Component

Human OATP1B1 / SLCO1B1

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

17 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Human SLCO1B1 transported Luteolin 3′-O-glucuronide in the fluorescence-based uptake assay.

    Human OATP1B1 / SLCO1B1 → Luteolin 3′-O-glucuronide source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Living-cell uptake using 2-APB fluorescence enhancement.
    limitations
    Transport capacity is not clinical efficacy or net organ flux.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    A circulating conjugate has a route into cells.
    primary_references
    The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740
    transport_effect
    raises Measured in a fluorescence-based uptake assay.
    transport_pool
    the hepatocyte-model cell in the uptake assay Measured in a fluorescence-based uptake assay.

    Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 172–178

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

    ## luteolin-slco1b1-3g A circulating conjugate has a route into cells. Human SLCO1B1 transported Luteolin 3′-O-glucuronide in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740
    Complete structured claim and evidence

  2. Human SLCO1B1 transported Luteolin 3′-O-sulfate in the fluorescence-based uptake assay.

    Human OATP1B1 / SLCO1B1 → Luteolin 3′-O-sulfate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Living-cell uptake using 2-APB fluorescence enhancement.
    limitations
    Transport capacity is not clinical efficacy or net organ flux.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    A circulating conjugate has a route into cells.
    primary_references
    The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740
    transport_effect
    raises Measured in a fluorescence-based uptake assay.
    transport_pool
    the hepatocyte-model cell in the uptake assay Measured in a fluorescence-based uptake assay.

    Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 188–194

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

    ## luteolin-slco1b1-3s A circulating conjugate has a route into cells. Human SLCO1B1 transported Luteolin 3′-O-sulfate in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740
    Complete structured claim and evidence

  3. Human SLCO1B1 transported Luteolin 7-O-glucuronide in the fluorescence-based uptake assay.

    Human OATP1B1 / SLCO1B1 → Luteolin 7-O-glucuronide source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Living-cell uptake using 2-APB fluorescence enhancement.
    limitations
    Transport capacity is not clinical efficacy or net organ flux.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    A circulating conjugate has a route into cells.
    primary_references
    The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740
    transport_effect
    raises Measured in a fluorescence-based uptake assay.
    transport_pool
    the hepatocyte-model cell in the uptake assay Measured in a fluorescence-based uptake assay.

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

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Living-cell uptake using 2-APB fluorescence enhancement. · source_derived_draft · unverified_draft

    ## luteolin-slco1b1-7g A circulating conjugate has a route into cells. Human SLCO1B1 transported Luteolin 7-O-glucuronide in the fluorescence-based uptake assay. Model: Living-cell uptake using 2-APB fluorescence enhancement. Limitations: Transport capacity is not clinical efficacy or net organ flux. Evidence access: Primary abstract The 2-aminoethyl diphenylborinate-based fluorescent method identifies quercetin and luteolin metabolites as substrates of Organic anion transporting polypeptides, OATP1B1 and OATP2B1. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38437885/ · DOI 10.1016/j.ejps.2024.106740
    Complete structured claim and evidence

  4. Myricetin 3′-O-sulfate was a substrate of human SLCO1B1.

    Human OATP1B1 / SLCO1B1 → Myricetin 3′-O-sulfate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Overexpressing-cell uptake with flavonoid fluorescence method.
    limitations
    Not a quantified human tissue delivery rate.
    nutrient_topic
    Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
    plain_language
    The sulfate is transported, not simply inactive waste.
    primary_references
    Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
    transport_effect
    raises Recorded as a substrate in the OATP1B1 uptake assay.
    transport_pool
    the hepatocyte-model cell in the uptake assay Recorded as a substrate in the OATP1B1 uptake assay.

    Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 204–210

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Overexpressing-cell uptake with flavonoid fluorescence method. · source_derived_draft · unverified_draft

    ## myricetin-sulfate-uptake-slco1b1 The sulfate is transported, not simply inactive waste. Myricetin 3′-O-sulfate was a substrate of human SLCO1B1. Model: Overexpressing-cell uptake with flavonoid fluorescence method. Limitations: Not a quantified human tissue delivery rate. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
    Complete structured claim and evidence

  5. OATP1B1 activity lowers plasma atorvastatin exposure by carrying the drug from portal blood into the hepatocyte, so reducing that activity raises the plasma concentration.

    Human OATP1B1 / SLCO1B1 → Plasma atorvastatin exposure source_derived_draftungraded
    Experimental context and source evidence
    duration
    Single dose in both designs
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Healthy human volunteers, by pharmacological inhibition and by reduced-function genotype
    exposure
    Rifampicin inhibition in one study and the SLCO1B1 c.521CC genotype in another
    limitations
    This is the mechanistic reading shared by an inhibitor study and a genotype study rather than a single measurement of transporter activity against exposure; neither study measured OATP1B1 activity directly in the participants.
    organism
    Healthy human volunteers, by pharmacological inhibition and by reduced-function genotype
    plain_language
    OATP1B1 activity lowers plasma atorvastatin exposure by carrying the drug from portal blood into the hepatocyte, so reducing that activity raises the plasma concentration.
    primary_references
    The effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. (2007). https://pubmed.ncbi.nlm.nih.gov/17192770/ DOI: 10.1038/sj.clpt.6100038
    route
    Oral atorvastatin
    tissue
    Hepatic sinusoidal uptake and systemic plasma exposure

    OATP1B1 activity and statin exposure: the step between transporter inhibition and drug concentration (2026-09-22) · lines 24–33

    Original AI-assisted curation of four primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Three of the four share one research group and are recorded as one line of evidence. Study-specific citations, doses and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## oatp1b1-activity-lowers-atorvastatin-exposure OATP1B1 activity lowers plasma atorvastatin exposure by carrying the drug from portal blood into the hepatocyte, so reducing that activity raises the plasma concentration. Model/species: Healthy human volunteers, by pharmacological inhibition and by reduced-function genotype Tissue/system: Hepatic sinusoidal uptake and systemic plasma exposure Exposure: Rifampicin inhibition in one study and the SLCO1B1 c.521CC genotype in another Route: Oral atorvastatin Duration: Single dose in both designs Limits: This is the mechanistic reading shared by an inhibitor study and a genotype study rather than a single measurement of transporter activity against exposure; neither study measured OATP1B1 activity directly in the participants. Primary reference: The effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. (2007). https://pubmed.ncbi.nlm.nih.gov/17192770/ DOI: 10.1038/sj.clpt.6100038 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  6. The SLCO1B1 c.521T>C variant decreases OATP1B1 transporting activity, markedly increasing plasma statin concentrations, and thereby enhances the risk of statin-induced myopathy and decreases the therapeutic index of statins.

    Human OATP1B1 / SLCO1B1 → Statin-associated muscle pain source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not applicable
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Review of human pharmacogenetic and pharmacokinetic studies
    exposure
    SLCO1B1 c.521T>C, protein p.V174A, rs4149056
    limitations
    This is a review statement summarising several studies rather than a single measurement, the effect differs between statins, and it describes the variant's effect on activity rather than a directly measured activity-to-myopathy relationship.
    organism
    Review of human pharmacogenetic and pharmacokinetic studies
    plain_language
    The SLCO1B1 c.521T>C variant decreases OATP1B1 transporting activity, markedly increasing plasma statin concentrations, and thereby enhances the risk of statin-induced myopathy and decreases the therapeutic index of statins.
    primary_references
    Organic anion transporting polypeptide 1B1: a genetically polymorphic transporter of major importance for hepatic drug uptake. (2011). https://pubmed.ncbi.nlm.nih.gov/21245207/ DOI: 10.1124/pr.110.002857
    route
    Oral statins
    tissue
    Hepatic uptake, plasma statin concentration and skeletal muscle injury

    OATP1B1 activity and statin exposure: the step between transporter inhibition and drug concentration (2026-09-22) · lines 68–77

