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The U.S. Food and Drug Administration has changed clopidogrel's prescribing information to highlight the potential impact of CYP2C19 genotype on clopidogrel pharmacokinetics and clinical response ( 289). Nevertheless, other studies have not confirmed associations between CYP2C19 polymorphisms and adverse outcomes in clopidogrel-treated patients ( 290). Future studies are needed to further clarify the risk associated with these genetic polymorphisms and to develop effective therapeutic strategies for carriers of allelic variants of responsible enzyme systems. Proton-pump inhibitors, Afatinib nmr most prominently omeprazole, can interfere with clopidogrel metabolism and result in diminished in vitro antiplatelet effect ( 291), but it does not appear that this pharmacokinetic effect translates into worse clinical outcomes ( 291?and?292). Prasugrel, an alternative thienopyridine, achieves greater PTPRJ inhibition of platelet aggregation than clopidogrel. In the TRITON-TIMI 38 trial(260) of prasugrel versus clopidogrel in patients with ACS for whom an invasive strategy was planned, patients with STEMI who were assigned to prasugrel had a lower 30-day rate of the composite primary outcome. This difference persisted to 15 months. In addition, the rate of stent thrombosis reported at 30 days was significantly lower with prasugrel (260?and?262). The loading dose of clopidogrel in TRITON-TIMI 38, which rarely was administered before coronary angiography and was limited to 300 mg, may have contributed to differences in efficacy and safety between treatment groups (262). The benefits of prasugrel relative to clopidogrel in STEMI must be weighed against the increase in the risk of bleeding associated with its use. Prasugrel should not be administered to patients with a history of stroke or transient ischemic attack and was not shown Selleckchem Dasatinib to be beneficial in patients ��75 years of age or patients who weigh