| Identification | Back Directory | [Name]
GS967 | [CAS]
1262618-39-2 | [Synonyms]
GS967
CS-1742
GS458967
GS-458967
GS 458967
GS967, >98%
GS967(GS-458967)
GS-967;GS 967;GS-458967; GS 458967; GS458967
6-(4-(trifluoroMethoxy)phenyl)-3-(trifluoroMethyl)-[1,2,4]triazolo[4,3-a]pyridine
1,2,4-Triazolo[4,3-a]pyridine, 6-[4-(trifluoromethoxy)phenyl]-3-(trifluoromethyl)- | [Molecular Formula]
C14H7F6N3O | [MDL Number]
MFCD28385879 | [MOL File]
1262618-39-2.mol | [Molecular Weight]
347.22 |
| Chemical Properties | Back Directory | [density ]
1.52±0.1 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
insoluble in H2O; ≥13.35 mg/mL in DMSO; ≥25.52 mg/mL in EtOH with ultrasonic | [form ]
solid | [pka]
-0.41±0.50(Predicted) |
| Hazard Information | Back Directory | [Uses]
GS967, also known as GS-458967, is a highly selective late sodium channel current blocker. The selective inhibition of late INa with GS967 can exert antiarrhythmic effects by suppressing EAD- and DAD-mediated extrasystolic activity in PFs and PV and SVC sleeve preparations. Selective late INa inhibition with GS967 exerts potent protective effects against ischemia-induced depolarization and repolarization abnormalities in both atria and ventricles. | [Biological Activity]
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] | [References]
1. belardinelli l, liu g, smith-maxwell c et al. a novel, potent, and selective inhibitor ofcardiac late sodium current suppresses experimental arrhythmias. j pharmacol exp ther. 2013 jan;344(1):23-32. |
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