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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
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 evidenceA single intravenous dose of rifampicin increased the total plasma exposure of atorvastatin acid by 6.8-fold in healthy volunteers.
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)
OATP1B1 activity lowers plasma atorvastatin exposure by carrying the drug from portal blood into the hepatocyte, so reducing that activity raises the plasma concentration.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.