piperine; micromolar concentrations evidence_span: {"source_cache": "artifacts/curcumin-research/18480186.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1155ca38a767b3c3fa7bd494d0ad5590eed70a47812b7a6f3d977b43aa8a922", "start_char": 0, "end_char": 1788, "text_sha256": "c1155ca38a767b3c3fa7bd494d0ad5590eed70a47812b7a6f3d977b43aa8a922"} [curcumin-p18480186] Curcuminoids inhibit multiple human cytochromes P450, UDP-glucuronosyltransferase, and sulfotransferase enzymes, whereas piperine is a relatively selective CYP3A4 inhibitor. (2008). https://pubmed.ncbi.nlm.nih.gov/18480186/ DOI: 10.1124/dmd.108.020552

evidence_access

Primary abstract

experimental_model

Enzyme activity testing accompanying a rat carvedilol study.

limitations

Later recombinant diclofenac assay showed no inhibition at 20 micromolar. Assay differences require matched replication; not a universal clinical interaction.

nutrient_topic

Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin

plain_language

An earlier enzyme assay reported greater inhibition.

primary_references

Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141

Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 220–226

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Enzyme activity testing accompanying a rat carvedilol study. · source_derived_draft · unverified_draft

## myricetin-cyp2c9-earlier An earlier enzyme assay reported greater inhibition. An earlier CYP assay reported myricetin inhibition of CYP2C9 with IC50 13 micromolar. Model: Enzyme activity testing accompanying a rat carvedilol study. Limitations: Later recombinant diclofenac assay showed no inhibition at 20 micromolar. Assay differences require matched replication; not a universal clinical interaction. Evidence access: Primary abstract Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141

evidence_access

Primary full text

experimental_model

Recombinant human enzymes; 5 micromolar substrate.

limitations

Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency.

nutrient_topic

Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin

plain_language

A transporter interaction does not imply strong CYP inhibition.

primary_references

Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 132–138

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzymes; 5 micromolar substrate. · source_derived_draft · unverified_draft

## myricetin-parent-cyp2c9 A transporter interaction does not imply strong CYP inhibition. At 20 micromolar, the parent did not inhibit diclofenac hydroxylation in the human CYP2C9 assay. Model: Recombinant human enzymes; 5 micromolar substrate. Limitations: Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

evidence_access

Primary full text

experimental_model

Recombinant human enzymes; 5 micromolar substrate.

limitations

Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency.

nutrient_topic

Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin

plain_language

A transporter interaction does not imply strong CYP inhibition.

primary_references

Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 180–186

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzymes; 5 micromolar substrate. · source_derived_draft · unverified_draft

## myricetin-sulfate-cyp2c9 A transporter interaction does not imply strong CYP inhibition. At 20 micromolar, the sulfate did not inhibit diclofenac hydroxylation in the human CYP2C9 assay. Model: Recombinant human enzymes; 5 micromolar substrate. Limitations: Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

acting_entity

s-allylcysteine

dose

SAC 0.01–1 mM; N-acetyl-SAC 1 mM

duration

Probe-specific incubation

evidence_access

Primary full-text HTML, methods/results

experimental_comparison

Test compound versus probe reaction without compound

experimental_model

Pooled human liver microsomes; probe substrate metabolism

interpretation_status

Source-derived research curation; not independent primary verification

limitations

Microsomal assay; not a clinical interaction or induction study.

nutrient_topic

S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC

organism

Human liver preparation

plain_language

A negative enzyme-interaction result is retained.

primary_references

[27725449] Evaluation of the Effects of S-Allyl-L-cysteine, S-Methyl-L-cysteine, trans-S-1-Propenyl-L-cysteine, and Their N-Acetylated and S-Oxidized Metabolites on Human CYP Activities. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27725449/ · DOI 10.1248/bpb.b16-00449

route

In vitro

tissue_or_cell_type

Pooled human liver microsomes; probe substrate metabolism

S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 392–399

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pooled human liver microsomes; probe substrate metabolism · source_derived_draft · unverified_draft

