Nutrient chapter

Red yeast rice

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

53 recorded mechanisms · 2 availability situations · 4 preserved sources. Draft and verified records 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.

The 28-brand analytical study treated monacolin K in red yeast rice as chemically identical to lovastatin.
Red yeast rice → Lovastatin / monacolin K lactone source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
2017 commercial-product chemical analysis.
limitations
Chemical identity does not make the whole mixture identical to a lovastatin tablet or establish equal exposure.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A constituent can be the same molecule as a prescription drug.
primary_references
[28641460] Variability in strength of red yeast rice supplements purchased from mainstream retailers. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28641460/ · DOI 10.1177/2047487317715714
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 12–18
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 2017 commercial-product chemical analysis. · source_derived_draft · unverified_draft
## red-yeast-rice-monacolin-identity A constituent can be the same molecule as a prescription drug. The 28-brand analytical study treated monacolin K in red yeast rice as chemically identical to lovastatin. Model: 2017 commercial-product chemical analysis. Limitations: Chemical identity does not make the whole mixture identical to a lovastatin tablet or establish equal exposure. Evidence access: Primary abstract [28641460] Variability in strength of red yeast rice supplements purchased from mainstream retailers. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28641460/ · DOI 10.1177/2047487317715714
Complete structured claim and evidence
Monacolin K was undetected in two of 28 brands; the other 26 ranged from 0.09 to 5.48 mg per 1,200 mg red yeast rice.
Red yeast rice → Lovastatin / monacolin K lactone source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
UHPLC-based analysis of products purchased for the 2017 study.
limitations
A historical sample, not a measurement of current products or batches.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Equal masses of product delivered very different measured amounts.
primary_references
[28641460] Variability in strength of red yeast rice supplements purchased from mainstream retailers. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28641460/ · DOI 10.1177/2047487317715714
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 20–26
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · UHPLC-based analysis of products purchased for the 2017 study. · source_derived_draft · unverified_draft
## red-yeast-rice-monacolin-variability Equal masses of product delivered very different measured amounts. Monacolin K was undetected in two of 28 brands; the other 26 ranged from 0.09 to 5.48 mg per 1,200 mg red yeast rice. Model: UHPLC-based analysis of products purchased for the 2017 study. Limitations: A historical sample, not a measurement of current products or batches. Evidence access: Primary abstract [28641460] Variability in strength of red yeast rice supplements purchased from mainstream retailers. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28641460/ · DOI 10.1177/2047487317715714
Complete structured claim and evidence
Twelve products labeled 600 mg per capsule contained 0.00–2.30 mg monacolin KA per capsule, alongside variable lactone and total monacolins.
Red yeast rice → Lovastatin hydroxy acid / monacolin KA source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Commercial formulations analyzed in 2006–2008.
limitations
Do not infer acid/lactone proportions from the red yeast rice mass on a label.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Acid-form content also varied.
primary_references
[20975018] Marked variability of monacolin levels in commercial red yeast rice products: buyer beware! · 2010 · https://pubmed.ncbi.nlm.nih.gov/20975018/ · DOI 10.1001/archinternmed.2010.382
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 28–34
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Commercial formulations analyzed in 2006–2008. · source_derived_draft · unverified_draft
## red-yeast-rice-acid-variability Acid-form content also varied. Twelve products labeled 600 mg per capsule contained 0.00–2.30 mg monacolin KA per capsule, alongside variable lactone and total monacolins. Model: Commercial formulations analyzed in 2006–2008. Limitations: Do not infer acid/lactone proportions from the red yeast rice mass on a label. Evidence access: Primary abstract [20975018] Marked variability of monacolin levels in commercial red yeast rice products: buyer beware! · 2010 · https://pubmed.ncbi.nlm.nih.gov/20975018/ · DOI 10.1001/archinternmed.2010.382
Complete structured claim and evidence
Four of twelve analyzed red yeast rice formulations had elevated citrinin levels in the reported survey.
Red yeast rice → Citrinin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
HPLC-MS/MS product survey.
limitations
This does not establish contamination of every product or a human toxicity threshold.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The contaminant was present in some tested products.
primary_references
[20975018] Marked variability of monacolin levels in commercial red yeast rice products: buyer beware! · 2010 · https://pubmed.ncbi.nlm.nih.gov/20975018/ · DOI 10.1001/archinternmed.2010.382
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 36–42
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · HPLC-MS/MS product survey. · source_derived_draft · unverified_draft
## red-yeast-rice-citrinin-detection The contaminant was present in some tested products. Four of twelve analyzed red yeast rice formulations had elevated citrinin levels in the reported survey. Model: HPLC-MS/MS product survey. Limitations: This does not establish contamination of every product or a human toxicity threshold. Evidence access: Primary abstract [20975018] Marked variability of monacolin levels in commercial red yeast rice products: buyer beware! · 2010 · https://pubmed.ncbi.nlm.nih.gov/20975018/ · DOI 10.1001/archinternmed.2010.382
Complete structured claim and evidence
The original monacolin K study prepared acid forms by saponifying lactones in 0.1 N NaOH at 50 degrees C for two hours.
Lovastatin / monacolin K lactone → Lovastatin hydroxy acid / monacolin KA source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary PDF, Methods p334
experimental_model
Chemical preparation for the 1980 biochemical study.
limitations
These laboratory conditions are not a claim about the rate or enzyme of human conversion.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Opening the lactone ring produces a different chemical form.
primary_references
[7380744] Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7380744/ · DOI 10.7164/antibiotics.33.334
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 44–50
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Chemical preparation for the 1980 biochemical study. · source_derived_draft · unverified_draft
## red-yeast-rice-acid-preparation Opening the lactone ring produces a different chemical form. The original monacolin K study prepared acid forms by saponifying lactones in 0.1 N NaOH at 50 degrees C for two hours. Model: Chemical preparation for the 1980 biochemical study. Limitations: These laboratory conditions are not a claim about the rate or enzyme of human conversion. Evidence access: Primary PDF, Methods p334 [7380744] Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7380744/ · DOI 10.7164/antibiotics.33.334
Complete structured claim and evidence
Monacolin K acid sodium salt competitively inhibited rat liver HMG-CoA reductase with respect to HMG-CoA; the reported Ki was 0.49 nM.
Monacolin K hydroxy-acid sodium salt → Rat HMG-CoA reductase / Hmgcr source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary PDF, p335 and Figure 3 visually inspected
experimental_model
Partially purified rat liver microsomal reductase; radiolabeled product assay.
limitations
Assay-specific inhibition constant, not a human plasma threshold or potency of an entire rice product.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The active preparation competed with the enzyme substrate.
primary_references
[7380744] Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7380744/ · DOI 10.7164/antibiotics.33.334
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 52–58
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Partially purified rat liver microsomal reductase; radiolabeled product assay. · source_derived_draft · unverified_draft
## red-yeast-rice-hmgcr-binding The active preparation competed with the enzyme substrate. Monacolin K acid sodium salt competitively inhibited rat liver HMG-CoA reductase with respect to HMG-CoA; the reported Ki was 0.49 nM. Model: Partially purified rat liver microsomal reductase; radiolabeled product assay. Limitations: Assay-specific inhibition constant, not a human plasma threshold or potency of an entire rice product. Evidence access: Primary PDF, p335 and Figure 3 visually inspected [7380744] Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7380744/ · DOI 10.7164/antibiotics.33.334
Complete structured claim and evidence
The same monacolin K inhibition was noncompetitive with respect to NADPH.
Monacolin K hydroxy-acid sodium salt → NADPH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary PDF, p335 visually inspected
experimental_model
Rat liver reductase kinetics in the 1980 study.
limitations
Not evidence of NADPH depletion, niacin deficiency or reversal by niacin supplementation.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The reducing cofactor and the competing substrate have different roles.
primary_references
[7380744] Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7380744/ · DOI 10.7164/antibiotics.33.334
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 60–66
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat liver reductase kinetics in the 1980 study. · source_derived_draft · unverified_draft
## red-yeast-rice-nadph-noncompetition The reducing cofactor and the competing substrate have different roles. The same monacolin K inhibition was noncompetitive with respect to NADPH. Model: Rat liver reductase kinetics in the 1980 study. Limitations: Not evidence of NADPH depletion, niacin deficiency or reversal by niacin supplementation. Evidence access: Primary PDF, p335 visually inspected [7380744] Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7380744/ · DOI 10.7164/antibiotics.33.334
Complete structured claim and evidence
Monacolin K inhibited lipid labeling from acetate or HMG-CoA, but did not inhibit incorporation from supplied mevalonate at concentrations up to 10 mM.
Lovastatin / monacolin K lactone → Mevalonate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary PDF, p335 visually inspected
experimental_model
Rat liver cell-free nonsaponifiable-lipid synthesis; lactone and acid preparations tested.
limitations
A biochemical bypass is not a clinical repletion strategy; the 10 mM figure applies to tested monacolin concentrations, not human exposure.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Supplying the downstream intermediate bypassed the inhibited step in this assay.
primary_references
[7380744] Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7380744/ · DOI 10.7164/antibiotics.33.334
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 68–74
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat liver cell-free nonsaponifiable-lipid synthesis; lactone and acid preparations tested. · source_derived_draft · unverified_draft
## red-yeast-rice-mevalonate-bypass Supplying the downstream intermediate bypassed the inhibited step in this assay. Monacolin K inhibited lipid labeling from acetate or HMG-CoA, but did not inhibit incorporation from supplied mevalonate at concentrations up to 10 mM. Model: Rat liver cell-free nonsaponifiable-lipid synthesis; lactone and acid preparations tested. Limitations: A biochemical bypass is not a clinical repletion strategy; the 10 mM figure applies to tested monacolin concentrations, not human exposure. Evidence access: Primary PDF, p335 visually inspected [7380744] Monacolin K, a new hypocholesterolemic agent that specifically inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase. · 1980 · https://pubmed.ncbi.nlm.nih.gov/7380744/ · DOI 10.7164/antibiotics.33.334
Complete structured claim and evidence
Human HMG-CoA reductase catalyzes mevalonate formation; substrate/cofactor-bound structures locate HMG-CoA and the nicotinamide cofactor in the catalytic domain.
