您好,欢迎来到化工原料网! [登录] [免费注册]
化工原料网
位置:首页 > 产品库 > AM 92016 hydrochloride
立即咨询
咨询类型:
     
*姓名:
*电话:
*单位:
Email:
*留言内容:
请详细说明您的需求。
*验证码:
 
AM 92016 hydrochloride
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
AM 92016 hydrochloride图片
CAS NO:133229-11-5
包装:10mg
规格:98%
市场价:2620元
分子量:483.84

产品介绍
Potassium channel blocker
CAS:133229-11-5
分子式:C19H24Cl2N2O4S.HCl
分子量:483.84
纯度:98%
存储:Store at -20°C

Background:

AM 92016 hydrochloride is a specific inhibitor of delayed rectifier potassium current [1].


Potassium channel is an ion channel and acts to reset the resting potential and shapes the action potential. Delayed rectifier potassium channel (IK) is activated by the influx of Na+ and discharges K+, which repolarizes the membrane. IK restricts the duration of the nerve impulse.


AM 92016 hydrochloride is a specific iK inhibitor. In guinea-pig and rabbit ventricular cells, AM 92016 significantly increased action potential duration with 20% and 90% repolarization levels, respectively. Also, AM 92016 (1 μM) inhibited IK activated by step depolarizations in a time-dependent way [1]. In rabbit sino-atrial node cells, AM 92016 (50 nM) significantly inhibited IK with IC50 value of 40 nM in a concentration-dependent way [2]. In vascular smooth muscle cells (VSMC), AM92016 hydrochloride inhibited NO-induced ERK1/2 dephosphorylation [3].


In guinea-pigs, AM 92016 (1-5 mg/kg) significantly increased heart rate, left ventricular systolic pressure, systolic arterial blood pressure and the contractile index dp dtmax. AM 92016 exhibited proarrhythmic activity [4].


参考文献:
[1].  Connors SP, Gill EW, Terrar DA. Actions and mechanisms of action of novel analogues of sotalol on guinea-pig and rabbit ventricular cells. Br J Pharmacol, 1992, 106(4): 958-965.
[2].  Lei M, Brown HF. Inhibition by Compound II, a sotalol analogue, of delayed rectifier current (iK) in rabbit isolated sino-atrial node cells. Naunyn Schmiedebergs Arch Pharmacol, 1998, 357(3): 260-267.
[3].  Palen DI, Belmadani S, Lucchesi PA, et al. Role of SHP-1, Kv.1.2, and cGMP in nitric oxide-induced ERK1/2 MAP kinase dephosphorylation in rat vascular smooth muscle cells. Cardiovasc Res, 2005, 68(2): 268-277.
[4].  Hagerty MJ, Wainwright CL, Kane KA. The in-vivo cardiovascular effects of a putative class III anti-arrhythmic drug, AM 92016. J Pharm Pharmacol, 1996, 48(4): 417-421.