Voltage-gated sodium (Na_V) channels are integral membrane proteins that play an essential role in the regulation of action potentials in neurons, myocytes and endocrine cells¹. Given their central role in electrical signaling, Na_Vs inhibitors have been extensively studied. Inhibitors of Na_vs have been found to be highly effective as local anesthetics, anticonvulsants and antiarrhythmic and in the prevention of myocardial ischemia and heart failure².  

Late Na⁺ current (I_NaL) is a phenomenon that occurs when Na_Vs in myocytes fail to regulate Na⁺ influx. Increased magnitude of late I_NaL is associated with pathological conditions. Inhibition of cardiac late I_Na is a strategy to suppress arrhythmias and Na⁺-dependent calcium overload associated with myocardial ischemia and heart failure³. 

GS967 is a potent and selective inhibitor of late I_Na. It was shown to inhibit ATX-II (#STA-700) induced late I_Na in ventricular myocytes and isolated hearts^4-5.  

Photogenic variant SCN8A, encoding the Na_V α subunit Nav1.6, is a known cause of epilepsy. Treatment of mice carrying the SCN8A mutation with G967 resulted in lower seizure burden and complete protection from seizure‐associated lethality⁶.