product name Clopidogrel
Description: Clopidogrel is an orally available, thienopyridine class antiplatelet agent. It is used to inhibit blood clots in coronary artery disease, peripheral vascular disease, cerebrovascular disease, and to prevent myocardial infarction (heart attack) and stroke. Clopidogrel works by irreversibly inhibiting a receptor called P2Y12, an adenosine diphosphate (ADP) chemoreceptor on platelet cell membranes. Clopidogrel acts by inhibiting the ADP receptor on platelet cell membranes. It is a prodrug, which requires CYP2C19 for its activation.
References: Eur J Pharmacol. 2012 Nov 15;695(1-3):112-9; Basic Res Cardiol. 2011 May;106(3):485-94.
419.9
Formula
C16H16ClNO2S.H2SO4
CAS No.
120202-66-6
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 83 mg/mL (197.7 mM)
Water: 78 mg/mL (185.7 mM)
Ethanol: 46 mg/mL (109.5 mM)
Solubility (In vivo)
Synonyms
SR-25990C
other peoduct :
| In Vitro |
In vitro activity: Clopidogrel is converted to its active metabolite by cytochrome P450 (CYP) enzymes. 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). 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. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | 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. 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. 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 ADPs effects provide a marked enhanced antithrombotic efficacy. |
| Animal model | |
| Formulation & Dosage | |
| References | Eur J Pharmacol. 2012 Nov 15;695(1-3):112-9; Basic Res Cardiol. 2011 May;106(3):485-94. |
