GS967

• CAT Number: I001057
• CAS Number: 1262618-39-2
• Molecular Formula: C14H7F6N3O
• Molecular Weight: 347.22
• Purity: ≥95%
• Target: Sodium Channel
• Solubility: 10 mM in DMSO
• Storage: Store at -20°C
• IUPAC Name: 6-[4-(trifluoromethoxy)phenyl]-3-(trifluoromethyl)-[1,2,4]triazolo[4,3-a]pyridine
• InChI: InChI=1S/C14H7F6N3O/c15-13(16,17)12-22-21-11-6-3-9(7-23(11)12)8-1-4-10(5-2-8)24-14(18,19)20/h1-7H
• InChIKey: FEVBKJITJDHASC-UHFFFAOYSA-N
• SMILES: C1=CC(=CC=C1C2=CN3C(=NN=C3C(F)(F)F)C=C2)OC(F)(F)F

GS967（Cat No.:I001057） is a novel, potent, and selective inhibitor of cardiac late sodium current(late INa); inhibits ATX-II-induced late I(Na) in ventricular myocytes and isolated hearts with IC50 values of 0.13 and 0.21 μM, respectively.If you need, please feel free to contact us, we will reply to you within 24 hours.

Reference

1:Mol Pharmacol. 2016 Jul;90(1):52-60. doi: 10.1124/mol.116.103358. Epub 2016 May 2. Use-Dependent Block of Human Cardiac Sodium Channels by GS967.Potet F,Vanoye CG,George AL Jr, PMID: 27136942 DOI: 10.1124/mol.116.103358 Abstract: GS-458967, 6-(4-(Trifluoromethoxy)phenyl)-3-(trifluoromethyl)-[1,2,4]triazolo[4,3-a]pyridine (GS967) is a recently described, novel, sodium channel inhibitor exhibiting potent antiarrhythmic effects in various in vitro and in vivo models. The antiarrhythmic mechanism has been attributed to preferential suppression of late sodium current. However, there has been no reported systematic investigation of the effects of this compound on isolated sodium channels. Here, we examined the effects of GS967 on peak (INaP) and late (INaL) sodium current recorded from cells that heterologously expressed human cardiac voltage-gated sodium channel, the principle cardiac sodium channel. As previously described, we observed that GS967 exerted tonic block of INaL (63%) to a significantly greater extent than INaP (19%). However, GS967 also caused a reduction of INaP in a frequency-dependent manner, consistent with use-dependent block (UDB). GS967 evoked more potent UDB of INaP (IC50 = 0.07 µM) than ranolazine (16 µM) and lidocaine (17 µM). Use-dependent block was best explained by a significant slowing of recovery from fast and slow inactivation with a significant enhancement of slow inactivation in the presence of GS967. Furthermore, GS967 was found to exert these same effects on a prototypical long QT syndrome mutation (delKPQ). An engineered mutation at an interaction site for local anesthetic agents (F1760A) partially attenuated the effect of GS967 on UDB, but had no effect on tonic INaL block. We conclude that GS967 is a preferential inhibitor of INaL, but it also exerts previously unreported strong effects on slow inactivation and recovery from inactivation, resulting in substantial UDB that is not entirely dependent on a known interaction site for local anesthetic agents. Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics.