Component

Peroxisomal fatty acyl-CoA beta-oxidase activity

Peroxisomal fatty acyl-CoA beta-oxidase activity. Species, exposure and limitations are retained in each linked claim.

1 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

Where it participates (unsigned role)

  1. Each drug tested produced concentration-dependent activation of peroxisome proliferator-activated receptor alpha and gamma isoforms and of peroxisomal fatty acyl-CoA beta-oxidase activity, with a rank order of stereoselectivity for alpha activation and fatty acyl oxidase stimulation of S(+)-ibuprofen greater than R(-)-ibuprofen, S(+)-ibuprofen being more potent than indomethacin and naproxen on these parameters, while on gamma the order was S(+)-naproxen greater than indomethacin greater than S(+)-ibuprofen greater than R(-)-ibuprofen.

    S(+)-ibuprofen → Human PPAR alpha / PPARA source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/11755111.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1dd77f4a1eebd7777285c424b1731f4744d0fa593e62cfbde0a92dbb6242b239", "start_char": 0, "end_char": 2074, "text_sha256": "1dd77f4a1eebd7777285c424b1731f4744d0fa593e62cfbde0a92dbb6242b239"}
    experimental_model
    Reporter and enzyme assays comparing ibuprofen isomers against naproxen and indomethacin across four readouts
    exposure
    S(+)- and R(-)-ibuprofen compared directly on cyclooxygenase-1 and -2, platelet function and nuclear receptor activation
    limitations
    The only record here that measures both enantiomers on the same panel, which is what makes the fold-differences meaningful. Several different assay systems are combined.
    nutrient_topic
    Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
    organism
    Rat, human and sheep systems
    plain_language
    Both hands switch on the fat-handling nuclear receptors, with a much smaller gap between them than at cyclooxygenase.
    primary_references
    [ibu-p11755111] Activation of peroxisome proliferator-activated receptor isoforms and inhibition of prostaglandin H(2) synthases by ibuprofen, naproxen, and indomethacin. (2001). https://pubmed.ncbi.nlm.nih.gov/11755111/ DOI: 10.1016/s0006-2952(01)00822-x
    tissue_or_cell_type
    Transfected cells, hepatoma cells, platelets and purified enzyme

    Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 331–342

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reporter and enzyme assays comparing ibuprofen isomers against naproxen and indomethacin across four readouts · source_derived_draft · unverified_draft

    ### ibu-both-isomers-hit-ppar Each drug tested produced concentration-dependent activation of peroxisome proliferator-activated receptor alpha and gamma isoforms and of peroxisomal fatty acyl-CoA beta-oxidase activity, with a rank order of stereoselectivity for alpha activation and fatty acyl oxidase stimulation of S(+)-ibuprofen greater than R(-)-ibuprofen, S(+)-ibuprofen being more potent than indomethacin and naproxen on these parameters, while on gamma the order was S(+)-naproxen greater than indomethacin greater than S(+)-ibuprofen greater than R(-)-ibuprofen. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: Both hands switch on the fat-handling nuclear receptors, with a much smaller gap between them than at cyclooxygenase. organism: Rat, human and sheep systems tissue_or_cell_type: Transfected cells, hepatoma cells, platelets and purified enzyme experimental_model: Reporter and enzyme assays comparing ibuprofen isomers against naproxen and indomethacin across four readouts limitations: The only record here that measures both enantiomers on the same panel, which is what makes the fold-differences meaningful. Several different assay systems are combined. exposure: S(+)- and R(-)-ibuprofen compared directly on cyclooxygenase-1 and -2, platelet function and nuclear receptor activation evidence_span: {"source_cache": "artifacts/ibuprofen-research/11755111.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1dd77f4a1eebd7777285c424b1731f4744d0fa593e62cfbde0a92dbb6242b239", "start_char": 0, "end_char": 2074, "text_sha256": "1dd77f4a1eebd7777285c424b1731f4744d0fa593e62cfbde0a92dbb6242b239"} [ibu-p11755111] Activation of peroxisome proliferator-activated receptor isoforms and inhibition of prostaglandin H(2) synthases by ibuprofen, naproxen, and indomethacin. (2001). https://pubmed.ncbi.nlm.nih.gov/11755111/ DOI: 10.1016/s0006-2952(01)00822-x
    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