    Original AI-assisted curation of four primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Three of the four share one research group and are recorded as one line of evidence. Study-specific citations, doses and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## oatp1b1-activity-lowers-statin-myopathy-risk The SLCO1B1 c.521T>C variant decreases OATP1B1 transporting activity, markedly increasing plasma statin concentrations, and thereby enhances the risk of statin-induced myopathy and decreases the therapeutic index of statins. Model/species: Review of human pharmacogenetic and pharmacokinetic studies Tissue/system: Hepatic uptake, plasma statin concentration and skeletal muscle injury Exposure: SLCO1B1 c.521T>C, protein p.V174A, rs4149056 Route: Oral statins Duration: Not applicable Limits: This is a review statement summarising several studies rather than a single measurement, the effect differs between statins, and it describes the variant's effect on activity rather than a directly measured activity-to-myopathy relationship. Primary reference: Organic anion transporting polypeptide 1B1: a genetically polymorphic transporter of major importance for hepatic drug uptake. (2011). https://pubmed.ncbi.nlm.nih.gov/21245207/ DOI: 10.1124/pr.110.002857 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

What acts on it

  1. Cyclosporin A inhibited OATP2-mediated uptake of labelled cerivastatin in transporter-expressing MDCKII cells with a Ki of 0.2 micromolar.

    Cyclosporine → Human OATP1B1 / SLCO1B1 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Human OATP2 (OATP1B1 / SLCO1B1) expressed in MDCKII cells
    exposure
    Cyclosporin A
    limitations
    The transporter is named OATP2 in this 2003 report, which is the protein now called OATP1B1 and encoded by SLCO1B1; the same entity is reused here rather than forked. The Ki is for cerivastatin as the probe substrate and does not transfer unchanged to other OATP1B1 substrates.
    organism
    Human OATP2 (OATP1B1 / SLCO1B1) expressed in MDCKII cells
    plain_language
    Cyclosporin A inhibited OATP2-mediated uptake of labelled cerivastatin in transporter-expressing MDCKII cells with a Ki of 0.2 micromolar.
    primary_references
    Inhibition of transporter-mediated hepatic uptake as a mechanism for drug-drug interaction between cerivastatin and cyclosporin A. (2003). https://pubmed.ncbi.nlm.nih.gov/12538813/ DOI: 10.1124/jpet.102.041921
    route
    In vitro
    tissue
    Hepatic sinusoidal uptake transport

    Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 146–146

    Original AI-assisted curation of seven primary studies resolved by PubMed title search, with every abstract read and all DOIs cross-checked against live PubMed metadata on 2026-09-23. No reference carries a recorded retraction, erratum or expression of concern. Each of the seven is a separate laboratory and each carries its own lineage key, so none of them can be counted twice as independent support. Study-specific concentrations, kinetic constants and limitations retained. Not publisher full text. · supports · Human OATP2 (OATP1B1 / SLCO1B1) expressed in MDCKII cells · source_derived_draft · unverified_draft

    Cyclosporin A inhibited OATP2-mediated uptake of labelled cerivastatin in transporter-expressing MDCKII cells with a Ki of 0.2 micromolar.
    Complete structured claim and evidence

  2. Luteolin 3′-O-glucuronide strongly inhibited OATP1B1 in vitro.

    Luteolin 3′-O-glucuronide → Human OATP1B1 / SLCO1B1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human transporter interaction assays.
    limitations
    No clinical drug-exposure change was measured.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    A transported metabolite can also compete with uptake.
    primary_references
    Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

    Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 228–234

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

    ## luteolin-oatp1b1-inhibition-glucuronide A transported metabolite can also compete with uptake. Luteolin 3′-O-glucuronide strongly inhibited OATP1B1 in vitro. Model: Human transporter interaction assays. Limitations: No clinical drug-exposure change was measured. Evidence access: Primary abstract Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078
    Complete structured claim and evidence

