产品
编 号：F247337
分子式：C34H30Br2N4
分子量：654.44
分子式：C34H30Br2N4
分子量：654.44
产品类型
规格
价格
是否有货
1mg
询价
询价
结构图
CAS No: 199934-16-2
产品详情
生物活性：
UCL 1684 (dibromide) is a first nanomolar, non-peptidic small conductance calcium-activated potassium (SK) channel blocker. UCL 1684 (dibromide) is effective in preventing the development of atrial fibrillation due to potent atrial-selective inhibition of INa. UCL 1684 (dibromide) causes atrial-selective prolongation of ERP secondary to induction of postrepolarization refractoriness.
体内研究：
UCL 1684 (dibromide) (3 mg/kg; i.v.) increases wenckebach cycle length to 115.0±5.1 % of baseline value.
体外研究：
UCL 1684 (dibromide) (0.5 μM; HEK cells) produces direct atrial-selective inhibition of sodium channel current (INa) and shifts SS inactivation of the cardiac sodium channels. UCL 1684 (dibromide) (0.5 μM) induces PRR, decreases V max, increases DTE, and extends the shortest S1-S1 interval.
UCL 1684 (dibromide) is a first nanomolar, non-peptidic small conductance calcium-activated potassium (SK) channel blocker. UCL 1684 (dibromide) is effective in preventing the development of atrial fibrillation due to potent atrial-selective inhibition of INa. UCL 1684 (dibromide) causes atrial-selective prolongation of ERP secondary to induction of postrepolarization refractoriness.
体内研究：
UCL 1684 (dibromide) (3 mg/kg; i.v.) increases wenckebach cycle length to 115.0±5.1 % of baseline value.
体外研究：
UCL 1684 (dibromide) (0.5 μM; HEK cells) produces direct atrial-selective inhibition of sodium channel current (INa) and shifts SS inactivation of the cardiac sodium channels. UCL 1684 (dibromide) (0.5 μM) induces PRR, decreases V max, increases DTE, and extends the shortest S1-S1 interval.
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