Component

CYP1A2 catalytic activity

CYP1A2 catalytic activity. Species, exposure and limitations are retained in each linked claim.

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 it acts on

  1. Caffeine-derived CYP1A2 indices correlated with clozapine clearance in the 14-person study.

    CYP1A2 catalytic activity → Plasma clozapine exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/7893591.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d568c4f2cdf1fc2d58f2ea22e395a7d7813cef2b1433fe25da51a2c40df5c545", "start_char": 0, "end_char": 849, "text_sha256": "d568c4f2cdf1fc2d58f2ea22e395a7d7813cef2b1433fe25da51a2c40df5c545"}
    experimental_model
    Clinical caffeine phenotyping and prior clozapine exposure
    exposure
    Caffeine test related to single-dose clozapine kinetics
    limitations
    Correlation supports enzyme relevance; no DIM administration or prediction of an individual clinical effect.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    14 healthy adults
    plain_language
    Enzyme activity was linked to drug handling in people, separately from any DIM exposure.
    primary_references
    [dim-p7893591] Clozapine disposition covaries with CYP1A2 activity determined by a caffeine test. (1994). https://pubmed.ncbi.nlm.nih.gov/7893591/ DOI: 10.1111/j.1365-2125.1994.tb04385.x
    tissue_or_cell_type
    CYP1A2 phenotype and clozapine disposition

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 688–699

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical caffeine phenotyping and prior clozapine exposure · source_derived_draft · unverified_draft

    ### dim-clozapine-phenotype Caffeine-derived CYP1A2 indices correlated with clozapine clearance in the 14-person study. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Enzyme activity was linked to drug handling in people, separately from any DIM exposure. organism: 14 healthy adults tissue_or_cell_type: CYP1A2 phenotype and clozapine disposition experimental_model: Clinical caffeine phenotyping and prior clozapine exposure limitations: Correlation supports enzyme relevance; no DIM administration or prediction of an individual clinical effect. exposure: Caffeine test related to single-dose clozapine kinetics evidence_span: {"source_cache": "artifacts/dim-research/7893591.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d568c4f2cdf1fc2d58f2ea22e395a7d7813cef2b1433fe25da51a2c40df5c545", "start_char": 0, "end_char": 849, "text_sha256": "d568c4f2cdf1fc2d58f2ea22e395a7d7813cef2b1433fe25da51a2c40df5c545"} [dim-p7893591] Clozapine disposition covaries with CYP1A2 activity determined by a caffeine test. (1994). https://pubmed.ncbi.nlm.nih.gov/7893591/ DOI: 10.1111/j.1365-2125.1994.tb04385.x
    Complete structured claim and evidence

What acts on it

  1. Added FMN restored CYP1A2 ethoxyresorufin activity in POR Y181D membranes to 37% of the wild-type system.

    Flavin mononucleotide → CYP1A2 catalytic activity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/dim-research/19884324.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f702cc9af1528241d8572b8bcafc23dacb5ed3cacf6bb77403e8aa40d21a214", "start_char": 0, "end_char": 1738, "text_sha256": "3f702cc9af1528241d8572b8bcafc23dacb5ed3cacf6bb77403e8aa40d21a214"}
    experimental_model
    Recombinant protein and engineered bacterial coexpression
    exposure
    POR mutation and added FMN
    limitations
    In-vitro rescue of one mutant; not a dietary-riboflavin deficiency experiment or evidence that FMN reverses a DIM-drug interaction.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human POR Y181D and human CYP1A2 in engineered systems
    plain_language
    A specific cofactor-binding defect could be partly rescued in the assay.
    primary_references
    [dim-p19884324] Human cytochrome P450 oxidoreductase deficiency caused by the Y181D mutation: molecular consequences and rescue of defect. (2010). https://pubmed.ncbi.nlm.nih.gov/19884324/ DOI: 10.1124/dmd.109.030445
    tissue_or_cell_type
    FMN-dependent electron transfer
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 285–296

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant protein and engineered bacterial coexpression · source_derived_draft · unverified_draft

    ### dim-por-fmn-rescue Added FMN restored CYP1A2 ethoxyresorufin activity in POR Y181D membranes to 37% of the wild-type system. Condition category: machinery_impairment nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A specific cofactor-binding defect could be partly rescued in the assay. organism: Human POR Y181D and human CYP1A2 in engineered systems tissue_or_cell_type: FMN-dependent electron transfer experimental_model: Recombinant protein and engineered bacterial coexpression limitations: In-vitro rescue of one mutant; not a dietary-riboflavin deficiency experiment or evidence that FMN reverses a DIM-drug interaction. exposure: POR mutation and added FMN evidence_span: {"source_cache": "artifacts/dim-research/19884324.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f702cc9af1528241d8572b8bcafc23dacb5ed3cacf6bb77403e8aa40d21a214", "start_char": 0, "end_char": 1738, "text_sha256": "3f702cc9af1528241d8572b8bcafc23dacb5ed3cacf6bb77403e8aa40d21a214"} [dim-p19884324] Human cytochrome P450 oxidoreductase deficiency caused by the Y181D mutation: molecular consequences and rescue of defect. (2010). https://pubmed.ncbi.nlm.nih.gov/19884324/ DOI: 10.1124/dmd.109.030445
    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