  3. Luteolin 3′-O-sulfate strongly inhibited OATP1B1 in vitro.

    Luteolin 3′-O-sulfate → Human OATP1B1 / SLCO1B1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human transporter interaction assays.
    limitations
    No clinical drug-exposure change was measured.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    A transported metabolite can also compete with uptake.
    primary_references
    Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078

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

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

    ## luteolin-oatp1b1-inhibition-sulfate A transported metabolite can also compete with uptake. Luteolin 3′-O-sulfate strongly inhibited OATP1B1 in vitro. Model: Human transporter interaction assays. Limitations: No clinical drug-exposure change was measured. Evidence access: Primary abstract Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36481402/ · DOI 10.1016/j.biopha.2022.114078
    Complete structured claim and evidence

  4. The parent inhibited human SLCO1B1 transport in vitro, IC50 6.4 micromolar.

    Myricetin → Human OATP1B1 / SLCO1B1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human transporter-overexpressing cells.
    limitations
    Probe-substrate potency is not a measured clinical drug interaction.
    nutrient_topic
    Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
    plain_language
    Transport competition can depend on the metabolite.
    primary_references
    Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

    Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 108–114

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter-overexpressing cells. · source_derived_draft · unverified_draft

    ## myricetin-parent-slco1b1 Transport competition can depend on the metabolite. The parent inhibited human SLCO1B1 transport in vitro, IC50 6.4 micromolar. Model: Human transporter-overexpressing cells. Limitations: Probe-substrate potency is not a measured clinical drug interaction. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
    Complete structured claim and evidence

  5. The sulfate inhibited human SLCO1B1 transport in vitro, IC50 1.7 micromolar.

    Myricetin 3′-O-sulfate → Human OATP1B1 / SLCO1B1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human transporter-overexpressing cells.
    limitations
    Probe-substrate potency is not a measured clinical drug interaction.
    nutrient_topic
    Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
    plain_language
    Transport competition can depend on the metabolite.
    primary_references
    Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

    Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 156–162

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter-overexpressing cells. · source_derived_draft · unverified_draft

    ## myricetin-sulfate-slco1b1 Transport competition can depend on the metabolite. The sulfate inhibited human SLCO1B1 transport in vitro, IC50 1.7 micromolar. Model: Human transporter-overexpressing cells. Limitations: Probe-substrate potency is not a measured clinical drug interaction. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. A genome-wide association study found a single strong association of statin myopathy with the rs4363657 variant within SLCO1B1, which encodes the hepatic uptake transporter OATP1B1.

    SLCO1B1 rs4363657 variant → Statin-associated muscle pain source_derived_draftungraded
    Experimental context and source evidence
    duration
    Trial duration, not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    85 subjects with definite or incipient myopathy and 90 controls, replicated in a separate trial
    exposure
    Simvastatin 80 mg daily, replication at simvastatin 40 mg daily
    limitations
    The statin was simvastatin, not atorvastatin, and the association is with a noncoding variant rather than a demonstrated change in transporter function in these subjects.
    organism
    85 subjects with definite or incipient myopathy and 90 controls, replicated in a separate trial
    plain_language
    A genome-wide association study found a single strong association of statin myopathy with the rs4363657 variant within SLCO1B1, which encodes the hepatic uptake transporter OATP1B1.
    primary_references
    SLCO1B1 variants and statin-induced myopathy--a genomewide study. (2008). https://pubmed.ncbi.nlm.nih.gov/18650507/ DOI: 10.1056/NEJMoa0801936
    route
    Oral
    tissue
    Hepatic statin uptake and skeletal muscle injury

    Atorvastatin: mechanism of action from target occupancy to isoprenoids, transport, muscle and metabolism (2026-09-22) · lines 133–142

