Component

Cerivastatin

Statin withdrawn after rhabdomyolysis reports, used here for the size of its gemfibrozil interaction.

4 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 acts on it

  1. Cyclosporin A inhibited the in vitro metabolism of labelled cerivastatin only at concentrations above 30 micromolar, two orders of magnitude above the concentrations that inhibited its transport.

    Cyclosporine → Cerivastatin 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
    In vitro cerivastatin metabolism
    exposure
    Cyclosporin A
    limitations
    Recorded as the measured null that separates the two candidate mechanisms for this interaction. The authors conclude the interaction is mainly transporter inhibition, which is an interpretation of these two numbers rather than a separate measurement.
    organism
    In vitro cerivastatin metabolism
    plain_language
    Cyclosporin A inhibited the in vitro metabolism of labelled cerivastatin only at concentrations above 30 micromolar, two orders of magnitude above the concentrations that inhibited its transport.
    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
    Drug metabolism

    Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 168–168

    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 · In vitro cerivastatin metabolism · source_derived_draft · unverified_draft

    Cyclosporin A inhibited the in vitro metabolism of labelled cerivastatin only at concentrations above 30 micromolar, two orders of magnitude above the concentrations that inhibited its transport.
    Complete structured claim and evidence

  2. Uptake of labelled cerivastatin into human hepatocytes from three donors was inhibited by cyclosporin A with Ki values of 0.3 to 0.7 micromolar, against Km values for the uptake itself of 3 to 18 micromolar, so more than 70 per cent of total uptake at therapeutic concentrations was carrier-mediated.

    Cyclosporine → Cerivastatin 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 hepatocytes from three donors
    exposure
    Cyclosporin A
    limitations
    The pool that falls is the hepatocyte interior. Plasma exposure is expected to move the other way and was not measured here. Three donors is a small panel for a kinetic range.
    organism
    Human hepatocytes from three donors
    plain_language
    Uptake of labelled cerivastatin into human hepatocytes from three donors was inhibited by cyclosporin A with Ki values of 0.3 to 0.7 micromolar, against Km values for the uptake itself of 3 to 18 micromolar, so more than 70 per cent of total uptake at therapeutic concentrations was carrier-mediated.
    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
    Hepatocyte interior

    Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 157–157

    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 hepatocytes from three donors · source_derived_draft · unverified_draft

    Uptake of labelled cerivastatin into human hepatocytes from three donors was inhibited by cyclosporin A with Ki values of 0.3 to 0.7 micromolar, against Km values for the uptake itself of 3 to 18 micromolar, so more than 70 per cent of total uptake at therapeutic concentrations was carrier-mediated.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Concomitant use of gemfibrozil with statins, and particularly with cerivastatin, increases the risk of rhabdomyolysis, and this study was undertaken because the mechanism of that potentially fatal interaction was unclear.

    Plasma cerivastatin exposure → 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
    Stated as the background to a 10-volunteer pharmacokinetic study
    exposure
    Gemfibrozil with cerivastatin
    limitations
    This is the study's framing of an established clinical association rather than a measurement made in it; no muscle outcome was recorded in the ten volunteers.
    organism
    Stated as the background to a 10-volunteer pharmacokinetic study
    plain_language
    Concomitant use of gemfibrozil with statins, and particularly with cerivastatin, increases the risk of rhabdomyolysis, and this study was undertaken because the mechanism of that potentially fatal interaction was unclear.
    primary_references
    Gemfibrozil greatly increases plasma concentrations of cerivastatin. (2002). https://pubmed.ncbi.nlm.nih.gov/12496749/ DOI: 10.1067/mcp.2002.128469
    route
    Oral
    tissue
    Skeletal muscle injury risk during combined treatment

    Statin plasma exposure and muscle injury: dose randomisation and a drug interaction (2026-09-22) · lines 57–66

    Original AI-assisted curation of three primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Two share a research group with the OATP1B1 collection and are recorded as one line of evidence with it. Study-specific doses, effect sizes and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## cerivastatin-exposure-and-rhabdomyolysis-risk Concomitant use of gemfibrozil with statins, and particularly with cerivastatin, increases the risk of rhabdomyolysis, and this study was undertaken because the mechanism of that potentially fatal interaction was unclear. Model/species: Stated as the background to a 10-volunteer pharmacokinetic study Tissue/system: Skeletal muscle injury risk during combined treatment Exposure: Gemfibrozil with cerivastatin Route: Oral Duration: Not applicable Limits: This is the study's framing of an established clinical association rather than a measurement made in it; no muscle outcome was recorded in the ten volunteers. Primary reference: Gemfibrozil greatly increases plasma concentrations of cerivastatin. (2002). https://pubmed.ncbi.nlm.nih.gov/12496749/ DOI: 10.1067/mcp.2002.128469 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. Gemfibrozil raised the plasma exposure of cerivastatin to 559 percent of control, with a range across subjects of 138 to 995 percent.

    Gemfibrozil → Plasma cerivastatin exposure source_derived_draftungraded
    Experimental context and source evidence
    duration
    3 days of gemfibrozil, 24 hours of sampling
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    10 healthy volunteers, randomised double-blind crossover
    exposure
    Gemfibrozil 600 mg twice daily for 3 days, then a single 0.3 mg cerivastatin dose
    limitations
    Metabolite M-23 exposure fell to 22 percent of control while the parent and other metabolites rose, so the interaction shifts the metabolic route rather than simply slowing clearance. Between-subject variation was wide.
    organism
    10 healthy volunteers, randomised double-blind crossover
    plain_language
    Gemfibrozil raised the plasma exposure of cerivastatin to 559 percent of control, with a range across subjects of 138 to 995 percent.
    primary_references
    Gemfibrozil greatly increases plasma concentrations of cerivastatin. (2002). https://pubmed.ncbi.nlm.nih.gov/12496749/ DOI: 10.1067/mcp.2002.128469
    route
    Oral
    tissue
    Plasma cerivastatin, cerivastatin lactone and its metabolites

    Statin plasma exposure and muscle injury: dose randomisation and a drug interaction (2026-09-22) · lines 46–55

    Original AI-assisted curation of three primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Two share a research group with the OATP1B1 collection and are recorded as one line of evidence with it. Study-specific doses, effect sizes and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## gemfibrozil-raises-cerivastatin-exposure Gemfibrozil raised the plasma exposure of cerivastatin to 559 percent of control, with a range across subjects of 138 to 995 percent. Model/species: 10 healthy volunteers, randomised double-blind crossover Tissue/system: Plasma cerivastatin, cerivastatin lactone and its metabolites Exposure: Gemfibrozil 600 mg twice daily for 3 days, then a single 0.3 mg cerivastatin dose Route: Oral Duration: 3 days of gemfibrozil, 24 hours of sampling Limits: Metabolite M-23 exposure fell to 22 percent of control while the parent and other metabolites rose, so the interaction shifts the metabolic route rather than simply slowing clearance. Between-subject variation was wide. Primary reference: Gemfibrozil greatly increases plasma concentrations of cerivastatin. (2002). https://pubmed.ncbi.nlm.nih.gov/12496749/ DOI: 10.1067/mcp.2002.128469 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