Component

Fluvoxamine

Fluvoxamine. Species, exposure and limitations are retained in each linked claim.

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. Fluvoxamine increased oral duloxetine AUC by 460% and peak concentration by 141% in the clinical study.

    Fluvoxamine → Plasma duloxetine exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/18307373.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2705ee887855e9dbe738ece57d4ad9d4b3d8cc0d67de45e63c01497a4a215149", "start_char": 0, "end_char": 2879, "text_sha256": "2705ee887855e9dbe738ece57d4ad9d4b3d8cc0d67de45e63c01497a4a215149"}
    experimental_model
    Enzyme phenotyping and clinical drug-interaction studies
    exposure
    Fluvoxamine with oral or intravenous duloxetine
    limitations
    The clinical exposure change was caused by fluvoxamine, not DIM. The study tests inhibition, not the inverse size of induction.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human enzyme systems and healthy adults
    plain_language
    Blocking metabolism increased exposure; this measured result must not be relabeled as a DIM study.
    primary_references
    [dim-p18307373] In vitro and in vivo evaluations of cytochrome P450 1A2 interactions with duloxetine. (2008). https://pubmed.ncbi.nlm.nih.gov/18307373/ DOI: 10.2165/00003088-200847030-00005
    tissue_or_cell_type
    Duloxetine metabolism and exposure

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 805–816

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme phenotyping and clinical drug-interaction studies · source_derived_draft · unverified_draft

    ### dim-duloxetine-inhibition Fluvoxamine increased oral duloxetine AUC by 460% and peak concentration by 141% in the clinical study. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking metabolism increased exposure; this measured result must not be relabeled as a DIM study. organism: Human enzyme systems and healthy adults tissue_or_cell_type: Duloxetine metabolism and exposure experimental_model: Enzyme phenotyping and clinical drug-interaction studies limitations: The clinical exposure change was caused by fluvoxamine, not DIM. The study tests inhibition, not the inverse size of induction. exposure: Fluvoxamine with oral or intravenous duloxetine evidence_span: {"source_cache": "artifacts/dim-research/18307373.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2705ee887855e9dbe738ece57d4ad9d4b3d8cc0d67de45e63c01497a4a215149", "start_char": 0, "end_char": 2879, "text_sha256": "2705ee887855e9dbe738ece57d4ad9d4b3d8cc0d67de45e63c01497a4a215149"} [dim-p18307373] In vitro and in vivo evaluations of cytochrome P450 1A2 interactions with duloxetine. (2008). https://pubmed.ncbi.nlm.nih.gov/18307373/ DOI: 10.2165/00003088-200847030-00005
    Complete structured claim and evidence

  2. Fluvoxamine increased melatonin AUC about 17-fold and peak concentration about 12-fold on average.

    Fluvoxamine → Circulating melatonin exposure, route and timing specified source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/10668847.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f3c51771fcf28fd453299490bdedee5088501fb2447e3683edd68b93590d544", "start_char": 0, "end_char": 1563, "text_sha256": "0f3c51771fcf28fd453299490bdedee5088501fb2447e3683edd68b93590d544"}
    experimental_model
    Single-dose drug interaction study
    exposure
    5 mg melatonin with or without 50 mg fluvoxamine
    limitations
    Very small study; one CYP2D6 poor metabolizer affected fluvoxamine exposure. Increased melatonin exposure is consistent with inhibited elimination, not proof of increased pineal synthesis.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Five healthy male volunteers
    plain_language
    Slowing clearance can sharply raise exposure to an unchanged swallowed dose.
    primary_references
    [melatonin-p10668847] Increased bioavailability of oral melatonin after fluvoxamine coadministration. (2000). https://pubmed.ncbi.nlm.nih.gov/10668847/ DOI: 10.1067/mcp.2000.104071
    tissue_or_cell_type
    Oral melatonin pharmacokinetics

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 695–706

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-dose drug interaction study · source_derived_draft · unverified_draft

    ### melatonin-fluvoxamine-exposure Fluvoxamine increased melatonin AUC about 17-fold and peak concentration about 12-fold on average. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Slowing clearance can sharply raise exposure to an unchanged swallowed dose. organism: Five healthy male volunteers tissue_or_cell_type: Oral melatonin pharmacokinetics experimental_model: Single-dose drug interaction study limitations: Very small study; one CYP2D6 poor metabolizer affected fluvoxamine exposure. Increased melatonin exposure is consistent with inhibited elimination, not proof of increased pineal synthesis. exposure: 5 mg melatonin with or without 50 mg fluvoxamine evidence_span: {"source_cache": "artifacts/melatonin-research/10668847.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f3c51771fcf28fd453299490bdedee5088501fb2447e3683edd68b93590d544", "start_char": 0, "end_char": 1563, "text_sha256": "0f3c51771fcf28fd453299490bdedee5088501fb2447e3683edd68b93590d544"} [melatonin-p10668847] Increased bioavailability of oral melatonin after fluvoxamine coadministration. (2000). https://pubmed.ncbi.nlm.nih.gov/10668847/ DOI: 10.1067/mcp.2000.104071
    Complete structured claim and evidence

  3. In human liver microsomes, fluvoxamine inhibited caffeine demethylated-metabolite formation with Ki values of 0.08–0.28 micromolar.

    Fluvoxamine → Human cytochrome P450 1A2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human liver microsomes; metabolite HPLC.
    limitations
    Not all three demethylations are exclusively CYP1A2-dependent.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    An enzyme experiment supports the observed clearance interaction.
    primary_references
    Fluvoxamine is a potent inhibitor of the metabolism of caffeine in vitro. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9868741/ · DOI 10.1111/j.1600-0773.1998.tb01476.x

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 212–218

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver microsomes; metabolite HPLC. · source_derived_draft · unverified_draft

    ## caf-cyp1a2-inhibition An enzyme experiment supports the observed clearance interaction. In human liver microsomes, fluvoxamine inhibited caffeine demethylated-metabolite formation with Ki values of 0.08–0.28 micromolar. Model: Human liver microsomes; metabolite HPLC. Limitations: Not all three demethylations are exclusively CYP1A2-dependent. Evidence access: Primary abstract Fluvoxamine is a potent inhibitor of the metabolism of caffeine in vitro. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9868741/ · DOI 10.1111/j.1600-0773.1998.tb01476.x
    Complete structured claim and evidence

  4. Median caffeine clearance fell from 107 to 21 mL/min during fluvoxamine treatment.

    Fluvoxamine → Caffeine clearance source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers.
    limitations
    Study used 200 mg caffeine and repeated fluvoxamine; not a prediction of the same effect size for every CYP1A2 inhibitor.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    Inhibiting the metabolic pathway slowed caffeine removal.
    primary_references
    A fluvoxamine-caffeine interaction study. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8807660/ · DOI 10.1097/00008571-199606000-00003

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 196–202

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers. · source_derived_draft · unverified_draft

    ## caf-fluvox-clear Inhibiting the metabolic pathway slowed caffeine removal. Median caffeine clearance fell from 107 to 21 mL/min during fluvoxamine treatment. Model: Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers. Limitations: Study used 200 mg caffeine and repeated fluvoxamine; not a prediction of the same effect size for every CYP1A2 inhibitor. Evidence access: Primary abstract A fluvoxamine-caffeine interaction study. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8807660/ · DOI 10.1097/00008571-199606000-00003
    Complete structured claim and evidence

  5. Caffeine half-life increased from five to 31 hours in the fluvoxamine crossover experiment.

    Fluvoxamine → Caffeine elimination half-life source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers.
    limitations
    Reported median under this regimen, not a universal caffeine half-life.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    The same dose remained in the body much longer.
    primary_references
    A fluvoxamine-caffeine interaction study. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8807660/ · DOI 10.1097/00008571-199606000-00003

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 204–210

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers. · source_derived_draft · unverified_draft

    ## caf-fluvox-half The same dose remained in the body much longer. Caffeine half-life increased from five to 31 hours in the fluvoxamine crossover experiment. Model: Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers. Limitations: Reported median under this regimen, not a universal caffeine half-life. Evidence access: Primary abstract A fluvoxamine-caffeine interaction study. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8807660/ · DOI 10.1097/00008571-199606000-00003
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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