    Original AI-assisted curation of twelve primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Findings obtained with mevastatin, simvastatin or the statin class are recorded against those subjects. Study-specific citations, doses, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## slco1b1-variant-and-statin-myopathy A genome-wide association study found a single strong association of statin myopathy with the rs4363657 variant within SLCO1B1, which encodes the hepatic uptake transporter OATP1B1. Model/species: 85 subjects with definite or incipient myopathy and 90 controls, replicated in a separate trial Tissue/system: Hepatic statin uptake and skeletal muscle injury Exposure: Simvastatin 80 mg daily, replication at simvastatin 40 mg daily Route: Oral Duration: Trial duration, not stated here Limits: The statin was simvastatin, not atorvastatin, and the association is with a noncoding variant rather than a demonstrated change in transporter function in these subjects. Primary reference: SLCO1B1 variants and statin-induced myopathy--a genomewide study. (2008). https://pubmed.ncbi.nlm.nih.gov/18650507/ DOI: 10.1056/NEJMoa0801936 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. Selected naringenin sulfate or glucuronide conjugates potently inhibited OATP1B1 and/or OATP2B1 in vitro.

    Naringenin sulfate conjugates → Human OATP1B1/OATP2B1 transport activity source_derived_draftungraded
    Experimental context and source evidence
    dose
    Naringenin metabolite concentration-response
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Transporter expression assays
    limitations
    The abstract does not assign every conjugate to each transporter or establish interaction at human free concentrations.
    nutrient_topic
    Naringenin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Naringenin
    organism
    Transporter expression assays
    plain_language
    Selected naringenin sulfate or glucuronide conjugates potently inhibited OATP1B1 and/or OATP2B1 in vitro.
    primary_references
    Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. (2023). https://pubmed.ncbi.nlm.nih.gov/36481402/ DOI: 10.1016/j.biopha.2022.114078
    route
    In vitro
    tissue
    OATP1B1 and OATP2B1 transport

    Naringenin: mechanism of action and interactions (2026-09-20) · lines 88–97

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Transporter expression assays · source_derived_draft · unverified_draft

    ## naringenin-oatp-inhibition Selected naringenin sulfate or glucuronide conjugates potently inhibited OATP1B1 and/or OATP2B1 in vitro. Model/species: Transporter expression assays Tissue/system: OATP1B1 and OATP2B1 transport Exposure: Naringenin metabolite concentration-response Route: In vitro Duration: Acute Limits: The abstract does not assign every conjugate to each transporter or establish interaction at human free concentrations. Primary reference: Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters. (2023). https://pubmed.ncbi.nlm.nih.gov/36481402/ DOI: 10.1016/j.biopha.2022.114078 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. A single intravenous dose of rifampicin increased the total plasma exposure of atorvastatin acid by 6.8-fold in healthy volunteers.

    Rifampicin → Plasma atorvastatin exposure source_derived_draftungraded
    Experimental context and source evidence
    duration
    Single dose, sampling to 24 hours
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    11 healthy human volunteers, randomised crossover
    exposure
    Two 40 mg oral atorvastatin doses one week apart, with one 30-minute intravenous infusion of 600 mg rifampicin on one of the two study days
    limitations
    Rifampicin is used here as a model hepatic uptake inhibitor and is not selective for OATP1B1; the lactone forms rose less than the acid, and a single intravenous dose avoids the enzyme induction that repeated oral rifampicin would cause.
    organism
    11 healthy human volunteers, randomised crossover
    plain_language
    A single intravenous dose of rifampicin increased the total plasma exposure of atorvastatin acid by 6.8-fold in healthy volunteers.
    primary_references
    The effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. (2007). https://pubmed.ncbi.nlm.nih.gov/17192770/ DOI: 10.1038/sj.clpt.6100038
    route
    Oral atorvastatin with intravenous rifampicin
    tissue
    Plasma atorvastatin acid and its hydroxy metabolites

    OATP1B1 activity and statin exposure: the step between transporter inhibition and drug concentration (2026-09-22) · lines 13–22

