Component

Clozapine N-oxide

Clozapine N-oxide. Species, exposure and limitations are retained in each linked claim.

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

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

Where it participates (unsigned role)

  1. CYP3A4 contributed to clozapine demethylation and N-oxidation.

    Human cytochrome P450 3A4 → Clozapine source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/9384460.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eb481193bb0d7564d728a25a9ddd63678e8234e628edca3f13ece910770279b6", "start_char": 0, "end_char": 1794, "text_sha256": "eb481193bb0d7564d728a25a9ddd63678e8234e628edca3f13ece910770279b6"}
    experimental_model
    Recombinant enzymes, antibodies and human liver microsomes
    exposure
    Enzyme-specific inhibition and metabolite formation
    limitations
    Identifies metabolic routes, not a trial of DIM with clozapine. Do not infer a dose change or magnitude of interaction.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human CYP enzymes
    plain_language
    Clozapine has more than one relevant route.
    primary_references
    [dim-p9384460] The involvement of CYP1A2 and CYP3A4 in the metabolism of clozapine. (1997). https://pubmed.ncbi.nlm.nih.gov/9384460/ DOI: 10.1046/j.1365-2125.1997.t01-1-00605.x
    tissue_or_cell_type
    Clozapine oxidation

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 675–686

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant enzymes, antibodies and human liver microsomes · source_derived_draft · unverified_draft

    ### dim-clozapine-3a4 CYP3A4 contributed to clozapine demethylation and N-oxidation. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Clozapine has more than one relevant route. organism: Human CYP enzymes tissue_or_cell_type: Clozapine oxidation experimental_model: Recombinant enzymes, antibodies and human liver microsomes limitations: Identifies metabolic routes, not a trial of DIM with clozapine. Do not infer a dose change or magnitude of interaction. exposure: Enzyme-specific inhibition and metabolite formation evidence_span: {"source_cache": "artifacts/dim-research/9384460.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eb481193bb0d7564d728a25a9ddd63678e8234e628edca3f13ece910770279b6", "start_char": 0, "end_char": 1794, "text_sha256": "eb481193bb0d7564d728a25a9ddd63678e8234e628edca3f13ece910770279b6"} [dim-p9384460] The involvement of CYP1A2 and CYP3A4 in the metabolism of clozapine. (1997). https://pubmed.ncbi.nlm.nih.gov/9384460/ DOI: 10.1046/j.1365-2125.1997.t01-1-00605.x
    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