ClopidogrelClopidogrel
MedChemExpress (MCE)
HY-15283
113665-84-2
Clopidogrelum
99.13%
-20°C, stored under nitrogen, away from moisture *In solvent : -80°C, 6 months
-20°C, 1 month (stored under nitrogen, away from moisture)
Room temperature in continental US
may vary elsewhere.
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.
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].
Mice[1] 13-week-old C57BL/6J male mice are used throughout the study. After 1 week of acclimation, 15 mice are injected I.P. with streptozotocin (STZ) at a dosage of 55 mg/kg body weight daily for five consecutive days. Additional 15 mice as controls (Ctrl) are injected with a vehicle solution (0.1 mol/L citrate acid buffer, pH 4.3-4.5). Seven days after the last STZ administration, hyperglycemic mice (3-hour fasting blood glucose ≥250 mg/dL) are considered T1D (DM). This time point is defined as a baseline. Three months after diabetes induction, five diabetic and five control mice are sacrificed and blood and kidneys harvested. The remaining animals are divided in four groups: Normal control with vehicle (Ctrl), Normal control with Clopidogrel (Ctrl+ Clo), T1D (DM) with vehicle, and DM with Clopidogrel treatment (DM+Clo) and are treated with 20 mg/kg b.w./day Clopidogrel or with vehicle administered in their drinking water for three additional months. At the end of experiment, mice are intraperitoneally anesthetized with Avertin (tribromoethanol, 350 mg/kg) and sacrificed to collect blood and kidneys for mRNA, protein, and histological analyses[1].
P2Y12 Receptor
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[1]. Zongyu Zheng, et al. Clopidogrel Reduces Fibronectin Accumulation and Improves Diabetes-Induced Renal Fibrosis. Int J Biol Sci. 2019 Jan. [Content Brief]
[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.