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Phase II drug-metabolising enzymes are principally *transferases* that catalyze conjugation reactions—such as glucuronidation, sulfation, acetylation, glutathione conjugation, and methylation—of both endogenous substrates and xenobiotics. The resulting conjugated products are typically less active and more hydrophilic, aiding rapid elimination via urine or feces. Critical Phase II enzymes include UDP-glucuronosyltransferases, sulfotransferases, N-acetyltransferases, glutathione S-transferases, and several methyltransferases. Genetic polymorphisms in these enzymes contribute to interindividual and interspecies differences in drug response and toxicity. These enzymes are central to pharmacogenomics, and alterations in their activity can be linked to cancer risk and adverse drug reactions
Drugs may act as substrates, inhibitors, or inducers of Phase II enzymes, modifying drug clearance, toxicity, and efficacy
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