The prodrug prasugrel is rapidly hydrolysed to a thiolactione in the intestines. The thiolactone metabolite is a substrate of CYP3A4, CYP2B6, CYP2C9 and CYP2C19. There are no in vitro or in vivo data indicating that prasugrel inhibits or induce the major CYP enzymes.

Prasugrel is indicated for prevention of atherotrombotic incidences in patients with acute coronary syndromes subjected to percutaneous coronary intervention. Administration to patients >75 years is generally not recommended.

Probably significant hepatic exposure with regard to the active thiolactone metabolite.

Prasugrel is a prodrug which is rapidly hydrolysed in the intestines to a thiolactone by human carboxylesterase 2 (Laizure 2010). The thiolactone is converted by CYP3A4, CYP2B6, and to a lesser extent by CYP2C9 and CYP2C19, to the active metabolite which is inactivated after S-metylation and conjugation with cysteine (Schrör 2011, Small 2010). In vitro studies have shown that it is unlikely that the main metabolites of prasugrel will inhibit CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A4 (Small 2010). Other in vitro data however, showed that the metabolite R-95913 inhibits CYP2C9, CYP2C19, CYP2D6 and CYP3A4. The data also indicated that the inhibitions best fit the competitive inhibition model, except for CYP2D6 which best fitted the non-competitive inhibition model (Rehmel 2006). In vitro studies have shown that prasugrel and its thiolactone metabolite R-95913 are mechanism-based inhibitors of CYP2B6, but have no potential to be a mechanism-based inhibitor of CYP2C19 (Nishiya 2009). In clinical use prasugrel does not inhibit CYP2C9, but is a weak inhibitor of CYP2B6 (Small 2010, Farid 2008). Unlike clopidogrel, very few drug-drug interactions have been reported for prasugrel (hulot 2011) and there are no in vitro or in vivo data indicating that prasugrel inhibits or induces the major CYP enzymes.