HMG-CoA reductase (HMGCR) → Mevalonate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human recombinant catalytic-domain crystallography and biochemical background.
limitations
Shared human machinery; the source is not an experiment administering red yeast rice.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
This enzyme supplies a shared precursor pathway.
primary_references
[10698924] Crystal structure of the catalytic portion of human HMG-CoA reductase: insights into regulation of activity and catalysis. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10698924/ · DOI 10.1093/emboj/19.5.819
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 76–82
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant catalytic-domain crystallography and biochemical background. · source_derived_draft · unverified_draft
## red-yeast-rice-human-mevalonate-machinery This enzyme supplies a shared precursor pathway. Human HMG-CoA reductase catalyzes mevalonate formation; substrate/cofactor-bound structures locate HMG-CoA and the nicotinamide cofactor in the catalytic domain. Model: Human recombinant catalytic-domain crystallography and biochemical background. Limitations: Shared human machinery; the source is not an experiment administering red yeast rice. Evidence access: Primary abstract [10698924] Crystal structure of the catalytic portion of human HMG-CoA reductase: insights into regulation of activity and catalysis. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10698924/ · DOI 10.1093/emboj/19.5.819
Complete structured claim and evidence
The 1990 human lovastatin report observed reductions in circulating CoQ10 during drug exposure in five hospitalized patients and a separately monitored volunteer.
Lovastatin / monacolin K lactone → Plasma coenzyme Q10 concentration source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Small uncontrolled clinical series, including pre-existing cardiac disease.
limitations
Does not establish causal cardiomyopathy, tissue deficiency or the same effect from a specified red yeast rice product.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A constituent has human CoQ observations, with major study limitations.
primary_references
[2247468] Lovastatin decreases coenzyme Q levels in humans. · 1990 · https://pubmed.ncbi.nlm.nih.gov/2247468/ · DOI 10.1073/pnas.87.22.8931
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 84–90
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Small uncontrolled clinical series, including pre-existing cardiac disease. · source_derived_draft · unverified_draft
## red-yeast-rice-human-lovastatin-coq A constituent has human CoQ observations, with major study limitations. The 1990 human lovastatin report observed reductions in circulating CoQ10 during drug exposure in five hospitalized patients and a separately monitored volunteer. Model: Small uncontrolled clinical series, including pre-existing cardiac disease. Limitations: Does not establish causal cardiomyopathy, tissue deficiency or the same effect from a specified red yeast rice product. Evidence access: Primary abstract [2247468] Lovastatin decreases coenzyme Q levels in humans. · 1990 · https://pubmed.ncbi.nlm.nih.gov/2247468/ · DOI 10.1073/pnas.87.22.8931
Complete structured claim and evidence
Acute red yeast rice gavage at 1 or 5 g/kg reduced hepatic CoQ10 in male ICR mice, with suppression still reported at 24 hours.
Red yeast rice preparation in the 2005 ICR mouse experiment → Mouse liver CoQ10 after acute red yeast rice gavage source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Soybean-oil preparation; eight mice per experimental subgroup, sampled from 0.5 to 24 hours.
limitations
High-dose rodent exposure; the abstract describes controls killed immediately, so time and feeding controls limit interpretation. No human dose equivalence is inferred.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The mixture itself was tested in mice at high doses.
primary_references
[15705235] Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15705235/ · DOI 10.1079/bjn20041285
trigger_kind
biomarker_context Imported condition classification; unverified.
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 92–98
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Soybean-oil preparation; eight mice per experimental subgroup, sampled from 0.5 to 24 hours. · source_derived_draft · unverified_draft
## red-yeast-rice-mouse-ryr-liver-coq The mixture itself was tested in mice at high doses. Acute red yeast rice gavage at 1 or 5 g/kg reduced hepatic CoQ10 in male ICR mice, with suppression still reported at 24 hours. Model: Soybean-oil preparation; eight mice per experimental subgroup, sampled from 0.5 to 24 hours. Limitations: High-dose rodent exposure; the abstract describes controls killed immediately, so time and feeding controls limit interpretation. No human dose equivalence is inferred. Evidence access: Primary abstract [15705235] Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15705235/ · DOI 10.1079/bjn20041285
Complete structured claim and evidence
The same acute mouse study reported lower cardiac CoQ10 after red yeast rice gavage, with greater suppression at the higher dose.
Red yeast rice preparation in the 2005 ICR mouse experiment → Mouse heart CoQ10 after acute red yeast rice gavage source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Male ICR mice, 1 or 5 g/kg oral gavage.
limitations
The abstract repeats the heart label in its time-course description; precise tissue-specific onset is not reconstructed from that ambiguous wording.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A second tissue showed a measured change.
primary_references
[15705235] Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15705235/ · DOI 10.1079/bjn20041285
trigger_kind
biomarker_context Imported condition classification; unverified.
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 100–106
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Male ICR mice, 1 or 5 g/kg oral gavage. · source_derived_draft · unverified_draft
## red-yeast-rice-mouse-ryr-heart-coq A second tissue showed a measured change. The same acute mouse study reported lower cardiac CoQ10 after red yeast rice gavage, with greater suppression at the higher dose. Model: Male ICR mice, 1 or 5 g/kg oral gavage. Limitations: The abstract repeats the heart label in its time-course description; precise tissue-specific onset is not reconstructed from that ambiguous wording. Evidence access: Primary abstract [15705235] Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15705235/ · DOI 10.1079/bjn20041285
Complete structured claim and evidence
The three 2012 red yeast rice product extracts inhibited human microsomal CYP1A2 more potently than pure lovastatin at matched nominal lovastatin concentrations.
LipoCol Forte, Xuezhikang and Cholestin extract panel studied in 2012 → Human cytochrome P450 1A2 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC3513969, CYP methods and results
experimental_model
Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system.
limitations
In-vitro inhibition is not a measured interaction with every drug using this enzyme; the additional responsible constituent was not identified.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The mixture changed an enzyme assay beyond its lovastatin content.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 108–114
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system. · source_derived_draft · unverified_draft
## red-yeast-rice-extract-cyp1a2 The mixture changed an enzyme assay beyond its lovastatin content. The three 2012 red yeast rice product extracts inhibited human microsomal CYP1A2 more potently than pure lovastatin at matched nominal lovastatin concentrations. Model: Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system. Limitations: In-vitro inhibition is not a measured interaction with every drug using this enzyme; the additional responsible constituent was not identified. Evidence access: Primary full text PMC3513969, CYP methods and results [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
The three 2012 red yeast rice product extracts inhibited human microsomal CYP2C19 more potently than pure lovastatin at matched nominal lovastatin concentrations.
LipoCol Forte, Xuezhikang and Cholestin extract panel studied in 2012 → Human cytochrome P450 2C19 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC3513969, CYP methods and results
experimental_model
Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system.
limitations
In-vitro inhibition is not a measured interaction with every drug using this enzyme; the additional responsible constituent was not identified.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The mixture changed an enzyme assay beyond its lovastatin content.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 116–122
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system. · source_derived_draft · unverified_draft
## red-yeast-rice-extract-cyp2c19 The mixture changed an enzyme assay beyond its lovastatin content. The three 2012 red yeast rice product extracts inhibited human microsomal CYP2C19 more potently than pure lovastatin at matched nominal lovastatin concentrations. Model: Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system. Limitations: In-vitro inhibition is not a measured interaction with every drug using this enzyme; the additional responsible constituent was not identified. Evidence access: Primary full text PMC3513969, CYP methods and results [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
The three 2012 red yeast rice product extracts inhibited human microsomal CYP3A4 more potently than pure lovastatin at matched nominal lovastatin concentrations.
LipoCol Forte, Xuezhikang and Cholestin extract panel studied in 2012 → Human cytochrome P450 3A4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC3513969, CYP methods and results
experimental_model
Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system.
limitations
In-vitro inhibition is not a measured interaction with every drug using this enzyme; the additional responsible constituent was not identified.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The mixture changed an enzyme assay beyond its lovastatin content.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 124–130
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system. · source_derived_draft · unverified_draft
## red-yeast-rice-extract-cyp3a4 The mixture changed an enzyme assay beyond its lovastatin content. The three 2012 red yeast rice product extracts inhibited human microsomal CYP3A4 more potently than pure lovastatin at matched nominal lovastatin concentrations. Model: Human liver microsomes; product concentrations normalized to 0.5–25 micromolar lovastatin, with an NADPH-generating system. Limitations: In-vitro inhibition is not a measured interaction with every drug using this enzyme; the additional responsible constituent was not identified. Evidence access: Primary full text PMC3513969, CYP methods and results [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
The three product extracts inhibited P-glycoprotein transport activity more potently than pure lovastatin in the study assay.
LipoCol Forte, Xuezhikang and Cholestin extract panel studied in 2012 → Human P-glycoprotein / ABCB1 / MDR1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC3513969
experimental_model
Canine MDCK cells engineered with human MDR1; radiolabeled digoxin probe.
limitations
Human transporter in a canine host cell; not a clinical digoxin-interaction magnitude.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
An efflux transporter provides another exposure-related route.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 132–138
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Canine MDCK cells engineered with human MDR1; radiolabeled digoxin probe. · source_derived_draft · unverified_draft
## red-yeast-rice-extract-pgp An efflux transporter provides another exposure-related route. The three product extracts inhibited P-glycoprotein transport activity more potently than pure lovastatin in the study assay. Model: Canine MDCK cells engineered with human MDR1; radiolabeled digoxin probe. Limitations: Human transporter in a canine host cell; not a clinical digoxin-interaction magnitude. Evidence access: Primary full text PMC3513969 [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
Lovastatin flux across Caco-2 monolayers was higher with the three product extracts than with pure lovastatin at a matched 25 micromolar concentration.
