Clopidogrel Bisulfate (SR-25990C, Clopidogrel hydrogen sulfate, Iscover, Plavix) is an oral, thienopyridine class antiplatelet agent.
Clopidogrel is converted to its active metabolite by cytochrome P450 (CYP) enzymes. [1] Clopidogrel (1 μM) also inhibits EGF-stimulated EGF receptor, PERK expression, and cell proliferation in RGM-1 cells (P<0.05), and causes much less inhibition of EGF-stimulated cell proliferation in EGF receptor over-expressed RGM-1 cells than in RGM-1 cells (22% vs. 32% reduction). [2] Clopidogrel increases blood vessel number, reduces polymorphonuclear count and decreases attachment and bone loss, also decreases osteoclast number in rats submitted or not to periodontal repair. Clopidogrel decreases CXCL4, CXCL12 and PDGF content compared with saline-treated rats, without affecting CXCL5. [3]
Clopidogrel (2mg and 10mg/kg/day) significantly decreases ulcer-induced gastric epithelial cell proliferation and ulcer-stimulated expressions of EGF receptor and phosphorylated extracellular signal-regulated kinase (PERK) at the ulcer margin of rats. [2] Clopidogrel improves endothelial function and NO bioavailability in rats with congestive heart failure. Clopidogrel-treated Congestive heart failure (CHF) rat displays enhances phosphorylation of AKT and eNOS. [4] The clopidogrel/aspirin combination shows only additive-type effects on bleeding time prolongation induced by ear transection in the rabbit, therefore showing that combined inhibition of cyclooxygenase and ADP's effects provide a marked enhanced antithrombotic efficacy. [5]
[1] Laine L, et al. Am J Gastroenterol, 2010, 105(1), 34-41. [2] Luo JC, et al. Eur J Pharmacol, 2012, 695(1-3), 112-119. [3] Coimbra LS, et al. J Clin Periodontol, 2014, 41(3), 295-302.