Introduction Platelets (PLTs) play an essential role in the development of ischemic stroke in terms of pathophysiology of thrombosis formation (1). Clopidogrel, an antithrombotic agent that inhibits PLT activation via adenosine diphosphate (ADP), has proven efficacy and safety in preventing recurrent ischemic strokes (1). Clopidogrel is a secondgeneration thienopyridine derivative prodrug and is converted to its active metabolite by cytochrome P450 enzyme system (mainly CYP2C19)