    Original AI-assisted curation of four primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Three of the four share one research group and are recorded as one line of evidence. Study-specific citations, doses and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## rifampicin-raises-atorvastatin-exposure A single intravenous dose of rifampicin increased the total plasma exposure of atorvastatin acid by 6.8-fold in healthy volunteers. Model/species: 11 healthy human volunteers, randomised crossover Tissue/system: Plasma atorvastatin acid and its hydroxy metabolites Exposure: Two 40 mg oral atorvastatin doses one week apart, with one 30-minute intravenous infusion of 600 mg rifampicin on one of the two study days Route: Oral atorvastatin with intravenous rifampicin Duration: Single dose, sampling to 24 hours Limits: Rifampicin is used here as a model hepatic uptake inhibitor and is not selective for OATP1B1; the lactone forms rose less than the acid, and a single intravenous dose avoids the enzyme induction that repeated oral rifampicin would cause. Primary reference: The effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. (2007). https://pubmed.ncbi.nlm.nih.gov/17192770/ DOI: 10.1038/sj.clpt.6100038 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  4. Volunteers with the SLCO1B1 c.521CC genotype had 144 percent greater plasma atorvastatin exposure than those with the c.521TT genotype.

    SLCO1B1 c.521T>C reduced-function variant → Plasma atorvastatin exposure source_derived_draftungraded
    Experimental context and source evidence
    duration
    Single dose with 48-hour sampling
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    32 healthy volunteers, 4 with c.521CC, 12 with c.521TC and 16 with c.521TT
    exposure
    Single 20 mg oral atorvastatin dose
    limitations
    Only four participants carried the c.521CC genotype, and 2-hydroxyatorvastatin exposure was 100 percent greater in the same comparison.
    organism
    32 healthy volunteers, 4 with c.521CC, 12 with c.521TC and 16 with c.521TT
    plain_language
    Volunteers with the SLCO1B1 c.521CC genotype had 144 percent greater plasma atorvastatin exposure than those with the c.521TT genotype.
    primary_references
    Different effects of SLCO1B1 polymorphism on the pharmacokinetics of atorvastatin and rosuvastatin. (2007). https://pubmed.ncbi.nlm.nih.gov/17473846/ DOI: 10.1038/sj.clpt.6100220
    route
    Oral
    tissue
    Plasma atorvastatin area under the concentration-time curve from 0 to 48 hours

    OATP1B1 activity and statin exposure: the step between transporter inhibition and drug concentration (2026-09-22) · lines 35–44

    Original AI-assisted curation of four primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Three of the four share one research group and are recorded as one line of evidence. Study-specific citations, doses and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## slco1b1-c521cc-raises-atorvastatin-exposure Volunteers with the SLCO1B1 c.521CC genotype had 144 percent greater plasma atorvastatin exposure than those with the c.521TT genotype. Model/species: 32 healthy volunteers, 4 with c.521CC, 12 with c.521TC and 16 with c.521TT Tissue/system: Plasma atorvastatin area under the concentration-time curve from 0 to 48 hours Exposure: Single 20 mg oral atorvastatin dose Route: Oral Duration: Single dose with 48-hour sampling Limits: Only four participants carried the c.521CC genotype, and 2-hydroxyatorvastatin exposure was 100 percent greater in the same comparison. Primary reference: Different effects of SLCO1B1 polymorphism on the pharmacokinetics of atorvastatin and rosuvastatin. (2007). https://pubmed.ncbi.nlm.nih.gov/17473846/ DOI: 10.1038/sj.clpt.6100220 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  5. The same SLCO1B1 c.521CC genotype raised rosuvastatin exposure by 65 percent, a smaller effect than on atorvastatin, which the authors describe as unexpected for the more hydrophilic statin.

