Component

Metabolism of anandamide by amidohydrolase

Metabolism of anandamide by amidohydrolase. 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

What acts on it

  1. The time-dependent reduction in potency of anandamide toward inhibition of cannabinoid agonist binding in rat cerebellar membranes was blocked by ibuprofen but not by acetylsalicylic acid, sulindac, acetaminophen or to any significant extent by ketoprofen and naproxen, a direct assay of anandamide amidase gave a half-maximal inhibitory concentration for ibuprofen of approximately 400 micromolar, and that potency was of the same order as required for inhibition of cyclooxygenase-2 in cell-free systems and as the peak plasma concentrations following a two times 200 milligram dose regimen, so following therapeutic doses the metabolism of anandamide may be affected.

    Ibuprofen → Metabolism of anandamide by amidohydrolase source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/9060042.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543", "start_char": 0, "end_char": 1394, "text_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543"}
    experimental_model
    Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay
    exposure
    Ibuprofen compared against acetylsalicylic acid, sulindac, acetaminophen, ketoprofen and naproxen
    limitations
    The comparator set is what distinguishes this from a class effect: five other drugs failed. The concentration required is high, and the authors relate it to peak plasma levels rather than measuring them.
    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
    plain_language
    Ibuprofen, and not the other painkillers tested, slows the destruction of the body’s own cannabis-like signal.
    primary_references
    [ibu-p9060042] Ibuprofen inhibits the metabolism of the endogenous cannabimimetic agent anandamide. (1997). https://pubmed.ncbi.nlm.nih.gov/9060042/ DOI: 10.1111/j.1600-0773.1997.tb00291.x
    tissue_or_cell_type
    Cerebellar membranes

    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 448–459

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay · source_derived_draft · unverified_draft

    ### ibu-blocks-anandamide-breakdown The time-dependent reduction in potency of anandamide toward inhibition of cannabinoid agonist binding in rat cerebellar membranes was blocked by ibuprofen but not by acetylsalicylic acid, sulindac, acetaminophen or to any significant extent by ketoprofen and naproxen, a direct assay of anandamide amidase gave a half-maximal inhibitory concentration for ibuprofen of approximately 400 micromolar, and that potency was of the same order as required for inhibition of cyclooxygenase-2 in cell-free systems and as the peak plasma concentrations following a two times 200 milligram dose regimen, so following therapeutic doses the metabolism of anandamide may be affected. 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: Ibuprofen, and not the other painkillers tested, slows the destruction of the body’s own cannabis-like signal. organism: Rat tissue_or_cell_type: Cerebellar membranes experimental_model: Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay limitations: The comparator set is what distinguishes this from a class effect: five other drugs failed. The concentration required is high, and the authors relate it to peak plasma levels rather than measuring them. exposure: Ibuprofen compared against acetylsalicylic acid, sulindac, acetaminophen, ketoprofen and naproxen evidence_span: {"source_cache": "artifacts/ibuprofen-research/9060042.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543", "start_char": 0, "end_char": 1394, "text_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543"} [ibu-p9060042] Ibuprofen inhibits the metabolism of the endogenous cannabimimetic agent anandamide. (1997). https://pubmed.ncbi.nlm.nih.gov/9060042/ DOI: 10.1111/j.1600-0773.1997.tb00291.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