## s-allylcysteine-cyp-null-cyp2c9 A negative enzyme-interaction result is retained. SAC showed little effect on tested human CYP2C9 activity over 0.01–1 mM. Model: Pooled human liver microsomes; probe substrate metabolism Limitations: Microsomal assay; not a clinical interaction or induction study. Evidence access: Primary full-text HTML, methods/results [27725449] Evaluation of the Effects of S-Allyl-L-cysteine, S-Methyl-L-cysteine, trans-S-1-Propenyl-L-cysteine, and Their N-Acetylated and S-Oxidized Metabolites on Human CYP Activities. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27725449/ · DOI 10.1248/bpb.b16-00449 Structured context: {"organism": "Human liver preparation", "tissue_or_cell_type": "Pooled human liver microsomes; probe substrate metabolism", "dose": "SAC 0.01–1 mM; N-acetyl-SAC 1 mM", "duration": "Probe-specific incubation", "route": "In vitro", "experimental_comparison": "Test compound versus probe reaction without compound", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}

evidence_span

{"source_cache": "artifacts/thc-research/16306858.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "686c5587340a5590db33367328f93f4be704262c3d92b53f627ff01b154943da", "start_char": 0, "end_char": 2129, "text_sha256": "686c5587340a5590db33367328f93f4be704262c3d92b53f627ff01b154943da"}

experimental_model

Randomised double-blind placebo-controlled crossover in 24 volunteers

exposure

Oral THC 10 mg versus cannabis extract containing 10 mg THC plus 5.4 mg cannabidiol

limitations

A human randomised crossover. The authors conclude the cannabidiol effect is small relative to other variability, so a pharmacokinetic explanation for extract-versus-THC differences is improbable at these doses.

nutrient_topic

THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC

organism

Human

plain_language

Cannabidiol does slow one step of THC breakdown, but not enough to explain much.

primary_references

[thc-p16306858] Randomized, double-blind, placebo-controlled study about the effects of cannabidiol (CBD) on the pharmacokinetics of Delta9-tetrahydrocannabinol (THC) after oral application of THC verses standardized cannabis extract. (2005). https://pubmed.ncbi.nlm.nih.gov/16306858/ DOI: 10.1097/01.ftd.0000177223.19294.5c

tissue_or_cell_type

Plasma

THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 556–567

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised double-blind placebo-controlled crossover in 24 volunteers · source_derived_draft · unverified_draft

### thc-cbd-inhibits-hydroxylation Evidence emerged that cannabidiol partially inhibits the CYP2C-catalysed hydroxylation of THC to 11-OH-THC, with the probability particularly high for oral intake, but the effect was small compared with the variability caused by other factors, and significantly higher exposure and shorter time to peak were found in women than men. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: Cannabidiol does slow one step of THC breakdown, but not enough to explain much. organism: Human tissue_or_cell_type: Plasma experimental_model: Randomised double-blind placebo-controlled crossover in 24 volunteers limitations: A human randomised crossover. The authors conclude the cannabidiol effect is small relative to other variability, so a pharmacokinetic explanation for extract-versus-THC differences is improbable at these doses. exposure: Oral THC 10 mg versus cannabis extract containing 10 mg THC plus 5.4 mg cannabidiol evidence_span: {"source_cache": "artifacts/thc-research/16306858.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "686c5587340a5590db33367328f93f4be704262c3d92b53f627ff01b154943da", "start_char": 0, "end_char": 2129, "text_sha256": "686c5587340a5590db33367328f93f4be704262c3d92b53f627ff01b154943da"} [thc-p16306858] Randomized, double-blind, placebo-controlled study about the effects of cannabidiol (CBD) on the pharmacokinetics of Delta9-tetrahydrocannabinol (THC) after oral application of THC verses standardized cannabis extract. (2005). https://pubmed.ncbi.nlm.nih.gov/16306858/ DOI: 10.1097/01.ftd.0000177223.19294.5c

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/thc-research/19005461.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "67758630ab5ff7fc0505e51bda1d2fa1b24ec91f1569d14717bf2ec83c03e34e", "start_char": 0, "end_char": 601, "text_sha256": "67758630ab5ff7fc0505e51bda1d2fa1b24ec91f1569d14717bf2ec83c03e34e"}

experimental_model

Oral THC in 43 healthy volunteers genotyped for CYP2C9

exposure

Oral THC across CYP2C9 genotypes

limitations

A pharmacogenetic study with a clear exposure difference. The sedation finding is described as a trend.

nutrient_topic

THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC

organism

Human

plain_language

People with two copies of one variant get three times the drug exposure from the same dose.

primary_references

[thc-p19005461] Interindividual variation in the pharmacokinetics of Delta9-tetrahydrocannabinol as related to genetic polymorphisms in CYP2C9. (2009). https://pubmed.ncbi.nlm.nih.gov/19005461/ DOI: 10.1038/clpt.2008.213

tissue_or_cell_type

Whole body

trigger_kind

machinery_impairment Imported condition classification; unverified.

THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 530–541

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral THC in 43 healthy volunteers genotyped for CYP2C9 · source_derived_draft · unverified_draft

### thc-cyp2c9-exposure The median area under the curve of THC was threefold higher and that of THC-COOH 70% lower in CYP2C9*3/*3 homozygotes than in CYP2C9*1/*1 homozygotes, with a trend toward increased sedation, while CYP2C9*2 status made no difference. Condition category: machinery_impairment nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: People with two copies of one variant get three times the drug exposure from the same dose. organism: Human tissue_or_cell_type: Whole body experimental_model: Oral THC in 43 healthy volunteers genotyped for CYP2C9 limitations: A pharmacogenetic study with a clear exposure difference. The sedation finding is described as a trend. exposure: Oral THC across CYP2C9 genotypes evidence_span: {"source_cache": "artifacts/thc-research/19005461.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "67758630ab5ff7fc0505e51bda1d2fa1b24ec91f1569d14717bf2ec83c03e34e", "start_char": 0, "end_char": 601, "text_sha256": "67758630ab5ff7fc0505e51bda1d2fa1b24ec91f1569d14717bf2ec83c03e34e"} [thc-p19005461] Interindividual variation in the pharmacokinetics of Delta9-tetrahydrocannabinol as related to genetic polymorphisms in CYP2C9. (2009). https://pubmed.ncbi.nlm.nih.gov/19005461/ DOI: 10.1038/clpt.2008.213

evidence_access

Primary abstract

experimental_model

Human CYP assays.

limitations

Restricted enzyme panel; not a blanket absence of interactions.

nutrient_topic

Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone

plain_language

The parent’s effects cannot simply be assigned to every metabolite.

primary_references

Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 244–250

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human CYP assays. · source_derived_draft · unverified_draft

## luteolin-conjugate-cyp The parent’s effects cannot simply be assigned to every metabolite. Tested luteolin conjugates had no or weak inhibition of CYP2C9, CYP2C19 and CYP3A4. Model: Human CYP assays. Limitations: Restricted enzyme panel; not a blanket absence of interactions. Evidence access: Primary abstract Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/sildenafil-research/10725306.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "21d73da8afc20cb90f2aa2d9bafe7bdbefd7d07037ffb493681414b09154f6d6", "start_char": 0, "end_char": 1190, "text_sha256": "21d73da8afc20cb90f2aa2d9bafe7bdbefd7d07037ffb493681414b09154f6d6"}

experimental_model

In vitro biotransformation in human liver microsomes and microsomes containing heterologously expressed cytochromes

exposure

Formation of the major circulating metabolite with chemical inhibitors and cDNA-expressed cytochromes

limitations

Assigns the clearance quantitatively across cytochromes and identifies the inhibitors that matter. In vitro microsomes.

nutrient_topic

Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. · Sildenafil

organism

Human

plain_language

Four fifths of the clearance runs through one enzyme, so anything blocking that enzyme raises the level of the drug.

primary_references

[sil-p10725306] In vitro biotransformation of sildenafil (Viagra): identification of human cytochromes and potential drug interactions. (2000). https://pubmed.ncbi.nlm.nih.gov/10725306/ DOI: 10.1016/s0090-9556(24)15055-6

tissue_or_cell_type

Liver microsomes

trigger_kind

machinery_impairment Imported condition classification; unverified.

Sildenafil: the enzyme it occupies instead of the substrate, why it cannot start a signal it can only preserve, the organic nitrate interaction that follows from that, the homologous retinal enzyme ten-fold away, and the pulmonary circulation where the same mechanism became a second indication (2026-09-22) · lines 457–468

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vitro biotransformation in human liver microsomes and microsomes containing heterologously expressed cytochromes · source_derived_draft · unverified_draft

