Component

Cyclosporine metabolite AM9

Primary cyclosporine metabolite formed by both CYP3A4 and CYP3A5, and the only one human kidney microsomes produced.

2 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. CYP3A5 formed only AM9 from cyclosporine, not AM1 or AM4N, with substrate inhibition and an apparent Km of 11.3 micromolar.

    Human cytochrome P450 3A5 → Cyclosporine metabolite AM9 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
    Heterologously expressed human CYP3A5
    exposure
    Cyclosporin A
    limitations
    A narrower product range than CYP3A4 in the same comparison. Recorded as the enzyme raising one named metabolite, with the two metabolites it did not form recorded as a null in the companion claim.
    organism
    Heterologously expressed human CYP3A5
    plain_language
    CYP3A5 formed only AM9 from cyclosporine, not AM1 or AM4N, with substrate inhibition and an apparent Km of 11.3 micromolar.
    primary_references
    In vitro metabolism of cyclosporine A by human kidney CYP3A5. (2004). https://pubmed.ncbi.nlm.nih.gov/15450954/ DOI: 10.1016/j.bcp.2004.07.012
    route
    In vitro
    tissue
    Oxidative drug metabolism

    Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 190–190

    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 · Heterologously expressed human CYP3A5 · source_derived_draft · unverified_draft

    CYP3A5 formed only AM9 from cyclosporine, not AM1 or AM4N, with substrate inhibition and an apparent Km of 11.3 micromolar.
    Complete structured claim and evidence

  2. Microsomes from human kidney produced only AM9, and the rate of formation at 2 and 20 micromolar cyclosporine was positively associated with detectable CYP3A5 protein and with the CYP3A5*1 allele in 4 of the 20 kidneys tested.

    Human kidney microsomal CYP3A activity, twenty-donor panel → Cyclosporine metabolite AM9 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 kidney microsomes from twenty donors
    exposure
    Cyclosporin A at 2 and 20 micromolar
    limitations
    Four of twenty kidneys carried the allele, so the genotype comparison rests on a small group. Ketoconazole at 200 nanomolar inhibited renal AM9 formation by 22 to 55 per cent across 2 to 45 micromolar cyclosporine, which supports a CYP3A route without isolating CYP3A5 from CYP3A4 pharmacologically.
    organism
    Human kidney microsomes from twenty donors
    plain_language
    Microsomes from human kidney produced only AM9, and the rate of formation at 2 and 20 micromolar cyclosporine was positively associated with detectable CYP3A5 protein and with the CYP3A5*1 allele in 4 of the 20 kidneys tested.
    primary_references
    In vitro metabolism of cyclosporine A by human kidney CYP3A5. (2004). https://pubmed.ncbi.nlm.nih.gov/15450954/ DOI: 10.1016/j.bcp.2004.07.012
    route
    In vitro
    tissue
    Renal drug metabolism

    Cyclosporine: the complex that inhibits calcineurin, a second cyclophilin, and the transport step that decides exposure (2026-09-23) · lines 212–212

    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 kidney microsomes from twenty donors · source_derived_draft · unverified_draft

    Microsomes from human kidney produced only AM9, and the rate of formation at 2 and 20 micromolar cyclosporine was positively associated with detectable CYP3A5 protein and with the CYP3A5*1 allele in 4 of the 20 kidneys tested.
    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