LipoCol Forte, Xuezhikang and Cholestin extract panel studied in 2012 → Human Caco-2 apical-to-basolateral lovastatin flux source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC3513969
experimental_model
Human intestinal-cell-line model.
limitations
Does not quantify intestinal absorption or oral bioavailability in humans.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A cell-layer transport result supported a mixture effect.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 140–146
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human intestinal-cell-line model. · source_derived_draft · unverified_draft
## red-yeast-rice-extract-caco2-flux A cell-layer transport result supported a mixture effect. Lovastatin flux across Caco-2 monolayers was higher with the three product extracts than with pure lovastatin at a matched 25 micromolar concentration. Model: Human intestinal-cell-line model. Limitations: Does not quantify intestinal absorption or oral bioavailability in humans. Evidence access: Primary full text PMC3513969 [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
In 14 volunteers, single doses of one, two or four LipoCol Forte capsules produced dose-related lovastatin and lovastatin-acid exposure; one capsule twice daily for five days produced no significant accumulation.
LipoCol Forte red yeast rice preparation studied in 2012 → Human plasma exposure to lovastatin hydroxy acid source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary full text PMC3513969
experimental_model
Human fed-state dose and repeat-dose study; 600 mg per capsule.
limitations
Does not establish identical kinetics for other formulations, chronic use or interacting-drug conditions.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The measured product had a defined short-term exposure profile.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
trigger_kind
biomarker_context Imported condition classification; unverified.
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 148–154
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human fed-state dose and repeat-dose study; 600 mg per capsule. · source_derived_draft · unverified_draft
## red-yeast-rice-lipocol-dose-response The measured product had a defined short-term exposure profile. In 14 volunteers, single doses of one, two or four LipoCol Forte capsules produced dose-related lovastatin and lovastatin-acid exposure; one capsule twice daily for five days produced no significant accumulation. Model: Human fed-state dose and repeat-dose study; 600 mg per capsule. Limitations: Does not establish identical kinetics for other formulations, chronic use or interacting-drug conditions. Evidence access: Primary full text PMC3513969 [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
One 600 mg LipoCol Forte capsule did not significantly change the measured pharmacokinetics of 5 mg nifedipine in 14 volunteers.
LipoCol Forte red yeast rice preparation studied in 2012 → Human nifedipine plasma exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC3513969
experimental_model
Human fasted-state single-dose pharmacokinetic comparison.
limitations
A null result for this dose does not exclude other drugs, preparations or exposures.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The predicted enzyme interaction was not demonstrated in this tested regimen.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 156–162
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human fasted-state single-dose pharmacokinetic comparison. · source_derived_draft · unverified_draft
## red-yeast-rice-nifedipine-null The predicted enzyme interaction was not demonstrated in this tested regimen. One 600 mg LipoCol Forte capsule did not significantly change the measured pharmacokinetics of 5 mg nifedipine in 14 volunteers. Model: Human fasted-state single-dose pharmacokinetic comparison. Limitations: A null result for this dose does not exclude other drugs, preparations or exposures. Evidence access: Primary full text PMC3513969 [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
Gemfibrozil 600 mg twice daily increased lovastatin-acid peak concentration and exposure area after LipoCol Forte in 13 volunteers.
Gemfibrozil → Human plasma exposure to lovastatin hydroxy acid source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary full text PMC3513969
experimental_model
Human short-course gemfibrozil followed by one LipoCol Forte capsule.
limitations
The trial did not establish a unique responsible transporter or enzyme, nor measure a muscle-injury incidence.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A coadministered drug increased exposure to the active acid.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
trigger_kind
biomarker_context Imported condition classification; unverified.
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 164–170
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human short-course gemfibrozil followed by one LipoCol Forte capsule. · source_derived_draft · unverified_draft
## red-yeast-rice-gemfibrozil-acid A coadministered drug increased exposure to the active acid. Gemfibrozil 600 mg twice daily increased lovastatin-acid peak concentration and exposure area after LipoCol Forte in 13 volunteers. Model: Human short-course gemfibrozil followed by one LipoCol Forte capsule. Limitations: The trial did not establish a unique responsible transporter or enzyme, nor measure a muscle-injury incidence. Evidence access: Primary full text PMC3513969 [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
Gemfibrozil did not significantly change parent lovastatin pharmacokinetic parameters in that LipoCol Forte experiment.
Gemfibrozil → Human plasma exposure to lovastatin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC3513969
experimental_model
Same 13 volunteers and dosing protocol.
limitations
The positive acid result must not be generalized to every measured chemical form.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The lactone and acid did not show the same interaction result.
primary_references
[23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 172–178
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same 13 volunteers and dosing protocol. · source_derived_draft · unverified_draft
## red-yeast-rice-gemfibrozil-lactone-null The lactone and acid did not show the same interaction result. Gemfibrozil did not significantly change parent lovastatin pharmacokinetic parameters in that LipoCol Forte experiment. Model: Same 13 volunteers and dosing protocol. Limitations: The positive acid result must not be generalized to every measured chemical form. Evidence access: Primary full text PMC3513969 [23227093] Interaction between Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implication for the Clinical Pharmacokinetics of Lovastatin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23227093/ · DOI 10.1155/2012/127043
Complete structured claim and evidence
Repeated double-strength grapefruit juice increased lovastatin peak concentration about 12-fold and exposure area about 15-fold after an 80 mg dose in ten volunteers.
Double-strength grapefruit juice in the 1998 lovastatin study → Human plasma exposure to lovastatin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Randomized crossover: 200 mL three times daily for two days, with further juice around the day-three dose.
limitations
Prescription lovastatin and intensive juice regimen; not a measured red yeast rice interaction or a multiplier for ordinary juice intake.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Food-related inhibition of first-pass handling can change drug exposure.
primary_references
[9585793] Grapefruit juice greatly increases serum concentrations of lovastatin and lovastatin acid. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9585793/ · DOI 10.1016/S0009-9236(98)90034-0
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 180–186
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized crossover: 200 mL three times daily for two days, with further juice around the day-three dose. · source_derived_draft · unverified_draft
## red-yeast-rice-grapefruit-lovastatin Food-related inhibition of first-pass handling can change drug exposure. Repeated double-strength grapefruit juice increased lovastatin peak concentration about 12-fold and exposure area about 15-fold after an 80 mg dose in ten volunteers. Model: Randomized crossover: 200 mL three times daily for two days, with further juice around the day-three dose. Limitations: Prescription lovastatin and intensive juice regimen; not a measured red yeast rice interaction or a multiplier for ordinary juice intake. Evidence access: Primary abstract [9585793] Grapefruit juice greatly increases serum concentrations of lovastatin and lovastatin acid. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9585793/ · DOI 10.1016/S0009-9236(98)90034-0
Complete structured claim and evidence
In the same experiment, lovastatin-acid peak concentration rose about fourfold and exposure area about fivefold.
Double-strength grapefruit juice in the 1998 lovastatin study → Human plasma exposure to lovastatin hydroxy acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Ten healthy volunteers; 80 mg prescription lovastatin.
limitations
First-pass CYP3A4 inhibition was the proposed explanation, not a measured effect on all red yeast rice products.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The two chemical forms had different exposure changes.
primary_references
[9585793] Grapefruit juice greatly increases serum concentrations of lovastatin and lovastatin acid. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9585793/ · DOI 10.1016/S0009-9236(98)90034-0
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 188–194
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ten healthy volunteers; 80 mg prescription lovastatin. · source_derived_draft · unverified_draft
## red-yeast-rice-grapefruit-acid The two chemical forms had different exposure changes. In the same experiment, lovastatin-acid peak concentration rose about fourfold and exposure area about fivefold. Model: Ten healthy volunteers; 80 mg prescription lovastatin. Limitations: First-pass CYP3A4 inhibition was the proposed explanation, not a measured effect on all red yeast rice products. Evidence access: Primary abstract [9585793] Grapefruit juice greatly increases serum concentrations of lovastatin and lovastatin acid. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9585793/ · DOI 10.1016/S0009-9236(98)90034-0
Complete structured claim and evidence
Itraconazole 100 mg daily for four days increased lovastatin peak concentration about 15-fold and exposure area more than 15-fold after a 40 mg dose in ten volunteers.
Itraconazole → Human plasma exposure to lovastatin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Randomized crossover prescription-lovastatin study; lovastatin-acid exposure also increased.
limitations
The numerical magnitude belongs to this drug regimen, not to untested red yeast rice preparations.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A drug interaction can substantially change constituent exposure.
primary_references
[9690949] Different effects of itraconazole on the pharmacokinetics of fluvastatin and lovastatin. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9690949/ · DOI 10.1046/j.1365-2125.1998.00034.x
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 196–202
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized crossover prescription-lovastatin study; lovastatin-acid exposure also increased. · source_derived_draft · unverified_draft
## red-yeast-rice-itraconazole A drug interaction can substantially change constituent exposure. Itraconazole 100 mg daily for four days increased lovastatin peak concentration about 15-fold and exposure area more than 15-fold after a 40 mg dose in ten volunteers. Model: Randomized crossover prescription-lovastatin study; lovastatin-acid exposure also increased. Limitations: The numerical magnitude belongs to this drug regimen, not to untested red yeast rice preparations. Evidence access: Primary abstract [9690949] Different effects of itraconazole on the pharmacokinetics of fluvastatin and lovastatin. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9690949/ · DOI 10.1046/j.1365-2125.1998.00034.x
Complete structured claim and evidence
Adding monascin increased hepatic AMPK phosphorylation in high-fat-diet-fed mice.
Monascin → Mouse hepatic AMPK activity in the Monascus pigment study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
C57BL/6 mouse liver; exposure dose not available in the accessed abstract.
limitations
Phosphorylation is not proof of direct AMPK binding or a demonstrated effect of every red yeast rice product.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A pigment changed an energy-regulation signal in mice.
