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Cytochrome P450 family members such as **cytochrome P450 3A4** and **cytochrome P450 2C9**, along with the **UDP-glucuronosyltransferase** family and other hepatic phase I/II metabolic enzymes, play central roles in the biotransformation of both exogenous substances—including most clinically used drugs—and endogenous compounds. These liver-expressed proteins catalyze oxidation/reduction reactions (*phase I*, mainly via cytochromes) or conjugation reactions (*phase II*, mainly via UGTs), facilitating detoxification and elimination from the body. Genetic variation among individuals leads to substantial differences in enzyme activity that impact efficacy/toxicity profiles across populations. These pathways are major determinants of pharmacokinetics and sources of clinically relevant drug-drug interactions.
Drugs may act as substrates, inhibitors or inducers of these metabolic pathways. Inhibition can increase plasma concentrations of co-administered drugs; induction can decrease them. Some drugs are prodrugs activated by these pathways; others are inactivated for excretion.
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