Human ABCG2 / breast cancer resistance protein

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

UGT1A9-expressing human HeLa cells.

limitations

Pharmacological inhibition; diglucuronide compensation was proposed, not proven in patients.

nutrient_topic

Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone

plain_language

Blocking export changes where metabolites accumulate.

primary_references

Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

trigger_kind

machinery_impairment Imported condition classification; unverified.

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 84–90

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · UGT1A9-expressing human HeLa cells. · source_derived_draft · unverified_draft

## luteolin-abcg2-blockade Blocking export changes where metabolites accumulate. Ko143 inhibition of ABCG2 reduced luteolin-monoglucuronide efflux and increased intracellular retention. Model: UGT1A9-expressing human HeLa cells. Limitations: Pharmacological inhibition; diglucuronide compensation was proposed, not proven in patients. Evidence access: Primary abstract Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0

evidence_span

{"source_cache": "artifacts/curcumin-research/22300367.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe", "start_char": 0, "end_char": 1713, "text_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe"}

experimental_model

Human pharmacokinetics, transporter vesicles and mouse knockout experiment

exposure

Human: curcumin 2 g before sulfasalazine 100 micrograms or 2 g; eight participants. Mouse: 300-400 mg/kg curcumin

limitations

Small dose- and formulation-specific drug study. Transporter inference is supported by separate assays, not a universal effect on every BCRP substrate.

nutrient_topic

Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin

organism

Human transporter/human participants; mouse claims separately scoped

plain_language

A drug-export transporter can be inhibited in the test system.

primary_references

[curcumin-p22300367] Pharmacokinetic interaction study of sulphasalazine in healthy subjects and the impact of curcumin as an in vivo inhibitor of BCRP. (2012). https://pubmed.ncbi.nlm.nih.gov/22300367/ DOI: 10.1111/j.1476-5381.2012.01887.x

tissue_or_cell_type

Intestinal drug transport and plasma

Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 775–786

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pharmacokinetics, transporter vesicles and mouse knockout experiment · source_derived_draft · unverified_draft

### curcumin-bcrp-inhibition Curcumin inhibited human BCRP-mediated sulfasalazine transport in vesicles, Ki 0.70 +/- 0.41 micromolar. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A drug-export transporter can be inhibited in the test system. organism: Human transporter/human participants; mouse claims separately scoped tissue_or_cell_type: Intestinal drug transport and plasma experimental_model: Human pharmacokinetics, transporter vesicles and mouse knockout experiment limitations: Small dose- and formulation-specific drug study. Transporter inference is supported by separate assays, not a universal effect on every BCRP substrate. exposure: Human: curcumin 2 g before sulfasalazine 100 micrograms or 2 g; eight participants. Mouse: 300-400 mg/kg curcumin evidence_span: {"source_cache": "artifacts/curcumin-research/22300367.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe", "start_char": 0, "end_char": 1713, "text_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe"} [curcumin-p22300367] Pharmacokinetic interaction study of sulphasalazine in healthy subjects and the impact of curcumin as an in vivo inhibitor of BCRP. (2012). https://pubmed.ncbi.nlm.nih.gov/22300367/ DOI: 10.1111/j.1476-5381.2012.01887.x

dose

Food-additive screen at 50 micromolar; concentration-response experiments

duration

Exact incubation interval not recovered from accessed primary material

evidence_access

Primary PubMed abstract and publisher supplementary screening table; assay detail gaps retained.

evidence_scope

literature_reviewed; source-specific experimental curation

experimental_model

Human ABCG2 / BCRP transporter in membrane-vesicle assay

limitations

Primary abstract and publisher supplementary screening table inspected; no unverified IC50 assigned. Vesicle inhibition does not establish increased drug absorption, vitamin depletion or inhibition of every ABC transporter.

nutrient_topic

Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine

organism

Human ABCG2 / BCRP transporter in membrane-vesicle assay

plain_language

Tartrazine inhibited human BCRP-mediated probe transport in the membrane-vesicle screen.