primary_references
[24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 204–210
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · C57BL/6 mouse liver; exposure dose not available in the accessed abstract. · source_derived_draft · unverified_draft
## red-yeast-rice-monascin-ampk A pigment changed an energy-regulation signal in mice. Adding monascin increased hepatic AMPK phosphorylation in high-fat-diet-fed mice. Model: C57BL/6 mouse liver; exposure dose not available in the accessed abstract. Limitations: Phosphorylation is not proof of direct AMPK binding or a demonstrated effect of every red yeast rice product. Evidence access: Primary abstract [24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
Complete structured claim and evidence
Monascin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study.
Monascin → Mouse peroxisome proliferator-activated receptor alpha / Ppara source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported.
limitations
The paper describes agonist activity; the accessed abstract does not resolve direct receptor affinity or establish a human clinical effect.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A transcriptional program provides a distinct route from statin inhibition.
primary_references
[24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 212–218
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported. · source_derived_draft · unverified_draft
## red-yeast-rice-monascin-ppara A transcriptional program provides a distinct route from statin inhibition. Monascin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study. Model: High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported. Limitations: The paper describes agonist activity; the accessed abstract does not resolve direct receptor affinity or establish a human clinical effect. Evidence access: Primary abstract [24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
Complete structured claim and evidence
Adding ankaflavin increased hepatic AMPK phosphorylation in high-fat-diet-fed mice.
Ankaflavin → Mouse hepatic AMPK activity in the Monascus pigment study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
C57BL/6 mouse liver; exposure dose not available in the accessed abstract.
limitations
Phosphorylation is not proof of direct AMPK binding or a demonstrated effect of every red yeast rice product.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A pigment changed an energy-regulation signal in mice.
primary_references
[24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 220–226
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · C57BL/6 mouse liver; exposure dose not available in the accessed abstract. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-ampk A pigment changed an energy-regulation signal in mice. Adding ankaflavin increased hepatic AMPK phosphorylation in high-fat-diet-fed mice. Model: C57BL/6 mouse liver; exposure dose not available in the accessed abstract. Limitations: Phosphorylation is not proof of direct AMPK binding or a demonstrated effect of every red yeast rice product. Evidence access: Primary abstract [24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
Complete structured claim and evidence
Ankaflavin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study.
Ankaflavin → Mouse peroxisome proliferator-activated receptor alpha / Ppara source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported.
limitations
The paper describes agonist activity; the accessed abstract does not resolve direct receptor affinity or establish a human clinical effect.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A transcriptional program provides a distinct route from statin inhibition.
primary_references
[24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 228–234
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-ppara A transcriptional program provides a distinct route from statin inhibition. Ankaflavin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study. Model: High-fat-diet C57BL/6 mice; related mouse FL83B hepatocyte experiments also reported. Limitations: The paper describes agonist activity; the accessed abstract does not resolve direct receptor affinity or establish a human clinical effect. Evidence access: Primary abstract [24275089] Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24275089/ · DOI 10.1016/j.fct.2013.11.015
Complete structured claim and evidence
GW9662 antagonism abolished tested insulin-sensitivity effects of ankaflavin in methylglyoxal-treated Wistar rats.
Rat peroxisome proliferator-activated receptor gamma / Pparg → Rat insulin-response endpoints during ankaflavin treatment source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Four-week rat model; methylglyoxal 600 mg/kg and ankaflavin 10 mg/kg as reported.
limitations
Drug-induced rodent model; not an established treatment for human diabetes.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Blocking the receptor helped test pathway involvement.
primary_references
[23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
trigger_kind
machinery_impairment Imported condition classification; unverified.
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 236–242
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Four-week rat model; methylglyoxal 600 mg/kg and ankaflavin 10 mg/kg as reported. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-pparg-blockade Blocking the receptor helped test pathway involvement. GW9662 antagonism abolished tested insulin-sensitivity effects of ankaflavin in methylglyoxal-treated Wistar rats. Model: Four-week rat model; methylglyoxal 600 mg/kg and ankaflavin 10 mg/kg as reported. Limitations: Drug-induced rodent model; not an established treatment for human diabetes. Evidence access: Primary abstract [23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Complete structured claim and evidence
Ankaflavin increased hepatic Nrf2 Ser40 phosphorylation without increasing measured Nrf2 mRNA or total protein in the rat experiment.
Ankaflavin → Rat Nrf2 / Nfe2l2 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Methylglyoxal-treated Wistar rats, four-week model.
limitations
Does not demonstrate direct binding to Nrf2 or KEAP1; effect cannot be assigned to dietary riboflavin.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Activation and abundance were different measured endpoints.
primary_references
[23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 244–250
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Methylglyoxal-treated Wistar rats, four-week model. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-nrf2 Activation and abundance were different measured endpoints. Ankaflavin increased hepatic Nrf2 Ser40 phosphorylation without increasing measured Nrf2 mRNA or total protein in the rat experiment. Model: Methylglyoxal-treated Wistar rats, four-week model. Limitations: Does not demonstrate direct binding to Nrf2 or KEAP1; effect cannot be assigned to dietary riboflavin. Evidence access: Primary abstract [23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Complete structured claim and evidence
Ankaflavin increased hepatic GCL and HO-1 transcriptional activation; these effects persisted despite PPAR-gamma antagonist treatment.
Ankaflavin → Rat hepatic glutamate-cysteine ligase expression in the ankaflavin study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Wistar rat methylglyoxal model with GW9662 comparison.
limitations
GCL subunit-specific effects were not resolved in the accessed abstract.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The antioxidant-expression route was not blocked in the same way as the insulin endpoints.
primary_references
[23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 252–258
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Wistar rat methylglyoxal model with GW9662 comparison. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-gcl The antioxidant-expression route was not blocked in the same way as the insulin endpoints. Ankaflavin increased hepatic GCL and HO-1 transcriptional activation; these effects persisted despite PPAR-gamma antagonist treatment. Model: Wistar rat methylglyoxal model with GW9662 comparison. Limitations: GCL subunit-specific effects were not resolved in the accessed abstract. Evidence access: Primary abstract [23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Complete structured claim and evidence
Ankaflavin increased glutathione measured in liver and pancreas of methylglyoxal-treated rats.
Ankaflavin → Rat hepatic and pancreatic glutathione during ankaflavin treatment source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Four-week Wistar rat model.
limitations
Does not establish dietary cysteine demand, human glutathione repletion or which flux caused the concentration change.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Glutathione connects this pigment to shared amino-acid-dependent defenses.
primary_references
[23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 260–266
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Four-week Wistar rat model. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-gsh Glutathione connects this pigment to shared amino-acid-dependent defenses. Ankaflavin increased glutathione measured in liver and pancreas of methylglyoxal-treated rats. Model: Four-week Wistar rat model. Limitations: Does not establish dietary cysteine demand, human glutathione repletion or which flux caused the concentration change. Evidence access: Primary abstract [23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Complete structured claim and evidence
Ankaflavin did not inhibit AGE generation in the reported cell-free experiment despite lower AGE endpoints in treated rats.
Ankaflavin → Direct AGE-generation assay in the ankaflavin study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
In-vitro glycation assay in the 2012 study.
limitations
Assay conditions differ from later pigment-rich mixture experiments; no automatic contradiction.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Direct chemical trapping and an organism-level effect are separate possibilities.
primary_references
[23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 268–274
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · In-vitro glycation assay in the 2012 study. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-glycation-null Direct chemical trapping and an organism-level effect are separate possibilities. Ankaflavin did not inhibit AGE generation in the reported cell-free experiment despite lower AGE endpoints in treated rats. Model: In-vitro glycation assay in the 2012 study. Limitations: Assay conditions differ from later pigment-rich mixture experiments; no automatic contradiction. Evidence access: Primary abstract [23022408] Ankaflavin: a natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23022408/ · DOI 10.1016/j.freeradbiomed.2012.09.025
Complete structured claim and evidence
Ankaflavin inhibited yeast alpha-glucosidase with an IC50 of 126.5 micromolar and mixed-type kinetics.
Ankaflavin → Saccharomyces cerevisiae alpha-glucosidase in the 2024 pigment assay source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC11120408
experimental_model
Saccharomyces cerevisiae enzyme, pNPG substrate, pH 6.8; one-hour preincubation and 30-minute reaction.
limitations
Yeast enzyme, not human intestinal maltase-glucoamylase or sucrase-isomaltase; potency is not clinical glucose lowering.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The isolated pigment inhibited a carbohydrate-cleaving enzyme preparation.
primary_references
[38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 276–282
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Saccharomyces cerevisiae enzyme, pNPG substrate, pH 6.8; one-hour preincubation and 30-minute reaction. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-glucosidase The isolated pigment inhibited a carbohydrate-cleaving enzyme preparation. Ankaflavin inhibited yeast alpha-glucosidase with an IC50 of 126.5 micromolar and mixed-type kinetics. Model: Saccharomyces cerevisiae enzyme, pNPG substrate, pH 6.8; one-hour preincubation and 30-minute reaction. Limitations: Yeast enzyme, not human intestinal maltase-glucoamylase or sucrase-isomaltase; potency is not clinical glucose lowering. Evidence access: Primary full text PMC11120408 [38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Complete structured claim and evidence
Docking proposed ankaflavin binding outside the catalytic center of the alpha-glucosidase model.
