Component

Rifampicin

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

3 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

What it acts on

  1. The rifampicin treatment abolished the induced C-glucosyl-cleaving activity.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/16141538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88", "start_char": 0, "end_char": 1356, "text_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88"}
    experimental_model
    Isolated anaerobic human-fecal bacterium and cell-free extracts
    exposure
    Mangiferin culture exposure, with transcription/translation inhibitors
    limitations
    One isolate; activity identity unresolved; not a prediction of every human microbiome.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Bacteroides sp. MANG
    plain_language
    Conversion requires functioning bacterial gene-expression machinery.
    primary_references
    [mangiferin-p16141538] Isolation of a human intestinal bacterium that transforms mangiferin to norathyriol and inducibility of the enzyme that cleaves a C-glucosyl bond. (2005). https://pubmed.ncbi.nlm.nih.gov/16141538/ DOI: 10.1248/bpb.28.1672
    tissue_or_cell_type
    Bacterial culture
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 119–130

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated anaerobic human-fecal bacterium and cell-free extracts · source_derived_draft · unverified_draft

    ### mangiferin-rifampicin-cleavage The rifampicin treatment abolished the induced C-glucosyl-cleaving activity. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Conversion requires functioning bacterial gene-expression machinery. organism: Bacteroides sp. MANG tissue_or_cell_type: Bacterial culture experimental_model: Isolated anaerobic human-fecal bacterium and cell-free extracts limitations: One isolate; activity identity unresolved; not a prediction of every human microbiome. exposure: Mangiferin culture exposure, with transcription/translation inhibitors evidence_span: {"source_cache": "artifacts/mangiferin-research/16141538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88", "start_char": 0, "end_char": 1356, "text_sha256": "9bf5373ce89587337b6d0520b931f202d44771dba205220b8e340b9fa7446b88"} [mangiferin-p16141538] Isolation of a human intestinal bacterium that transforms mangiferin to norathyriol and inducibility of the enzyme that cleaves a C-glucosyl bond. (2005). https://pubmed.ncbi.nlm.nih.gov/16141538/ DOI: 10.1248/bpb.28.1672
    Complete structured claim and evidence
  2. A single intravenous dose of rifampicin increased the total plasma exposure of atorvastatin acid by 6.8-fold in healthy volunteers.

    Rifampicin → Plasma atorvastatin exposure source_derived_draftungraded
    Experimental context and source evidence
    duration
    Single dose, sampling to 24 hours
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    11 healthy human volunteers, randomised crossover
    exposure
    Two 40 mg oral atorvastatin doses one week apart, with one 30-minute intravenous infusion of 600 mg rifampicin on one of the two study days
    limitations
    Rifampicin is used here as a model hepatic uptake inhibitor and is not selective for OATP1B1; the lactone forms rose less than the acid, and a single intravenous dose avoids the enzyme induction that repeated oral rifampicin would cause.
    organism
    11 healthy human volunteers, randomised crossover
    plain_language
    A single intravenous dose of rifampicin increased the total plasma exposure of atorvastatin acid by 6.8-fold in healthy volunteers.
    primary_references
    The effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. (2007). https://pubmed.ncbi.nlm.nih.gov/17192770/ DOI: 10.1038/sj.clpt.6100038
    route
    Oral atorvastatin with intravenous rifampicin
    tissue
    Plasma atorvastatin acid and its hydroxy metabolites

    OATP1B1 activity and statin exposure: the step between transporter inhibition and drug concentration (2026-09-22) · lines 13–22

    Original AI-assisted curation of four primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Three of the four share one research group and are recorded as one line of evidence. Study-specific citations, doses and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## rifampicin-raises-atorvastatin-exposure A single intravenous dose of rifampicin increased the total plasma exposure of atorvastatin acid by 6.8-fold in healthy volunteers. Model/species: 11 healthy human volunteers, randomised crossover Tissue/system: Plasma atorvastatin acid and its hydroxy metabolites Exposure: Two 40 mg oral atorvastatin doses one week apart, with one 30-minute intravenous infusion of 600 mg rifampicin on one of the two study days Route: Oral atorvastatin with intravenous rifampicin Duration: Single dose, sampling to 24 hours Limits: Rifampicin is used here as a model hepatic uptake inhibitor and is not selective for OATP1B1; the lactone forms rose less than the acid, and a single intravenous dose avoids the enzyme induction that repeated oral rifampicin would cause. Primary reference: The effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. (2007). https://pubmed.ncbi.nlm.nih.gov/17192770/ DOI: 10.1038/sj.clpt.6100038 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. OATP1B1 activity lowers plasma atorvastatin exposure by carrying the drug from portal blood into the hepatocyte, so reducing that activity raises the plasma concentration.

    Human OATP1B1 / SLCO1B1 → Plasma atorvastatin exposure source_derived_draftungraded
    Experimental context and source evidence
    duration
    Single dose in both designs
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Healthy human volunteers, by pharmacological inhibition and by reduced-function genotype
    exposure
    Rifampicin inhibition in one study and the SLCO1B1 c.521CC genotype in another
    limitations
    This is the mechanistic reading shared by an inhibitor study and a genotype study rather than a single measurement of transporter activity against exposure; neither study measured OATP1B1 activity directly in the participants.
    organism
    Healthy human volunteers, by pharmacological inhibition and by reduced-function genotype
    plain_language
    OATP1B1 activity lowers plasma atorvastatin exposure by carrying the drug from portal blood into the hepatocyte, so reducing that activity raises the plasma concentration.
    primary_references
    The effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. (2007). https://pubmed.ncbi.nlm.nih.gov/17192770/ DOI: 10.1038/sj.clpt.6100038
    route
    Oral atorvastatin
    tissue
    Hepatic sinusoidal uptake and systemic plasma exposure

    OATP1B1 activity and statin exposure: the step between transporter inhibition and drug concentration (2026-09-22) · lines 24–33

    Original AI-assisted curation of four primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Three of the four share one research group and are recorded as one line of evidence. Study-specific citations, doses and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## oatp1b1-activity-lowers-atorvastatin-exposure OATP1B1 activity lowers plasma atorvastatin exposure by carrying the drug from portal blood into the hepatocyte, so reducing that activity raises the plasma concentration. Model/species: Healthy human volunteers, by pharmacological inhibition and by reduced-function genotype Tissue/system: Hepatic sinusoidal uptake and systemic plasma exposure Exposure: Rifampicin inhibition in one study and the SLCO1B1 c.521CC genotype in another Route: Oral atorvastatin Duration: Single dose in both designs Limits: This is the mechanistic reading shared by an inhibitor study and a genotype study rather than a single measurement of transporter activity against exposure; neither study measured OATP1B1 activity directly in the participants. Primary reference: The effect of OATP1B transporter inhibition on the pharmacokinetics of atorvastatin in healthy volunteers. (2007). https://pubmed.ncbi.nlm.nih.gov/17192770/ DOI: 10.1038/sj.clpt.6100038 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