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Article

Different flecainide sensitivity of hNav1.4 channels and myotonic mutants explained by state-dependent block.

The Journal of physiology - 15 Jan 2004

Desaphy Jean-François, De Luca Annamaria, Didonna Maria Paola, George Alfred L, Camerino Conte Diana, Luca Annamaria D E

Abstract excerpt

Flecainide, a class IC antiarrhythmic, was shown to improve myotonia caused by sodium channel mutations in situations where the class IB antiarrhythmic drug mexiletine was less efficient. Yet little is known about molecular interactions between flecainide and human skeletal muscle sodium (hNa(v)1.4) channels. Whole-cell sodium currents (I(Na)) were recorded in tsA201 cells expressing wild-type (WT) and mutant...

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Identifiers

PMID: 14608015
DOI: 10.1113/jphysiol.2003.046995
PMCID: PMC1664778

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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