Ankaflavin → Saccharomyces cerevisiae alpha-glucosidase in the 2024 pigment assay source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC11120408
experimental_model
Computational analysis accompanying enzyme kinetics.
limitations
No ligand-bound crystal structure or direct human-enzyme result follows.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The proposed contact site remains a model.
primary_references
[38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 284–290
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Computational analysis accompanying enzyme kinetics. · source_derived_draft · unverified_draft
## red-yeast-rice-ankaflavin-docking The proposed contact site remains a model. Docking proposed ankaflavin binding outside the catalytic center of the alpha-glucosidase model. Model: Computational analysis accompanying enzyme kinetics. Limitations: No ligand-bound crystal structure or direct human-enzyme result follows. Evidence access: Primary full text PMC11120408 [38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Complete structured claim and evidence
Monascin inhibited yeast alpha-glucosidase with an IC50 of 302.6 micromolar and mixed-type kinetics.
Monascin → Saccharomyces cerevisiae alpha-glucosidase in the 2024 pigment assay source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC11120408
experimental_model
Saccharomyces cerevisiae enzyme, pNPG substrate, pH 6.8; one-hour preincubation and 30-minute reaction.
limitations
Yeast enzyme, not human intestinal maltase-glucoamylase or sucrase-isomaltase; potency is not clinical glucose lowering.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The isolated pigment inhibited a carbohydrate-cleaving enzyme preparation.
primary_references
[38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 292–298
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Saccharomyces cerevisiae enzyme, pNPG substrate, pH 6.8; one-hour preincubation and 30-minute reaction. · source_derived_draft · unverified_draft
## red-yeast-rice-monascin-glucosidase The isolated pigment inhibited a carbohydrate-cleaving enzyme preparation. Monascin inhibited yeast alpha-glucosidase with an IC50 of 302.6 micromolar and mixed-type kinetics. Model: Saccharomyces cerevisiae enzyme, pNPG substrate, pH 6.8; one-hour preincubation and 30-minute reaction. Limitations: Yeast enzyme, not human intestinal maltase-glucoamylase or sucrase-isomaltase; potency is not clinical glucose lowering. Evidence access: Primary full text PMC11120408 [38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Complete structured claim and evidence
Docking proposed monascin binding outside the catalytic center of the alpha-glucosidase model.
Monascin → Saccharomyces cerevisiae alpha-glucosidase in the 2024 pigment assay source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC11120408
experimental_model
Computational analysis accompanying enzyme kinetics.
limitations
No ligand-bound crystal structure or direct human-enzyme result follows.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The proposed contact site remains a model.
primary_references
[38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 300–306
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Computational analysis accompanying enzyme kinetics. · source_derived_draft · unverified_draft
## red-yeast-rice-monascin-docking The proposed contact site remains a model. Docking proposed monascin binding outside the catalytic center of the alpha-glucosidase model. Model: Computational analysis accompanying enzyme kinetics. Limitations: No ligand-bound crystal structure or direct human-enzyme result follows. Evidence access: Primary full text PMC11120408 [38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Complete structured claim and evidence
The pigment-rich fermentation product at 0.2 mg/mL reduced fluorescent AGE formation by 87.1% in the BSA–fructose assay.
Pigment-rich Monascus fermentation product studied in 2024 → Bovine serum albumin–fructose glycation assay source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text PMC11120408
experimental_model
Cell-free bovine albumin and fructose experiment.
limitations
Not purified ankaflavin alone, and fluorescence inhibition is not a clinical diabetes endpoint.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A particular mixture changed a glycation readout.
primary_references
[38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 308–314
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free bovine albumin and fructose experiment. · source_derived_draft · unverified_draft
## red-yeast-rice-mixture-glycation A particular mixture changed a glycation readout. The pigment-rich fermentation product at 0.2 mg/mL reduced fluorescent AGE formation by 87.1% in the BSA–fructose assay. Model: Cell-free bovine albumin and fructose experiment. Limitations: Not purified ankaflavin alone, and fluorescence inhibition is not a clinical diabetes endpoint. Evidence access: Primary full text PMC11120408 [38790873] Revealing the Hypoglycemic Effect of Red Yeast Rice: Perspectives from the Inhibition of α-Glucosidase and the Anti-Glycation Capability by Ankaflavin and Monascin. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38790873/ · DOI 10.3390/foods13101573
Complete structured claim and evidence
Citrinin exposure reduced ATP in rat proximal-tubule suspensions before or during ensuing cell injury.
Citrinin → Rat renal proximal-tubule ATP during citrinin exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
125–500 micromolar citrinin; reported ATP declines 22–48% at selected 0.5–1.5 hour time points.
limitations
Not a measured amount ingested from red yeast rice; lower exposures and human relevance require separate data.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Energy loss was measured in the kidney-cell preparation.
primary_references
[1853344] The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1853344/ · DOI 10.1016/0041-008x(91)90008-3
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 316–322
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 125–500 micromolar citrinin; reported ATP declines 22–48% at selected 0.5–1.5 hour time points. · source_derived_draft · unverified_draft
## red-yeast-rice-citrinin-atp Energy loss was measured in the kidney-cell preparation. Citrinin exposure reduced ATP in rat proximal-tubule suspensions before or during ensuing cell injury. Model: 125–500 micromolar citrinin; reported ATP declines 22–48% at selected 0.5–1.5 hour time points. Limitations: Not a measured amount ingested from red yeast rice; lower exposures and human relevance require separate data. Evidence access: Primary abstract [1853344] The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1853344/ · DOI 10.1016/0041-008x(91)90008-3
Complete structured claim and evidence
Deferoxamine pretreatment prevented iron-mediated lipid peroxidation but did not protect rat tubules from citrinin-induced death.
Deferoxamine → Rat renal proximal-tubule death after citrinin exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat proximal-tubule suspensions; 1 mM deferoxamine pretreatment.
limitations
Does not exclude every oxidative mechanism or establish ferroptosis; distinguishes marker suppression from survival rescue.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Blocking one injury marker did not rescue the cells.
primary_references
[1853344] The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1853344/ · DOI 10.1016/0041-008x(91)90008-3
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 324–330
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat proximal-tubule suspensions; 1 mM deferoxamine pretreatment. · source_derived_draft · unverified_draft
## red-yeast-rice-citrinin-iron-rescue-failure Blocking one injury marker did not rescue the cells. Deferoxamine pretreatment prevented iron-mediated lipid peroxidation but did not protect rat tubules from citrinin-induced death. Model: Rat proximal-tubule suspensions; 1 mM deferoxamine pretreatment. Limitations: Does not exclude every oxidative mechanism or establish ferroptosis; distinguishes marker suppression from survival rescue. Evidence access: Primary abstract [1853344] The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1853344/ · DOI 10.1016/0041-008x(91)90008-3
Complete structured claim and evidence
Citrinin lowered respiratory control, ADP/O ratio and membrane potential in rat renal cortical mitochondria.
Citrinin → Rat renal cortical mitochondrial phosphorylation efficiency source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Isolated rat mitochondria; the enzyme-panel experiments included 1 mM citrinin.
limitations
Multiple effects were reported; this is not a selective single-complex inhibitor or a human exposure threshold.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Mitochondrial oxygen use and ATP production became less efficiently coupled.
primary_references
[1556379] Mechanism of citrinin-induced dysfunction of mitochondria. I. Effects on respiration, enzyme activities and membrane potential of renal cortical mitochondria. · 1992 · https://pubmed.ncbi.nlm.nih.gov/1556379/ · DOI 10.1002/jat.2550120209
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 332–338
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Isolated rat mitochondria; the enzyme-panel experiments included 1 mM citrinin. · source_derived_draft · unverified_draft
## red-yeast-rice-citrinin-coupling Mitochondrial oxygen use and ATP production became less efficiently coupled. Citrinin lowered respiratory control, ADP/O ratio and membrane potential in rat renal cortical mitochondria. Model: Isolated rat mitochondria; the enzyme-panel experiments included 1 mM citrinin. Limitations: Multiple effects were reported; this is not a selective single-complex inhibitor or a human exposure threshold. Evidence access: Primary abstract [1556379] Mechanism of citrinin-induced dysfunction of mitochondria. I. Effects on respiration, enzyme activities and membrane potential of renal cortical mitochondria. · 1992 · https://pubmed.ncbi.nlm.nih.gov/1556379/ · DOI 10.1002/jat.2550120209
Complete structured claim and evidence
In 62 statin-intolerant participants, the studied red yeast rice regimen reduced LDL by 43 mg/dL at 12 weeks and 35 mg/dL at 24 weeks, versus 11 and 15 mg/dL with placebo.
Red yeast rice preparation in the Becker 2009 trial → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
1,800 mg twice daily for 24 weeks; both groups also entered a lifestyle program.
limitations
Small selected population; formulation-specific lipid result, not proof of cardiovascular-event reduction.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
This particular preparation lowered LDL in a randomized trial.
primary_references
[19528562] Red yeast rice for dyslipidemia in statin-intolerant patients: a randomized trial. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19528562/ · DOI 10.7326/0003-4819-150-12-200906160-00006
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 340–346
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 1,800 mg twice daily for 24 weeks; both groups also entered a lifestyle program. · source_derived_draft · unverified_draft
## red-yeast-rice-becker-ldl This particular preparation lowered LDL in a randomized trial. In 62 statin-intolerant participants, the studied red yeast rice regimen reduced LDL by 43 mg/dL at 12 weeks and 35 mg/dL at 24 weeks, versus 11 and 15 mg/dL with placebo. Model: 1,800 mg twice daily for 24 weeks; both groups also entered a lifestyle program. Limitations: Small selected population; formulation-specific lipid result, not proof of cardiovascular-event reduction. Evidence access: Primary abstract [19528562] Red yeast rice for dyslipidemia in statin-intolerant patients: a randomized trial. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19528562/ · DOI 10.7326/0003-4819-150-12-200906160-00006
Complete structured claim and evidence
Pain, CPK and liver-enzyme results did not differ significantly between groups in the 24-week trial.
Red yeast rice preparation in the Becker 2009 trial → Pain and creatine-kinase endpoints in the Becker red yeast rice trial source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
62 previously statin-intolerant participants.
limitations
Insufficient to exclude rare muscle or liver injury, or establish that all red yeast rice is safer than statins.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
The trial retained tolerability outcomes as well as LDL changes.
primary_references
[19528562] Red yeast rice for dyslipidemia in statin-intolerant patients: a randomized trial. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19528562/ · DOI 10.7326/0003-4819-150-12-200906160-00006