    SLCO1B1 c.521T>C reduced-function variant → Plasma rosuvastatin exposure source_derived_draftungraded
    Experimental context and source evidence
    duration
    Single dose with 48-hour sampling
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    The same 32 healthy volunteers
    exposure
    Single 10 mg oral rosuvastatin dose, one week apart from the atorvastatin dose
    limitations
    A within-study comparison of two statins at different doses, so the ratio of effects is not a dose-matched comparison.
    organism
    The same 32 healthy volunteers
    plain_language
    The same SLCO1B1 c.521CC genotype raised rosuvastatin exposure by 65 percent, a smaller effect than on atorvastatin, which the authors describe as unexpected for the more hydrophilic statin.
    primary_references
    Different effects of SLCO1B1 polymorphism on the pharmacokinetics of atorvastatin and rosuvastatin. (2007). https://pubmed.ncbi.nlm.nih.gov/17473846/ DOI: 10.1038/sj.clpt.6100220
    route
    Oral
    tissue
    Plasma rosuvastatin area under the concentration-time curve and peak concentration

    OATP1B1 activity and statin exposure: the step between transporter inhibition and drug concentration (2026-09-22) · lines 46–55

    Original AI-assisted curation of four primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Three of the four share one research group and are recorded as one line of evidence. Study-specific citations, doses and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## slco1b1-c521cc-raises-rosuvastatin-exposure-less The same SLCO1B1 c.521CC genotype raised rosuvastatin exposure by 65 percent, a smaller effect than on atorvastatin, which the authors describe as unexpected for the more hydrophilic statin. Model/species: The same 32 healthy volunteers Tissue/system: Plasma rosuvastatin area under the concentration-time curve and peak concentration Exposure: Single 10 mg oral rosuvastatin dose, one week apart from the atorvastatin dose Route: Oral Duration: Single dose with 48-hour sampling Limits: A within-study comparison of two statins at different doses, so the ratio of effects is not a dose-matched comparison. Primary reference: Different effects of SLCO1B1 polymorphism on the pharmacokinetics of atorvastatin and rosuvastatin. (2007). https://pubmed.ncbi.nlm.nih.gov/17473846/ DOI: 10.1038/sj.clpt.6100220 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  6. Volunteers with the SLCO1B1 c.521CC genotype had 221 percent greater plasma exposure to active simvastatin acid than those with the c.521TT genotype.

    SLCO1B1 c.521T>C reduced-function variant → Plasma simvastatin exposure source_derived_draftungraded
    Experimental context and source evidence
    duration
    Single dose with 12-hour sampling
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    4 volunteers with c.521CC, 12 with c.521TC and 16 with c.521TT
    exposure
    Single 40 mg oral simvastatin dose
    limitations
    Peak concentration was 200 percent higher and occurred earlier in c.521CC carriers; the four-carrier group is small.
    organism
    4 volunteers with c.521CC, 12 with c.521TC and 16 with c.521TT
    plain_language
    Volunteers with the SLCO1B1 c.521CC genotype had 221 percent greater plasma exposure to active simvastatin acid than those with the c.521TT genotype.
    primary_references
    SLCO1B1 polymorphism markedly affects the pharmacokinetics of simvastatin acid. (2006). https://pubmed.ncbi.nlm.nih.gov/17108811/ DOI: 10.1097/01.fpc.0000230416.82349.90
    route
    Oral
    tissue
    Plasma simvastatin lactone and active simvastatin acid

    OATP1B1 activity and statin exposure: the step between transporter inhibition and drug concentration (2026-09-22) · lines 57–66

    Original AI-assisted curation of four primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Three of the four share one research group and are recorded as one line of evidence. Study-specific citations, doses and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## slco1b1-c521cc-raises-simvastatin-acid-exposure Volunteers with the SLCO1B1 c.521CC genotype had 221 percent greater plasma exposure to active simvastatin acid than those with the c.521TT genotype. Model/species: 4 volunteers with c.521CC, 12 with c.521TC and 16 with c.521TT Tissue/system: Plasma simvastatin lactone and active simvastatin acid Exposure: Single 40 mg oral simvastatin dose Route: Oral Duration: Single dose with 12-hour sampling Limits: Peak concentration was 200 percent higher and occurred earlier in c.521CC carriers; the four-carrier group is small. Primary reference: SLCO1B1 polymorphism markedly affects the pharmacokinetics of simvastatin acid. (2006). https://pubmed.ncbi.nlm.nih.gov/17108811/ DOI: 10.1097/01.fpc.0000230416.82349.90 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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