primary_references

Interaction of Food Additives with Intestinal Efflux Transporters. (2017). https://pubmed.ncbi.nlm.nih.gov/28921988/ DOI: 10.1021/acs.molpharmaceut.7b00563

route

In vitro exposure to membrane vesicles

tissue

Probe-substrate efflux

Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 215–224

Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human ABCG2 / BCRP transporter in membrane-vesicle assay · source_derived_draft · unverified_draft

## tartrazine-bcrp-inhibition Tartrazine inhibited human BCRP-mediated probe transport in the membrane-vesicle screen. Model/species: Human ABCG2 / BCRP transporter in membrane-vesicle assay Tissue: Probe-substrate efflux Exposure: Food-additive screen at 50 micromolar; concentration-response experiments Route: In vitro exposure to membrane vesicles Duration: Exact incubation interval not recovered from accessed primary material Limits: Primary abstract and publisher supplementary screening table inspected; no unverified IC50 assigned. Vesicle inhibition does not establish increased drug absorption, vitamin depletion or inhibition of every ABC transporter. Primary reference: Interaction of Food Additives with Intestinal Efflux Transporters. (2017). https://pubmed.ncbi.nlm.nih.gov/28921988/ DOI: 10.1021/acs.molpharmaceut.7b00563 Access: Primary PubMed abstract and publisher supplementary screening table; assay detail gaps retained.

evidence_span

{"source_cache": "artifacts/curcumin-research/22300367.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe", "start_char": 0, "end_char": 1713, "text_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe"}

experimental_model

Human pharmacokinetics, transporter vesicles and mouse knockout experiment

exposure

Human: curcumin 2 g before sulfasalazine 100 micrograms or 2 g; eight participants. Mouse: 300-400 mg/kg curcumin

limitations

Small dose- and formulation-specific drug study. Transporter inference is supported by separate assays, not a universal effect on every BCRP substrate.

nutrient_topic

Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin

organism

Human transporter/human participants; mouse claims separately scoped

plain_language

The human experiment measured more sulfasalazine in blood.

primary_references

[curcumin-p22300367] Pharmacokinetic interaction study of sulphasalazine in healthy subjects and the impact of curcumin as an in vivo inhibitor of BCRP. (2012). https://pubmed.ncbi.nlm.nih.gov/22300367/ DOI: 10.1111/j.1476-5381.2012.01887.x

tissue_or_cell_type

Intestinal drug transport and plasma

Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 801–812

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pharmacokinetics, transporter vesicles and mouse knockout experiment · source_derived_draft · unverified_draft

### curcumin-sulfasalazine-exposure Sulfasalazine AUC increased 2.0-fold at the microdose and 3.2-fold at the therapeutic dose. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The human experiment measured more sulfasalazine in blood. organism: Human transporter/human participants; mouse claims separately scoped tissue_or_cell_type: Intestinal drug transport and plasma experimental_model: Human pharmacokinetics, transporter vesicles and mouse knockout experiment limitations: Small dose- and formulation-specific drug study. Transporter inference is supported by separate assays, not a universal effect on every BCRP substrate. exposure: Human: curcumin 2 g before sulfasalazine 100 micrograms or 2 g; eight participants. Mouse: 300-400 mg/kg curcumin evidence_span: {"source_cache": "artifacts/curcumin-research/22300367.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe", "start_char": 0, "end_char": 1713, "text_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe"} [curcumin-p22300367] Pharmacokinetic interaction study of sulphasalazine in healthy subjects and the impact of curcumin as an in vivo inhibitor of BCRP. (2012). https://pubmed.ncbi.nlm.nih.gov/22300367/ DOI: 10.1111/j.1476-5381.2012.01887.x

dose

Tartrazine 200 micromolar apically with sulfasalazine 500 micromolar; Ko-143 comparator

duration

Samples at 20, 40, 60, 90 and 120 min

evidence_access

Primary full-text methods/results and metadata.

evidence_scope

literature_reviewed; source-specific experimental curation

experimental_model

Human Caco-2 intestinal monolayers

limitations

Cell-monolayer null result is not a clinical drug-interaction trial; transporter accessibility can differ from inside-out vesicles. Bilateral addition also had a limited effect, at most twofold.