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 348–354
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 62 previously statin-intolerant participants. · source_derived_draft · unverified_draft
## red-yeast-rice-becker-tolerability The trial retained tolerability outcomes as well as LDL changes. Pain, CPK and liver-enzyme results did not differ significantly between groups in the 24-week trial. Model: 62 previously statin-intolerant participants. Limitations: Insufficient to exclude rare muscle or liver injury, or establish that all red yeast rice is safer than statins. Evidence access: Primary abstract [19528562] Red yeast rice for dyslipidemia in statin-intolerant patients: a randomized trial. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19528562/ · DOI 10.7326/0003-4819-150-12-200906160-00006
Complete structured claim and evidence
The red yeast rice arm of SPORT did not significantly lower LDL versus placebo after 28 days; rosuvastatin 5 mg did.
Red yeast rice preparation in the SPORT trial → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Single-center randomized trial; 190 participants completed all study arms combined.
limitations
Do not treat 190 as the red yeast rice sample size. Different product, duration and population from the Becker or Xuezhikang trials.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
Another preparation and protocol did not demonstrate the same lipid result.
primary_references
[36351465] Comparative Effects of Low-Dose Rosuvastatin, Placebo, and Dietary Supplements on Lipids and Inflammatory Biomarkers. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36351465/ · DOI 10.1016/j.jacc.2022.10.013
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 356–362
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Single-center randomized trial; 190 participants completed all study arms combined. · source_derived_draft · unverified_draft
## red-yeast-rice-sport-null Another preparation and protocol did not demonstrate the same lipid result. The red yeast rice arm of SPORT did not significantly lower LDL versus placebo after 28 days; rosuvastatin 5 mg did. Model: Single-center randomized trial; 190 participants completed all study arms combined. Limitations: Do not treat 190 as the red yeast rice sample size. Different product, duration and population from the Becker or Xuezhikang trials. Evidence access: Primary abstract [36351465] Comparative Effects of Low-Dose Rosuvastatin, Placebo, and Dietary Supplements on Lipids and Inflammatory Biomarkers. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36351465/ · DOI 10.1016/j.jacc.2022.10.013
Complete structured claim and evidence
Over an average 4.5 years, major coronary events occurred in 5.7% of the Xuezhikang group versus 10.4% of placebo in nearly 5,000 Chinese patients with prior myocardial infarction.
Xuezhikang preparation in the coronary secondary-prevention trial → Major coronary events in the Xuezhikang secondary-prevention trial source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Randomized secondary-prevention trial; partially purified Xuezhikang preparation.
limitations
Not proof for arbitrary supplements, primary prevention or isolated pigment effects; event reduction is not itself a molecular mechanism.
nutrient_topic
Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
plain_language
A specific extract had cardiovascular-outcome evidence in a defined population.
primary_references
[18549841] Effect of Xuezhikang, an extract from red yeast Chinese rice, on coronary events in a Chinese population with previous myocardial infarction. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18549841/ · DOI 10.1016/j.amjcard.2008.02.056
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 364–370
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized secondary-prevention trial; partially purified Xuezhikang preparation. · source_derived_draft · unverified_draft
## red-yeast-rice-xuezhikang-events A specific extract had cardiovascular-outcome evidence in a defined population. Over an average 4.5 years, major coronary events occurred in 5.7% of the Xuezhikang group versus 10.4% of placebo in nearly 5,000 Chinese patients with prior myocardial infarction. Model: Randomized secondary-prevention trial; partially purified Xuezhikang preparation. Limitations: Not proof for arbitrary supplements, primary prevention or isolated pigment effects; event reduction is not itself a molecular mechanism. Evidence access: Primary abstract [18549841] Effect of Xuezhikang, an extract from red yeast Chinese rice, on coronary events in a Chinese population with previous myocardial infarction. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18549841/ · DOI 10.1016/j.amjcard.2008.02.056
Complete structured claim and evidence
At 10 µM gamma-tocotrienol, HepG2 HMG-CoA reductase degradation increased 2.4-fold and its half-life fell from 3.73 to 1.59 h, measured by [35S]methionine pulse-chase and immunoprecipitation.
Gamma-tocotrienol → HMG-CoA reductase protein degradation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Radiolabeled protein pulse-chase and HMGCR immunoprecipitation
exposure
10 µM gamma-tocotrienol; reported HMGCR half-life 3.73 h control versus 1.59 h treated.
limitations
Primary abstract only; these data do not by themselves identify Insig proteins or prove direct binding to the reductase. Human supplementation effects cannot be inferred.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Homo sapiens
plain_language
Gamma-tocotrienol made the cholesterol-synthesis enzyme turn over faster in cultured human liver tumor cells.
primary_references
[parker1993] Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. (1993). https://pubmed.ncbi.nlm.nih.gov/8388388/ DOI: 10.1016/s0021-9258(18)82115-9
tissue_or_cell_type
Hepatoma cell culture
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1115–1126
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled protein pulse-chase and HMGCR immunoprecipitation · source_derived_draft · unverified_draft
### e-sig-gamma-te-hmgcr-turnover At 10 µM gamma-tocotrienol, HepG2 HMG-CoA reductase degradation increased 2.4-fold and its half-life fell from 3.73 to 1.59 h, measured by [35S]methionine pulse-chase and immunoprecipitation. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Gamma-tocotrienol made the cholesterol-synthesis enzyme turn over faster in cultured human liver tumor cells. organism: Homo sapiens tissue_or_cell_type: Hepatoma cell culture experimental_model: Radiolabeled protein pulse-chase and HMGCR immunoprecipitation limitations: Primary abstract only; these data do not by themselves identify Insig proteins or prove direct binding to the reductase. Human supplementation effects cannot be inferred. exposure: 10 µM gamma-tocotrienol; reported HMGCR half-life 3.73 h control versus 1.59 h treated. cross_nutrient: false [parker1993] Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. (1993). https://pubmed.ncbi.nlm.nih.gov/8388388/ DOI: 10.1016/s0021-9258(18)82115-9
Complete structured claim and evidence
Delta-tocotrienol stimulated HMG-CoA reductase ubiquitination in isolated SV-589 fibroblast membrane fractions supplemented with ubiquitin-activating enzyme; gamma-tocotrienol showed the same activity. The reconstituted result supported action without further tocotrienol metabolism.
Delta-tocotrienol → HMG-CoA reductase ubiquitination source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Isolated membranes from sterol-depleted SV-589 human fibroblasts; FLAG-ubiquitin and purified E1 assay
exposure
Figure 5B: purified E1 5 µg/mL, FLAG-ubiquitin 0.1 mg/mL, ubiquitin-aldehyde 0.01 mg/mL and ATP-regenerating system; tocotrienol concentration not fully retrieved.
limitations
The assay does not prove direct molecular binding of tocotrienol to HMGCR or INSIG. No human cholesterol outcome follows from this reconstituted experiment.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Homo sapiens
plain_language
These tocotrienols promoted attachment of degradation tags to the cholesterol-synthesis enzyme in isolated cell membranes.
primary_references
[song2006] Insig-dependent ubiquitination and degradation of 3-hydroxy-3-methylglutaryl coenzyme a reductase stimulated by delta- and gamma-tocotrienols. (2006). https://pubmed.ncbi.nlm.nih.gov/16831864/ DOI: 10.1074/jbc.m605575200
tissue_or_cell_type
Fibroblast-derived membrane fractions
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1128–1139
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated membranes from sterol-depleted SV-589 human fibroblasts; FLAG-ubiquitin and purified E1 assay · source_derived_draft · unverified_draft
### e-sig-delta-te-hmgcr-ubiquitination Delta-tocotrienol stimulated HMG-CoA reductase ubiquitination in isolated SV-589 fibroblast membrane fractions supplemented with ubiquitin-activating enzyme; gamma-tocotrienol showed the same activity. The reconstituted result supported action without further tocotrienol metabolism. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: These tocotrienols promoted attachment of degradation tags to the cholesterol-synthesis enzyme in isolated cell membranes. organism: Homo sapiens tissue_or_cell_type: Fibroblast-derived membrane fractions experimental_model: Isolated membranes from sterol-depleted SV-589 human fibroblasts; FLAG-ubiquitin and purified E1 assay limitations: The assay does not prove direct molecular binding of tocotrienol to HMGCR or INSIG. No human cholesterol outcome follows from this reconstituted experiment. exposure: Figure 5B: purified E1 5 µg/mL, FLAG-ubiquitin 0.1 mg/mL, ubiquitin-aldehyde 0.01 mg/mL and ATP-regenerating system; tocotrienol concentration not fully retrieved. cross_nutrient: false [song2006] Insig-dependent ubiquitination and degradation of 3-hydroxy-3-methylglutaryl coenzyme a reductase stimulated by delta- and gamma-tocotrienols. (2006). https://pubmed.ncbi.nlm.nih.gov/16831864/ DOI: 10.1074/jbc.m605575200
Complete structured claim and evidence
Combined RNAi against INSIG1 and INSIG2 abolished gamma- and delta-tocotrienol-stimulated degradation of endogenous HMG-CoA reductase in sterol-depleted SV-589 fibroblasts supplied with 10 mM mevalonate.
Combined INSIG1 and INSIG2 depletion → HMG-CoA reductase protein degradation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
experimental_model
Combined INSIG1/INSIG2 RNA interference in immortalized human SV-589 fibroblasts
exposure
Sterol depletion 16 h; gamma- or delta-tocotrienol plus 10 mM mevalonate for 5 h; tocotrienol concentration not retrieved from the accessible Figure 3 text.
limitations
Combined knockdown establishes a machinery requirement in this model, not the unique role of either INSIG isoform or nutritional deficiency. Does not quantify viability or predict supplement benefit.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Homo sapiens
plain_language
Removing both INSIG regulators prevented these tocotrienols from accelerating loss of the reductase protein in this cell experiment.
primary_references
[song2006] Insig-dependent ubiquitination and degradation of 3-hydroxy-3-methylglutaryl coenzyme a reductase stimulated by delta- and gamma-tocotrienols. (2006). https://pubmed.ncbi.nlm.nih.gov/16831864/ DOI: 10.1074/jbc.m605575200
tissue_or_cell_type
Human fibroblast cell culture
trigger_kind
machinery_impairment Imported condition classification; unverified.
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1141–1152
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Combined INSIG1/INSIG2 RNA interference in immortalized human SV-589 fibroblasts · source_derived_draft · unverified_draft
### e-sig-insig-depletion-hmgcr-turnover Combined RNAi against INSIG1 and INSIG2 abolished gamma- and delta-tocotrienol-stimulated degradation of endogenous HMG-CoA reductase in sterol-depleted SV-589 fibroblasts supplied with 10 mM mevalonate. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing both INSIG regulators prevented these tocotrienols from accelerating loss of the reductase protein in this cell experiment. organism: Homo sapiens tissue_or_cell_type: Human fibroblast cell culture experimental_model: Combined INSIG1/INSIG2 RNA interference in immortalized human SV-589 fibroblasts limitations: Combined knockdown establishes a machinery requirement in this model, not the unique role of either INSIG isoform or nutritional deficiency. Does not quantify viability or predict supplement benefit. exposure: Sterol depletion 16 h; gamma- or delta-tocotrienol plus 10 mM mevalonate for 5 h; tocotrienol concentration not retrieved from the accessible Figure 3 text. cross_nutrient: false [song2006] Insig-dependent ubiquitination and degradation of 3-hydroxy-3-methylglutaryl coenzyme a reductase stimulated by delta- and gamma-tocotrienols. (2006). https://pubmed.ncbi.nlm.nih.gov/16831864/ DOI: 10.1074/jbc.m605575200
Complete structured claim and evidence
