Animal experiment:

Rats: Ventricular tachycardia or fibrillation are induced either by local aconitine injection (50 μg) in the left ventricular muscle of adult male rats or by arterial perfusion of 0.1 mM hydrogen peroxide in aged male rats. The left ventricular epicardial surface of the isolated-perfused hearts is optically mapped using fluorescent voltage-sensitive dye, and microelectrode recordings of action potentials are made adjacent to the aconitine injection site. The suppressive and preventive effects of GS967 (1 μM) against EAD/DAD-mediated ventricular tachycardia or fibrillation are then determined[2]. Rabbits: To determine the effect of GS967 on the inducibility of TdP by clofilium in the presence of methoxamine, rabbits are first treated with either vehicle or GS967 (in randomized manner) given as a 60 μg/kg bolus, followed by a 16 μg/kg/min infusion that is maintained for the duration of an experiment. After 10 minutes, methoxamine is infused intravenously at 15 μg/kg/min, followed 10 minutes later by clofilium at 100 nmol/kg/min. The incidences of premature ventricular contractions (PVCs), ventricular tachycardia (VT; defined as three or more consecutive abnormal beats), and TdP are determined from the ECG recordings[1].

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]

Reference:
1.  Belardinelli L, Liu G, Smith-Maxwell C et al. A novel, potent, and selective inhibitor of
cardiac late sodium current suppresses experimental arrhythmias.  J Pharmacol Exp
Ther.  2013 Jan;344(1):23-32.