| Bioactivity | Clopidogrel is an orally active platelet inhibitor that targets P2Y12 receptor. Clopidogrel is used to inhibit blood clots in coronary artery disease, peripheral vascular disease, and cerebrovascular disease. |
| Target | P2Y12 receptor. |
| In Vivo | Clopidogrel, administered during the last three months, significantly decreases blood glucose, collagen and fibronectin expression compared to vehicle-treated diabetic mice. Clopidogrel markedly ameliorates hyperglycemia-induced renal fibrosis[1]. The combination therapy of clopidogrel and aspirin (dual-antiplatelet therapy) has been shown to be significantly beneficial compared to aspirin monotherapy and has also shown to decrease sub-acute stent thrombosis as well as recurrent ischemic events following ACS[2]. |
| Name | Clopidogrel |
| CAS | 113665-84-2 |
| Formula | C16H16ClNO2S |
| Molar Mass | 321.82 |
| Appearance | Oil |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | -20°C, stored under nitrogen, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen, away from moisture) |
| Reference | [1]. Zongyu Zheng, et al. Clopidogrel Reduces Fibronectin Accumulation and Improves Diabetes-Induced Renal Fibrosis. Int J Biol Sci. 2019 Jan. [2]. An insight into the interaction between clopidogrel and proton pump inhibitors By Shah, Bhavik S.; Parmar, Sanjay A.; Mahajan, Shailaja; Mehta, Anita A. From Current Drug Metabolism (2012), 13(2),225-235. |