### sil-cyp3a4-carries-the-clearance Formation of the major circulating metabolite in human liver microsomes had a Michaelis constant of 14.4 micromolar, of the chemical inhibitors screened only ketoconazole showed detectable inhibition, biotransformation was inhibited by ketoconazole and ritonavir with half-maximal concentrations below 0.02 micromolar, and using microsomes containing cDNA-expressed cytochromes the reaction was mediated by CYP3A4, CYP2C9, CYP2C19 and CYP2D6 with estimated relative contributions to net intrinsic clearance of 79% for CYP3A4 and 20% for CYP2C9 and less than 2% for the other two. Condition category: machinery_impairment nutrient_topic: Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. plain_language: Four fifths of the clearance runs through one enzyme, so anything blocking that enzyme raises the level of the drug. organism: Human tissue_or_cell_type: Liver microsomes experimental_model: In vitro biotransformation in human liver microsomes and microsomes containing heterologously expressed cytochromes limitations: Assigns the clearance quantitatively across cytochromes and identifies the inhibitors that matter. In vitro microsomes. exposure: Formation of the major circulating metabolite with chemical inhibitors and cDNA-expressed cytochromes evidence_span: {"source_cache": "artifacts/sildenafil-research/10725306.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "21d73da8afc20cb90f2aa2d9bafe7bdbefd7d07037ffb493681414b09154f6d6", "start_char": 0, "end_char": 1190, "text_sha256": "21d73da8afc20cb90f2aa2d9bafe7bdbefd7d07037ffb493681414b09154f6d6"} [sil-p10725306] In vitro biotransformation of sildenafil (Viagra): identification of human cytochromes and potential drug interactions. (2000). https://pubmed.ncbi.nlm.nih.gov/10725306/ DOI: 10.1016/s0090-9556(24)15055-6

evidence_span

{"source_cache": "artifacts/ibuprofen-research/15606441.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "60cffa777fc0b9881548e974376299ec7e970c2785586766150896cbf0561af9", "start_char": 0, "end_char": 1795, "text_sha256": "60cffa777fc0b9881548e974376299ec7e970c2785586766150896cbf0561af9"}

experimental_model

Genotype screening of 355 Spanish Caucasians with pharmacokinetics in 25 individuals grouped by CYP2C8 genotype

exposure

400 milligrams ibuprofen, with R-ibuprofen disposition followed by genotype

limitations

A clear gene-dose effect on the enantiomer that CYP2C9 does not handle. One population, and 25 individuals across the genotype groups.

nutrient_topic

Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen

organism

Human

plain_language

A common variant makes the R half linger more than four times as long.

primary_references

[ibu-p15606441] The effect of the cytochrome P450 CYP2C8 polymorphism on the disposition of (R)-ibuprofen enantiomer in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/15606441/ DOI: 10.1111/j.1365-2125.2004.02183.x

tissue_or_cell_type

Plasma

Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 227–238

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genotype screening of 355 Spanish Caucasians with pharmacokinetics in 25 individuals grouped by CYP2C8 genotype · source_derived_draft · unverified_draft

### ibu-cyp2c8-and-the-r-hand The CYP2C8*3 allele influenced the pharmacokinetics of R-ibuprofen in a gene-dose manner, with plasma half-life after 400 milligrams of 2.0 hours in CYP2C8*1/*1, 4.2 hours in *1/*3 and 9.0 hours in *3/*3 individuals, alongside significant trends in area under the curve and clearance, and the allele frequency of 0.17 in this Spanish Caucasian population was higher than reported elsewhere and was associated with CYP2C9*2 at 2.4-fold the expected frequency. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: A common variant makes the R half linger more than four times as long. organism: Human tissue_or_cell_type: Plasma experimental_model: Genotype screening of 355 Spanish Caucasians with pharmacokinetics in 25 individuals grouped by CYP2C8 genotype limitations: A clear gene-dose effect on the enantiomer that CYP2C9 does not handle. One population, and 25 individuals across the genotype groups. exposure: 400 milligrams ibuprofen, with R-ibuprofen disposition followed by genotype evidence_span: {"source_cache": "artifacts/ibuprofen-research/15606441.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "60cffa777fc0b9881548e974376299ec7e970c2785586766150896cbf0561af9", "start_char": 0, "end_char": 1795, "text_sha256": "60cffa777fc0b9881548e974376299ec7e970c2785586766150896cbf0561af9"} [ibu-p15606441] The effect of the cytochrome P450 CYP2C8 polymorphism on the disposition of (R)-ibuprofen enantiomer in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/15606441/ DOI: 10.1111/j.1365-2125.2004.02183.x

