Component

Sulfasalazine

Salicylazosulfapyridine, the drug tested against jejunal folate hydrolase.

6 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. Sulfasalazine competitively inhibited human jejunal brush-border folate hydrolase, with reported Ki 0.13 mM.

    Sulfasalazine → Human glutamate carboxypeptidase II / FOLH1 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Partially purified human jejunal brush-border enzyme
    exposure
    In-vitro inhibitor concentration series
    limitations
    Does not quantify clinical malabsorption or establish every drug mechanism.
    nutrient_topic
    Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
    organism
    Homo sapiens
    plain_language
    This drug can inhibit the folate digestion enzyme.
    primary_references
    [reisenauer1981] Human jejunal brush border folate conjugase. Characteristics and inhibition by salicylazosulfapyridine (1981). https://pubmed.ncbi.nlm.nih.gov/6113848/ DOI: 10.1016/0005-2744(81)90271-0
    tissue_or_cell_type
    Jejunal brush border

    Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 94–104

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Partially purified human jejunal brush-border enzyme · source_derived_draft · unverified_draft

    ### folate-sulfasalazine-conjugase-inhibition Sulfasalazine competitively inhibited human jejunal brush-border folate hydrolase, with reported Ki 0.13 mM. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: This drug can inhibit the folate digestion enzyme. organism: Homo sapiens tissue_or_cell_type: Jejunal brush border experimental_model: Partially purified human jejunal brush-border enzyme limitations: Does not quantify clinical malabsorption or establish every drug mechanism. exposure: In-vitro inhibitor concentration series [reisenauer1981] Human jejunal brush border folate conjugase. Characteristics and inhibition by salicylazosulfapyridine (1981). https://pubmed.ncbi.nlm.nih.gov/6113848/ DOI: 10.1016/0005-2744(81)90271-0
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Curcumin inhibited human BCRP-mediated sulfasalazine transport in vesicles, Ki 0.70 +/- 0.41 micromolar.

    Curcumin → Human ABCG2 / breast cancer resistance protein source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence

  2. Curcumin increased sulfasalazine AUC about eightfold in wild-type mice but not in Bcrp-null mice.

    Experimental mouse Abcg2 knockout → Mouse sulfasalazine plasma exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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
    Mus musculus
    plain_language
    Removing the transporter removed this interaction in the mouse experiment.
    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
    Plasma pharmacokinetics
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 814–825

    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-loss Curcumin increased sulfasalazine AUC about eightfold in wild-type mice but not in Bcrp-null mice. Condition category: machinery_impairment nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the transporter removed this interaction in the mouse experiment. organism: Mus musculus tissue_or_cell_type: Plasma pharmacokinetics 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
    Complete structured claim and evidence

  3. Sulfasalazine was transported by OATP2B1 in transfected cells, Km 1.7 +/- 0.3 micromolar.

    Human organic anion transporting polypeptide 2B1 / SLCO2B1 → Human transporter-mediated sulfasalazine uptake in vitro source_derived_draftungraded
    Experimental context and source evidence
    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
    An uptake transporter also affects the drug's handling.
    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 788–799

    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-oatp-uptake Sulfasalazine was transported by OATP2B1 in transfected cells, Km 1.7 +/- 0.3 micromolar. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An uptake transporter also affects the drug's handling. 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
    Complete structured claim and evidence

  4. Sulfasalazine AUC increased 2.0-fold at the microdose and 3.2-fold at the therapeutic dose.

    Curcumin → Human sulfasalazine plasma exposure source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence

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

    Tartrazine → Sulfasalazine permeability through human Caco-2 monolayers source_derived_draftungraded
    Experimental context and source evidence
    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.
    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