Simvastatin, alone or with ezetimibe, lowered plasma CoQ; CoQ change correlated with LDL-cholesterol change and the CoQ-to-LDL ratio increased.
Simvastatin → Plasma coenzyme Q10 concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/coq10-research/16872244.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65abd11b5f58ce1125f554d52ed5203575d7a3ba0d20b789abce16148f3b5e27", "start_char": 0, "end_char": 2245, "text_sha256": "65abd11b5f58ce1125f554d52ed5203575d7a3ba0d20b789abce16148f3b5e27"}
experimental_model
Randomized three-arm parallel study
exposure
Simvastatin 40 mg/day, ezetimibe 10 mg/day or both for 14 days
limitations
Plasma measurements and correlation; neither tissue CoQ nor mitochondrial dysfunction was demonstrated.
nutrient_topic
Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
organism
72 healthy men
plain_language
The blood concentration also depends on the particles carrying CoQ.
primary_references
[coq10-p16872244] Effect of ezetimibe and/or simvastatin on coenzyme Q10 levels in plasma: a randomised trial. (2006). https://pubmed.ncbi.nlm.nih.gov/16872244/ DOI: 10.2165/00002018-200629080-00007
tissue_or_cell_type
Plasma CoQ and lipoprotein concentrations
Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 931–942
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-arm parallel study · source_derived_draft · unverified_draft
### coq10-statin-plasma-carriers Simvastatin, alone or with ezetimibe, lowered plasma CoQ; CoQ change correlated with LDL-cholesterol change and the CoQ-to-LDL ratio increased. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The blood concentration also depends on the particles carrying CoQ. organism: 72 healthy men tissue_or_cell_type: Plasma CoQ and lipoprotein concentrations experimental_model: Randomized three-arm parallel study limitations: Plasma measurements and correlation; neither tissue CoQ nor mitochondrial dysfunction was demonstrated. exposure: Simvastatin 40 mg/day, ezetimibe 10 mg/day or both for 14 days evidence_span: {"source_cache": "artifacts/coq10-research/16872244.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65abd11b5f58ce1125f554d52ed5203575d7a3ba0d20b789abce16148f3b5e27", "start_char": 0, "end_char": 2245, "text_sha256": "65abd11b5f58ce1125f554d52ed5203575d7a3ba0d20b789abce16148f3b5e27"} [coq10-p16872244] Effect of ezetimibe and/or simvastatin on coenzyme Q10 levels in plasma: a randomised trial. (2006). https://pubmed.ncbi.nlm.nih.gov/16872244/ DOI: 10.2165/00002018-200629080-00007
Complete structured claim and evidence
Ubiquinol did not reduce pain severity or interference versus placebo in confirmed simvastatin myalgia.
Reduced CoQ10 → Statin-associated muscle pain source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/coq10-research/25545331.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837", "start_char": 0, "end_char": 1976, "text_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837"}
experimental_model
Randomized double-blind trial after blinded symptom confirmation
exposure
600 mg/day ubiquinol with simvastatin 20 mg/day for eight weeks
limitations
Small confirmed-myalgia sample; null outcome is not proof that every other regimen is ineffective.
nutrient_topic
Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
organism
41 subjects with confirmed simvastatin myalgia
plain_language
A more strictly selected trial did not reproduce the pain benefit.
primary_references
[coq10-p25545331] A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. (2015). https://pubmed.ncbi.nlm.nih.gov/25545331/ DOI: 10.1016/j.atherosclerosis.2014.12.016
tissue_or_cell_type
Pain, muscle performance and serum CoQ
Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1165–1176
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind trial after blinded symptom confirmation · source_derived_draft · unverified_draft
### coq10-statin-pain-null Ubiquinol did not reduce pain severity or interference versus placebo in confirmed simvastatin myalgia. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A more strictly selected trial did not reproduce the pain benefit. organism: 41 subjects with confirmed simvastatin myalgia tissue_or_cell_type: Pain, muscle performance and serum CoQ experimental_model: Randomized double-blind trial after blinded symptom confirmation limitations: Small confirmed-myalgia sample; null outcome is not proof that every other regimen is ineffective. exposure: 600 mg/day ubiquinol with simvastatin 20 mg/day for eight weeks evidence_span: {"source_cache": "artifacts/coq10-research/25545331.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837", "start_char": 0, "end_char": 1976, "text_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837"} [coq10-p25545331] A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. (2015). https://pubmed.ncbi.nlm.nih.gov/25545331/ DOI: 10.1016/j.atherosclerosis.2014.12.016
Complete structured claim and evidence
Pain severity and interference improved relative to placebo after 30 days of CoQ in the 50-patient study.
Coenzyme Q10 / CoQ10 redox system → Statin-associated muscle pain source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/coq10-research/25375075.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1b3bae22ef80093dd226d2bebbc1791ac08e3952c694f801a72f308fd7258e4", "start_char": 0, "end_char": 1622, "text_sha256": "c1b3bae22ef80093dd226d2bebbc1791ac08e3952c694f801a72f308fd7258e4"}
experimental_model
Randomized placebo-controlled study
exposure
CoQ10 50 mg twice daily for 30 days
limitations
Small short study; symptoms were not confirmed by a blinded statin-placebo lead-in as in the later trial.
nutrient_topic
Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
organism
50 statin-treated patients reporting mild-to-moderate muscle symptoms
plain_language
One trial found less muscle pain with added CoQ.
primary_references
[coq10-p25375075] Coenzyme Q10 supplementation decreases statin-related mild-to-moderate muscle symptoms: a randomized clinical study. (2014). https://pubmed.ncbi.nlm.nih.gov/25375075/ DOI: 10.12659/msm.890777
tissue_or_cell_type
Brief Pain Inventory scores
Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1152–1163
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized placebo-controlled study · source_derived_draft · unverified_draft
### coq10-statin-pain-positive Pain severity and interference improved relative to placebo after 30 days of CoQ in the 50-patient study. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: One trial found less muscle pain with added CoQ. organism: 50 statin-treated patients reporting mild-to-moderate muscle symptoms tissue_or_cell_type: Brief Pain Inventory scores experimental_model: Randomized placebo-controlled study limitations: Small short study; symptoms were not confirmed by a blinded statin-placebo lead-in as in the later trial. exposure: CoQ10 50 mg twice daily for 30 days evidence_span: {"source_cache": "artifacts/coq10-research/25375075.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1b3bae22ef80093dd226d2bebbc1791ac08e3952c694f801a72f308fd7258e4", "start_char": 0, "end_char": 1622, "text_sha256": "c1b3bae22ef80093dd226d2bebbc1791ac08e3952c694f801a72f308fd7258e4"} [coq10-p25375075] Coenzyme Q10 supplementation decreases statin-related mild-to-moderate muscle symptoms: a randomized clinical study. (2014). https://pubmed.ncbi.nlm.nih.gov/25375075/ DOI: 10.12659/msm.890777
Complete structured claim and evidence
Complex I transferred electrons from NADH to ubiquinone-10 in reconstituted membranes.
Mitochondrial respiratory complex I → Ubiquinone-10 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/coq10-research/29133414.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "139122e8a567596e6ec1b4bd361567d0e5cd4e3329fec72d47b949a86d29610d", "start_char": 0, "end_char": 1770, "text_sha256": "139122e8a567596e6ec1b4bd361567d0e5cd4e3329fec72d47b949a86d29610d"}
experimental_model
Proteoliposome enzyme kinetics
exposure
Ubiquinones with one to ten isoprenoid units
limitations
Purified enzyme system; short-chain analogues do not have identical binding and release kinetics to Q10.
nutrient_topic
Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
organism
Mammalian complex I preparation
plain_language
CoQ receives electrons from the first respiratory complex.
primary_references
[coq10-p29133414] Correlating kinetic and structural data on ubiquinone binding and reduction by respiratory complex I. (2017). https://pubmed.ncbi.nlm.nih.gov/29133414/ DOI: 10.1073/pnas.1714074114
tissue_or_cell_type
Membrane quinone channel
Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 385–396
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proteoliposome enzyme kinetics · source_derived_draft · unverified_draft
### coq10-complex-i-q Complex I transferred electrons from NADH to ubiquinone-10 in reconstituted membranes. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: CoQ receives electrons from the first respiratory complex. organism: Mammalian complex I preparation tissue_or_cell_type: Membrane quinone channel experimental_model: Proteoliposome enzyme kinetics limitations: Purified enzyme system; short-chain analogues do not have identical binding and release kinetics to Q10. exposure: Ubiquinones with one to ten isoprenoid units evidence_span: {"source_cache": "artifacts/coq10-research/29133414.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "139122e8a567596e6ec1b4bd361567d0e5cd4e3329fec72d47b949a86d29610d", "start_char": 0, "end_char": 1770, "text_sha256": "139122e8a567596e6ec1b4bd361567d0e5cd4e3329fec72d47b949a86d29610d"} [coq10-p29133414] Correlating kinetic and structural data on ubiquinone binding and reduction by respiratory complex I. (2017). https://pubmed.ncbi.nlm.nih.gov/29133414/ DOI: 10.1073/pnas.1714074114
Complete structured claim and evidence
Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step.
Human glutamate-cysteine ligase catalytic subunit / GCLC → Gamma-glutamylcysteine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sulforaphane-research/30581542.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77cf6674cf9b9bc140a228588a53c937966fd3a67397c1c4970221c5cc58a0b1", "start_char": 762, "end_char": 1092, "text_sha256": "927fa13b085700c20b578ecabc7c8c17a66ea4600b90809e3061d12bcaea3849"}
experimental_model
Human enzyme mutagenesis, kinetics and molecular dynamics
exposure
S-loop variants; established biosynthetic reactions described in the introduction
limitations
Reaction descriptions are background chemistry in a primary enzyme paper, not evidence that sulforaphane corrects inherited GSS deficiency.
nutrient_topic
Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
organism
Human GSS
plain_language
The induced machinery still needs its amino-acid building blocks.
primary_references
[sulforaphane-p30581542] Genetic Mutations in the S-loop of Human Glutathione Synthetase: Links Between Substrate Binding, Active Site Structure and Allostery. (2019). https://pubmed.ncbi.nlm.nih.gov/30581542/ DOI: 10.1016/j.csbj.2018.11.008
tissue_or_cell_type
Glutathione synthesis and substrate binding
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 840–851
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human enzyme mutagenesis, kinetics and molecular dynamics · source_derived_draft · unverified_draft
### sulforaphane-gcl-first-step Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The induced machinery still needs its amino-acid building blocks. organism: Human GSS tissue_or_cell_type: Glutathione synthesis and substrate binding experimental_model: Human enzyme mutagenesis, kinetics and molecular dynamics limitations: Reaction descriptions are background chemistry in a primary enzyme paper, not evidence that sulforaphane corrects inherited GSS deficiency. exposure: S-loop variants; established biosynthetic reactions described in the introduction evidence_span: {"source_cache": "artifacts/sulforaphane-research/30581542.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77cf6674cf9b9bc140a228588a53c937966fd3a67397c1c4970221c5cc58a0b1", "start_char": 762, "end_char": 1092, "text_sha256": "927fa13b085700c20b578ecabc7c8c17a66ea4600b90809e3061d12bcaea3849"} [sulforaphane-p30581542] Genetic Mutations in the S-loop of Human Glutathione Synthetase: Links Between Substrate Binding, Active Site Structure and Allostery. (2019). https://pubmed.ncbi.nlm.nih.gov/30581542/ DOI: 10.1016/j.csbj.2018.11.008
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.

