K201 是一种 Ca2+ 依赖性阻滞剂，通过稳定兰尼碱受体来防止缺血性心脏和骨骼肌 (SkM) 中的肌质网异常 Ca(2+) 泄漏。

K201 is a Ca2+-dependent blocker and prevents abnormal Ca(2+) leak from the sarcoplasmic reticulum in the ischemic heart and skeletal muscle (SkM) by stabilizing the ryanodine receptors.

In isolated cardiac and SkM SR microsomes, K201 slowed the rate of SR Ca(2+) loading, suggesting potential SERCA block and/or RyR agonism. K201 displayed Ca(2+)-dependent inhibition of SERCA-dependent ATPase activity, which was measured in microsomes incubated with 200, 2, and 0.25 μM Ca(2+) and with the half-maximal K201 inhibitory doses (IC50) estimated at 130, 19, and 9 μM (cardiac muscle) and 104, 13, and 5 μM (SkM SR). K201 (≥5 μM) increased RyR1-mediated Ca(2+) release from SkM microsomes. Maximal K201 doses at 80 μM produced ~37% of the increase in SkM SR Ca(2+) release observed with the RyR agonist caffeine. K201 (≥5 μM) increased the open probability (Po) of very active ("high-activity") RyR1 of SkM reconstituted into bilayers, but it had no effect on "low-activity" channels. Likewise, K201 activated cardiac RyR2 under systolic Ca(2+) conditions (~5 μM; channels at Po ~0.3) but not under diastolic Ca(2+) conditions (~100 nM; Po< 0.01)[1].

1038410-88-6

C25H33ClN2O2S

461.06

JTV-519;K-201

DMSO:Soluble
Powder: -20°C for 3 years
In solvent: -80°C for 2 years