[HTML][HTML] Molecular basis of ranolazine block of LQT-3 mutant sodium channels: evidence for site of action

S Fredj, KJ Sampson, H Liu, RS Kass - British journal of …, 2006 - ncbi.nlm.nih.gov
S Fredj, KJ Sampson, H Liu, RS Kass
British journal of pharmacology, 2006ncbi.nlm.nih.gov
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.
Abstract
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.
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