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Overview
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Background
GS967 is a potent, selective and novel inhibitor of cardiac late sodium current (late INa) with IC50=0.13 μM in ventricular myocytes and IC50=0.21μM in isolated hearts. [1]
When Na+ channels in myocytes fail to inactivate after opening, Na+ influx continues throughout the AP plateau. The resulting Na+ current (INa) is referred to as late INa. Its magnitude is increased in many pathologic conditions, such as in the failing and/or ischemic heart, in the heart exposed to oxidative stress, and in hearts of patients with congenital long QT3 syndromes. [1]
In rabbit isolated ventricular myocytes, inhibition of peak INa by GS967 is in a concentration- and voltage-dependent manner with minimal use-dependent, it also decreases the Na+ and Ca2+ overload. In rabbit-isolated heart, GS967 abolishes TdP Induced by ATX-II or E-4031. [1]
In anesthetized rabbit, GS967 reduces MAPD90 but did not alter cardiac conduction time; it also prevents the Induction of arrhythmic activity and TdP by clofilium and decreases the Incidence of ischemia-Induced arrhythmias. [1]
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