Product dose and gemfibrozil change active-metabolite exposure

Condition: biomarker_context · Dose escalation or gemfibrozil coadministration.

Normal role: Chemical form and clearance influence drug exposure.

Recorded consequence: Measured product-specific pharmacokinetic changes.

Scope: Healthy volunteers.

PPAR-gamma blockade changes the pigment response

Condition: machinery_impairment · GW9662 during ankaflavin treatment.

Normal role: PPAR-gamma signaling can affect insulin-response endpoints.

Recorded consequence: Loss of tested metabolic effects.

Scope: Methylglyoxal-treated rats.

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20)AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · unverified_draftRead preserved source
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Statin-associated muscle pain: improvement in one trial, absent in othersThe 2014 study found pain relief, whereas the 2015 trial found no benefit after symptoms were confirmed with blinded simvastatin/placebo exposure. A 2022 trial also found no pain benefit or increase in muscle CoQ. These challenge a general claim of CoQ efficacy for statin-associated muscle pain; selection, formulation, dose and duration differed.Read the recorded disagreement

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Red yeast rice

The mechanisms

The 28-brand analytical study treated monacolin K in red yeast rice as chemically identical to lovastatin.

Monacolin K was undetected in two of 28 brands; the other 26 ranged from 0.09 to 5.48 mg per 1,200 mg red yeast rice.

Twelve products labeled 600 mg per capsule contained 0.00–2.30 mg monacolin KA per capsule, alongside variable lactone and total monacolins.

Four of twelve analyzed red yeast rice formulations had elevated citrinin levels in the reported survey.

The original monacolin K study prepared acid forms by saponifying lactones in 0.1 N NaOH at 50 degrees C for two hours.

Monacolin K acid sodium salt competitively inhibited rat liver HMG-CoA reductase with respect to HMG-CoA; the reported Ki was 0.49 nM.

The same monacolin K inhibition was noncompetitive with respect to NADPH.

Monacolin K inhibited lipid labeling from acetate or HMG-CoA, but did not inhibit incorporation from supplied mevalonate at concentrations up to 10 mM.

Human HMG-CoA reductase catalyzes mevalonate formation; substrate/cofactor-bound structures locate HMG-CoA and the nicotinamide cofactor in the catalytic domain.

The 1990 human lovastatin report observed reductions in circulating CoQ10 during drug exposure in five hospitalized patients and a separately monitored volunteer.

Acute red yeast rice gavage at 1 or 5 g/kg reduced hepatic CoQ10 in male ICR mice, with suppression still reported at 24 hours.

The same acute mouse study reported lower cardiac CoQ10 after red yeast rice gavage, with greater suppression at the higher dose.

The three 2012 red yeast rice product extracts inhibited human microsomal CYP1A2 more potently than pure lovastatin at matched nominal lovastatin concentrations.

The three 2012 red yeast rice product extracts inhibited human microsomal CYP2C19 more potently than pure lovastatin at matched nominal lovastatin concentrations.

The three 2012 red yeast rice product extracts inhibited human microsomal CYP3A4 more potently than pure lovastatin at matched nominal lovastatin concentrations.

The three product extracts inhibited P-glycoprotein transport activity more potently than pure lovastatin in the study assay.

Lovastatin flux across Caco-2 monolayers was higher with the three product extracts than with pure lovastatin at a matched 25 micromolar concentration.

In 14 volunteers, single doses of one, two or four LipoCol Forte capsules produced dose-related lovastatin and lovastatin-acid exposure; one capsule twice daily for five days produced no significant accumulation.

One 600 mg LipoCol Forte capsule did not significantly change the measured pharmacokinetics of 5 mg nifedipine in 14 volunteers.

Gemfibrozil 600 mg twice daily increased lovastatin-acid peak concentration and exposure area after LipoCol Forte in 13 volunteers.

Gemfibrozil did not significantly change parent lovastatin pharmacokinetic parameters in that LipoCol Forte experiment.

Repeated double-strength grapefruit juice increased lovastatin peak concentration about 12-fold and exposure area about 15-fold after an 80 mg dose in ten volunteers.

In the same experiment, lovastatin-acid peak concentration rose about fourfold and exposure area about fivefold.

Itraconazole 100 mg daily for four days increased lovastatin peak concentration about 15-fold and exposure area more than 15-fold after a 40 mg dose in ten volunteers.

Adding monascin increased hepatic AMPK phosphorylation in high-fat-diet-fed mice.

Monascin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study.

Adding ankaflavin increased hepatic AMPK phosphorylation in high-fat-diet-fed mice.

Ankaflavin increased hepatic PPAR-alpha expression and promoted a fatty-acid-oxidation program in the mouse study.

GW9662 antagonism abolished tested insulin-sensitivity effects of ankaflavin in methylglyoxal-treated Wistar rats.

Ankaflavin increased hepatic Nrf2 Ser40 phosphorylation without increasing measured Nrf2 mRNA or total protein in the rat experiment.

Ankaflavin increased hepatic GCL and HO-1 transcriptional activation; these effects persisted despite PPAR-gamma antagonist treatment.

Ankaflavin increased glutathione measured in liver and pancreas of methylglyoxal-treated rats.

Ankaflavin did not inhibit AGE generation in the reported cell-free experiment despite lower AGE endpoints in treated rats.

Ankaflavin inhibited yeast alpha-glucosidase with an IC50 of 126.5 micromolar and mixed-type kinetics.

Docking proposed ankaflavin binding outside the catalytic center of the alpha-glucosidase model.

Monascin inhibited yeast alpha-glucosidase with an IC50 of 302.6 micromolar and mixed-type kinetics.

Docking proposed monascin binding outside the catalytic center of the alpha-glucosidase model.

The pigment-rich fermentation product at 0.2 mg/mL reduced fluorescent AGE formation by 87.1% in the BSA–fructose assay.

Citrinin exposure reduced ATP in rat proximal-tubule suspensions before or during ensuing cell injury.

Deferoxamine pretreatment prevented iron-mediated lipid peroxidation but did not protect rat tubules from citrinin-induced death.

Citrinin lowered respiratory control, ADP/O ratio and membrane potential in rat renal cortical mitochondria.

In 62 statin-intolerant participants, the studied red yeast rice regimen reduced LDL by 43 mg/dL at 12 weeks and 35 mg/dL at 24 weeks, versus 11 and 15 mg/dL with placebo.

Pain, CPK and liver-enzyme results did not differ significantly between groups in the 24-week trial.

The red yeast rice arm of SPORT did not significantly lower LDL versus placebo after 28 days; rosuvastatin 5 mg did.

Over an average 4.5 years, major coronary events occurred in 5.7% of the Xuezhikang group versus 10.4% of placebo in nearly 5,000 Chinese patients with prior myocardial infarction.

At 10 µM gamma-tocotrienol, HepG2 HMG-CoA reductase degradation increased 2.4-fold and its half-life fell from 3.73 to 1.59 h, measured by [35S]methionine pulse-chase and immunoprecipitation.

Delta-tocotrienol stimulated HMG-CoA reductase ubiquitination in isolated SV-589 fibroblast membrane fractions supplemented with ubiquitin-activating enzyme; gamma-tocotrienol showed the same activity. The reconstituted result supported action without further tocotrienol metabolism.

Combined RNAi against INSIG1 and INSIG2 abolished gamma- and delta-tocotrienol-stimulated degradation of endogenous HMG-CoA reductase in sterol-depleted SV-589 fibroblasts supplied with 10 mM mevalonate.

Simvastatin, alone or with ezetimibe, lowered plasma CoQ; CoQ change correlated with LDL-cholesterol change and the CoQ-to-LDL ratio increased.

Ubiquinol did not reduce pain severity or interference versus placebo in confirmed simvastatin myalgia.

Pain severity and interference improved relative to placebo after 30 days of CoQ in the 50-patient study.

Complex I transferred electrons from NADH to ubiquinone-10 in reconstituted membranes.

Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step.

Availability and dependencies

The sources

Recorded disagreements

Open questions in this collection