evidence_span

{"source_cache": "artifacts/ibuprofen-research/9296349.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19179a5f8220c1d4037113812f8968e2730ecf07c6ad94997d2661d7c6c75afb", "start_char": 0, "end_char": 2012, "text_sha256": "19179a5f8220c1d4037113812f8968e2730ecf07c6ad94997d2661d7c6c75afb"}

experimental_model

Human liver microsomes and complementary-DNA-expressed cytochromes with a bank of fourteen microsomal preparations

exposure

Both enantiomers of ibuprofen assayed for 2- and 3-hydroxylation, with sulfaphenazole, retinol and arachidonic acid as inhibitors

limitations

Assigns each enantiomer to a different cytochrome by direct comparison in the same system. In vitro microsomes, though the authors note the selectivities matched those seen in vivo.

nutrient_topic

Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen

organism

Human

plain_language

The body uses two different clearance enzymes for the two hands of the same molecule.

primary_references

[ibu-p9296349] Regioselective and stereoselective metabolism of ibuprofen by human cytochrome P450 2C. (1997). https://pubmed.ncbi.nlm.nih.gov/9296349/ DOI: 10.1016/s0006-2952(97)00143-3

tissue_or_cell_type

Liver microsomes

Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 201–212

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human liver microsomes and complementary-DNA-expressed cytochromes with a bank of fourteen microsomal preparations · source_derived_draft · unverified_draft

### ibu-different-cytochromes Complementary-DNA-expressed CYP2C9 favoured formation of S-2- and S-3-hydroxyibuprofen while CYP2C8 favoured R-2-hydroxyibuprofen formation, high-affinity Km values for S-ibuprofen hydroxylation were 38 and 21 micromolar against 47 and 29 micromolar for R-ibuprofen, sulfaphenazole competitively inhibited all four hydroxylations with submicromolar Ki values, and the regio- and stereoselectivities observed in vitro were consistent with those noted in vivo. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The body uses two different clearance enzymes for the two hands of the same molecule. organism: Human tissue_or_cell_type: Liver microsomes experimental_model: Human liver microsomes and complementary-DNA-expressed cytochromes with a bank of fourteen microsomal preparations limitations: Assigns each enantiomer to a different cytochrome by direct comparison in the same system. In vitro microsomes, though the authors note the selectivities matched those seen in vivo. exposure: Both enantiomers of ibuprofen assayed for 2- and 3-hydroxylation, with sulfaphenazole, retinol and arachidonic acid as inhibitors evidence_span: {"source_cache": "artifacts/ibuprofen-research/9296349.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19179a5f8220c1d4037113812f8968e2730ecf07c6ad94997d2661d7c6c75afb", "start_char": 0, "end_char": 2012, "text_sha256": "19179a5f8220c1d4037113812f8968e2730ecf07c6ad94997d2661d7c6c75afb"} [ibu-p9296349] Regioselective and stereoselective metabolism of ibuprofen by human cytochrome P450 2C. (1997). https://pubmed.ncbi.nlm.nih.gov/9296349/ DOI: 10.1016/s0006-2952(97)00143-3

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/ibuprofen-research/12152005.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "314477c44dbb699b0fe3d9ab14eb7da427d88538177b4e4267ef0ad25fd407da", "start_char": 0, "end_char": 1822, "text_sha256": "314477c44dbb699b0fe3d9ab14eb7da427d88538177b4e4267ef0ad25fd407da"}

experimental_model

Population pharmacokinetic study in 21 healthy volunteers across all combinations of CYP2C9 variants

exposure

600 milligrams oral racemic ibuprofen, with thromboxane B2 and prostaglandin E2 measured ex vivo

limitations

Links a genotype to both the drug level and the enzyme effect in the same subjects. Twenty-one volunteers spread across genotype groups, so each group is small.

nutrient_topic

Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen

organism

Human

plain_language

People who clear the active half slowly get both more drug and more effect from the same tablet.

primary_references

[ibu-p12152005] Enantiospecific effects of cytochrome P450 2C9 amino acid variants on ibuprofen pharmacokinetics and on the inhibition of cyclooxygenases 1 and 2. (2002). https://pubmed.ncbi.nlm.nih.gov/12152005/ DOI: 10.1067/mcp.2002.125726

tissue_or_cell_type

Plasma, platelets and monocytes

trigger_kind

machinery_impairment Imported condition classification; unverified.

Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 214–225

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Population pharmacokinetic study in 21 healthy volunteers across all combinations of CYP2C9 variants · source_derived_draft · unverified_draft

### ibu-slow-clearance-more-effect Population mean S-ibuprofen clearances were 3.25, 2.38 and 1.52 litres per hour in carriers of CYP2C9 genotypes *1/*1, *1/*3 and *3/*3 respectively while the *2 variant had no significant effect, and ex vivo formation of thromboxane B2 reflecting cyclooxygenase-1 inhibition depended significantly on the polymorphism, with maximal inhibition and the area under the effect-time curve larger in carriers of the slow genotypes, the same trend holding for prostaglandin E2. Condition category: machinery_impairment nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: People who clear the active half slowly get both more drug and more effect from the same tablet. organism: Human tissue_or_cell_type: Plasma, platelets and monocytes experimental_model: Population pharmacokinetic study in 21 healthy volunteers across all combinations of CYP2C9 variants limitations: Links a genotype to both the drug level and the enzyme effect in the same subjects. Twenty-one volunteers spread across genotype groups, so each group is small. exposure: 600 milligrams oral racemic ibuprofen, with thromboxane B2 and prostaglandin E2 measured ex vivo evidence_span: {"source_cache": "artifacts/ibuprofen-research/12152005.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "314477c44dbb699b0fe3d9ab14eb7da427d88538177b4e4267ef0ad25fd407da", "start_char": 0, "end_char": 1822, "text_sha256": "314477c44dbb699b0fe3d9ab14eb7da427d88538177b4e4267ef0ad25fd407da"} [ibu-p12152005] Enantiospecific effects of cytochrome P450 2C9 amino acid variants on ibuprofen pharmacokinetics and on the inhibition of cyclooxygenases 1 and 2. (2002). https://pubmed.ncbi.nlm.nih.gov/12152005/ DOI: 10.1067/mcp.2002.125726

evidence_span

{"source_cache": "artifacts/berberine-research/21870106.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12e465c3c0a8ce995697a6fb9bf77c079e38b413e82c8b4f2a82e45a3dbf8ae5", "start_char": 0, "end_char": 1817, "text_sha256": "12e465c3c0a8ce995697a6fb9bf77c079e38b413e82c8b4f2a82e45a3dbf8ae5"}

experimental_model

Two-phase randomized crossover enzyme-phenotyping study

exposure

Berberine 300 mg three times daily for 14 days versus placebo

limitations

Small short-term study. Probe metabolic ratios are not percentage inhibition of every substrate. No universal dose-adjustment rule; no statistically significant effect is not equivalence.

nutrient_topic

Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine

organism

Healthy human male volunteers; 17 completed

plain_language

The drug-to-active-metabolite ratio changed in people.

primary_references

[berberine-p21870106] Repeated administration of berberine inhibits cytochromes P450 in humans. (2012). https://pubmed.ncbi.nlm.nih.gov/21870106/ DOI: 10.1007/s00228-011-1108-2

tissue_or_cell_type

Oral probe pharmacokinetics and urinary metabolite ratios

Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 649–660

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two-phase randomized crossover enzyme-phenotyping study · source_derived_draft · unverified_draft

### berberine-human-cyp-2c9 Berberine approximately doubled the losartan/E-3174 ratio, indicating reduced CYP2C9 activity. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug-to-active-metabolite ratio changed in people. organism: Healthy human male volunteers; 17 completed tissue_or_cell_type: Oral probe pharmacokinetics and urinary metabolite ratios experimental_model: Two-phase randomized crossover enzyme-phenotyping study limitations: Small short-term study. Probe metabolic ratios are not percentage inhibition of every substrate. No universal dose-adjustment rule; no statistically significant effect is not equivalence. exposure: Berberine 300 mg three times daily for 14 days versus placebo evidence_span: {"source_cache": "artifacts/berberine-research/21870106.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12e465c3c0a8ce995697a6fb9bf77c079e38b413e82c8b4f2a82e45a3dbf8ae5", "start_char": 0, "end_char": 1817, "text_sha256": "12e465c3c0a8ce995697a6fb9bf77c079e38b413e82c8b4f2a82e45a3dbf8ae5"} [berberine-p21870106] Repeated administration of berberine inhibits cytochromes P450 in humans. (2012). https://pubmed.ncbi.nlm.nih.gov/21870106/ DOI: 10.1007/s00228-011-1108-2