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Polymorphically acetylated aminoglutethimide in humans

R C Coombes, A B Foster, S J Harland

    British Journal of Cancer
    |September 1, 1982
    PubMed
    Summary
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    Slow acetylators excrete more aminoglutethimide (AG), while fast acetylators excrete more of its metabolite, N-acetylAG. This indicates that AG undergoes polymorphic acetylation in humans.

    Area of Science:

    • Pharmacology
    • Biochemistry
    • Human Metabolism

    Background:

    • Aminoglutethimide (AG) is a drug known to be metabolized in humans.
    • Individual differences in drug metabolism can significantly impact therapeutic efficacy and toxicity.
    • Acetylator phenotype, determined by N-acetyltransferase enzymes, is a key factor in drug metabolism variability.

    Purpose of the Study:

    • To investigate the urinary excretion of aminoglutethimide (AG) and its metabolites in relation to acetylator phenotype.
    • To determine if AG undergoes polymorphic acetylation in humans.

    Main Methods:

    • 10 healthy volunteers were phenotyped as fast or slow acetylators using sulphadimidine.
    • Urinary excretion of AG, N-acetylAG, N-formylAG, and nitroG was measured over 24 hours after AG administration.

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    Main Results:

    • Slow acetylators excreted a higher percentage of AG (28%) compared to fast acetylators (12%).
    • Fast acetylators excreted more N-acetylAG (8.8%) than slow acetylators (3.9%).
    • NitroG and N-formylAG were minor metabolites, with nitroG showing higher excretion in slow acetylators.

    Conclusions:

    • Aminoglutethimide (AG) is subject to polymorphic acetylation in humans.
    • Acetylator phenotype influences the metabolic profile of AG, affecting the relative excretion of the parent drug and its major metabolite.