BMS-191095 is a selective activator of mitochondrial ATP-sensitive potassium ( mitoKATP ) channels. BMS-191095 inhibits human platelet aggregation by opening mitochondrial K(ATP) channels.
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Product Description
BMS-191095 is a selective activator of mitochondrial ATP-sensitive potassium ( mitoKATP ) channels. BMS-191095 inhibits human platelet aggregation by opening mitochondrial K(ATP) channels .
In Vitro
BMS-191095 (50 μmol/L) induces mitochondrial depolarization of vascular smooth muscle (VSM) cells from SD rats. BMS-191095 (10-100 μmol/L) dose-dependently induces vasodilation in endothelium denuded cerebral arteries. BMS-191095 (50 μmol/L) increases the frequency of calcium sparks in VSM cells. BMS-191095 (0-1500 μM) inhibits human platelet aggregation induced by collagen and thrombin with IC 50 values of 63.9 and 104.8 μM, respectively. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
BMS-191095 (2.5 or 25 μg; intraventricular infusion, 30 min/60 min/24 hours before the induction of ischemia, once) reduces neuronal damage in rats with transient focal cerebral ischemia. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Male Wistar rats with the induction of ischemia induced by middle cerebral artery occlusion (MCAO)Dosage: 2.5 or 25 μg Administration: Intraventricular infusion; 30 min/60 min/24 hours before the induction of ischemia, once Result: Reduced total infarct volume in rats with of pretreat dose of 25 mg and 24 h before MCA. Induced a rapid mitochondrial depolarization.
