VK-II-86 prevents hypokalaemia-induced arrhythmogenesis by normalizing calcium homeostasis and repolarization reserve. VK-II-86 may provide an effective treatment in hypokalaemia and other arrhythmias caused by delayed repolarization or Ca 2+ overload.

2021年12月7日 · VK-II-86 prevents hypokalaemia-induced arrhythmogenesis by normalizing calcium homeostasis and repolarization reserve. VK-II-86 may provide an effective treatment in hypokalaemia and other arrhythmias caused by delayed repolarization or Ca 2+ overload.

VK-II-86 is a Carvedilol analogue lacking antagonist activity at β-adrenoceptors, in hypokalaemia. VK-II-86 prevents hypokalaemia-induced ventricular arrhythmia through multi-channel effects. VK-II-86 prevents all hypokalaemia-induced changes in ion channel activity and oxidative stress.

VK-II-86 is an inhibitor of store-overload-induced calcium release (SOICR) and a derivative of carvedilol (Item No. 15418). 1 It inhibits SOICR in HEK293 cells expressing the ryanodine receptor 2 (RyR2) R4496C (RyR2 R4496C) mutation (IC 50 = 16.8 µM), a mutation that results in spontaneous calcium release from the endoplasmic reticulum.

In an in vitro cell culture model, VK-II-86 was shown to be effective in decreasing store-overload induced Ca 2+ release in cells treated with the class I kinase inhibitors, CX-4545 (silmitasertib) and sunitinib .

2011年7月10日 · VK-II-86 prevented stress-induced ventricular tachyarrhythmias in RyR2-mutant mice and did so more effectively when combined with either of the selective beta blockers metoprolol or bisoprolol. Combining SOICR inhibition with optimal beta blockade has the potential to provide antiarrhythmic therapy that can be tailored to individual patients.

2018年12月25日 · Carvedilol and VK-II-86 are effective to prevent ouabain-induced apoptosis and spontaneous contractions indicative of arrhythmogenic activity without affecting inotropy and demonstrated to be effective in human models, thus emerging as a therapeutic tool for the prevention of digitalis-induced arrhy …

VK-II-36 是一种 carvedilol 类似物，可抑制肌浆网钙释放，但不阻断 β 受体。VK-II-36 抑制早期和延迟后去极化诱发的触发活动，可用于研究局灶性室性心律失常。- 高纯度，全球文献引用。

We found that VK-II-86 alone prevented stress-induced VTs in RyR2 mutant mice, and was more effective when combined with a selective beta-blocker metoprolol or bisoprolol. Thus, SOICR inhibition combined with optimal beta-blockade presents a new, promising and potentially patient-tailorable anti-arrhythmic approach.

VK-II-86 is a Carvedilol (HY-B0006) analogue lacking antagonist activity at β-adrenoceptors, in hypokalaemia. VK-II-86 prevents hypokalaemia-induced ventricular arrhythmia through multi-channel effects.