Component

SLCO1B1 c.521T>C reduced-function variant

Coding variant p.V174A, rs4149056, which decreases OATP1B1 transporting activity. Kept separate from the rs4363657 association signal until the ledger resolves whether they are one factor.

5 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. 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

  2. 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

  3. 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

Where it participates (unsigned role)

  1. 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

  2. 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

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.

    Evidence, AI assistance and curation standards