The hERG (KV11.1) potassium channel underlies the rapid delayed rectifier current, IKr, which is a major determinant of cardiac repolarization. IKr strongly modulates action potential duration (APD) and the QT interval at the cellular and organ levels, respectively. Loss of function mutations in hERG results in altered channel gating or impaired intracellular trafficking and reduced cell surface expression. These molecular defects give rise to a congenital form of the long-QT Syndrome type 2 (LQT2) and its associated arrhythmia, torsade de pointes (TdP). Recent studies have focused on the use of hERG channel agonists, such as NS-3623, as potential drug candidates for the treatment of cardiac arrhythmic disorders . The molecular mechanism of action NS-3623 is to primarily activate the native HERG channels underlying the IKr of the cardiomyocytes with an EC50 value of 10.5 μM.
产品描述
An Opener of KV11.1 (hERG) Channels
产品形式
The hERG (KV11.1) potassium channel underlies the rapid delayed rectifier current, IKr, which is a major determinant of cardiac repolarization. IKr strongly modulates action potential duration (APD) and the QT interval at the cellular and organ levels, respectively. Loss of function mutations in hERG results in altered channel gating or impaired intracellular trafficking and reduced cell surface expression. These molecular defects give rise to a congenital form of the long-QT Syndrome type 2 (LQT2) and its associated arrhythmia, torsade de pointes (TdP). Recent studies have focused on the use of hERG channel agonists, such as NS-3623, as potential drug candidates for the treatment of cardiac arrhythmic disorders . The molecular mechanism of action NS-3623 is to primarily activate the native HERG channels underlying the IKr of the cardiomyocytes with an EC50 value of 10.5 μM.