nutrient_topic

Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine

organism

Human Caco-2 intestinal monolayers

plain_language

Apically applied tartrazine did not change sulfasalazine permeability through Caco-2 monolayers.

primary_references

Food Additives Inhibit Intestinal Drug Transporters but Have Limited Effect on In Vitro Drug Permeability. (2025). https://pubmed.ncbi.nlm.nih.gov/40773056/ DOI: 10.1021/acs.molpharmaceut.5c00705

route

In vitro apical addition

tissue

Transepithelial drug transport

Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 248–257

Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human Caco-2 intestinal monolayers · source_derived_draft · unverified_draft

## tartrazine-sulfasalazine-null Apically applied tartrazine did not change sulfasalazine permeability through Caco-2 monolayers. Model/species: Human Caco-2 intestinal monolayers Tissue: Transepithelial drug transport Exposure: Tartrazine 200 micromolar apically with sulfasalazine 500 micromolar; Ko-143 comparator Route: In vitro apical addition Duration: Samples at 20, 40, 60, 90 and 120 min Limits: Cell-monolayer null result is not a clinical drug-interaction trial; transporter accessibility can differ from inside-out vesicles. Bilateral addition also had a limited effect, at most twofold. Primary reference: Food Additives Inhibit Intestinal Drug Transporters but Have Limited Effect on In Vitro Drug Permeability. (2025). https://pubmed.ncbi.nlm.nih.gov/40773056/ DOI: 10.1021/acs.molpharmaceut.5c00705 Access: Primary full-text methods/results and metadata.

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/mebendazole-research/25862759.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3", "start_char": 0, "end_char": 1682, "text_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3"}

experimental_model

Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics

exposure

Polymorphs A, B and C, alone and with the transporter inhibitor elacridar

limitations

Carries the polymorph distinction across from the anthelmintic use into the oncology use and finds it decides brain exposure. Mouse models, and elacridar is an experimental tool rather than a co-therapy.

nutrient_topic

Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole

organism

Mouse

plain_language

The same crystal form that works against worms is the one that gets into the brain; the inert form stays out of the blood entirely.

primary_references

[mbz-p25862759] Brain Penetration and Efficacy of Different Mebendazole Polymorphs in a Mouse Brain Tumor Model. (2015). https://pubmed.ncbi.nlm.nih.gov/25862759/ DOI: 10.1158/1078-0432.ccr-14-2681

tissue_or_cell_type

Brain and plasma

trigger_kind

biomarker_context Imported condition classification; unverified.

Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 524–535

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics · source_derived_draft · unverified_draft

### mbz-polymorph-decides-brain-levels Polymorph B and polymorph C both increased survival in a GL261 glioma model with B exhibiting greater toxicity, polymorph A showed no benefit, B and C both reached brain concentrations exceeding the GL261 half-maximal inhibitory concentration 29-fold, polymorph C demonstrated a 24-hour brain-to-plasma area-under-curve ratio of 0.82 while B showed higher plasma exposure and a lower ratio, polymorph A presented markedly lower levels in both plasma and brain, and combination with elacridar significantly improved the efficacy of polymorph C in glioma and medulloblastoma models. Condition category: biomarker_context nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: The same crystal form that works against worms is the one that gets into the brain; the inert form stays out of the blood entirely. organism: Mouse tissue_or_cell_type: Brain and plasma experimental_model: Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics limitations: Carries the polymorph distinction across from the anthelmintic use into the oncology use and finds it decides brain exposure. Mouse models, and elacridar is an experimental tool rather than a co-therapy. exposure: Polymorphs A, B and C, alone and with the transporter inhibitor elacridar evidence_span: {"source_cache": "artifacts/mebendazole-research/25862759.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3", "start_char": 0, "end_char": 1682, "text_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3"} [mbz-p25862759] Brain Penetration and Efficacy of Different Mebendazole Polymorphs in a Mouse Brain Tumor Model. (2015). https://pubmed.ncbi.nlm.nih.gov/25862759/ DOI: 10.1158/1078-0432.ccr-14-2681