What type of metabolism does Prasugrel undergo to activate its prodrug form?

Prasugrel is a prodrug that requires metabolic activation to exert its antiplatelet effect. The key metabolic process for transforming Prasugrel into its active form is through hydrolytic metabolism, specifically facilitated by esterases in the liver and plasma. This hydrolysis results in the conversion of Prasugrel to its active metabolite, which then inhibits platelet aggregation by irreversibly binding to the P2Y12 ADP receptor on platelet cell membranes.

Understanding this metabolic pathway is crucial, as it highlights the unique aspect of Prasugrel compared to other antiplatelet medications that may utilize cytochrome P450 enzymes for activation. This difference can impact aspects such as the pharmacokinetics of the drug and the variability in patient responses, related to genetic factors affecting esterase activity compared to those affecting CYP enzymes.