Article
Molecular basis of ranolazine block of LQT-3 mutant sodium channels: evidence for site of action.
British journal of pharmacology - 1 May 2006
Fredj Sandra, Sampson Kevin J, Liu Huajun, Kass Robert S
Abstract excerpt
1 We studied the effects of ranolazine, an antianginal agent with promise as an antiarrhythmic drug, on wild-type (WT) and long QT syndrome variant 3 (LQT-3) mutant Na(+) channels expressed in human embryonic kidney (HEK) 293 cells and knock-in mouse cardiomyocytes and used site-directed mutagenesis to probe the site of action of the drug. 2 We find preferential ranolazine block of sustained vs peak Na(+) channel...
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