What sets clopidogrel apart from other P2Y12 inhibitors? {Ans: Clopidogrel is absorbed in the intestine and activated in the liver. For clopidogrel to be activated it requires two oxidative steps. CYP2C19 is a liver enzyme, specifically the cytochrome P450 enzyme, that is heavily responsible for developing Clopidogrel's active metabolite. Genetic polymorphisms of CYP2C19 inhibit Clopidogrel metabolism and activation making it ineffective. Clopidogrel requires the active metabolite from CYP2C19 to be effective in preventing clot formation. Taking PPI decreases the effectiveness of Clopidogrel. P2Y12 inhibitors share a lot of similarities, but clopidogrel does stand apart in one specific way. The effectiveness of clopidogrel is dependent on the CYP2C19 genotype. As stated in my initial post, clopidogrel is metabolized by CYP2C19, making any variation in the gene to lead to alterations in the drug response. These variations can be linked to an increased risk for major adverse cardiovascular events. Unlike clopidogrel, CYP2C19 genotype does not affect other P2Y12 inhibitors, such as prasugrel and ticagrelor.}Statement: Although a large portion of this ethnic group has health care provided by the U.S. Indian Health Service, little research has been done related to racial considerations in pharmacokinetics or other therapies. Although research with the AI/AN