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. 2016 May 10;7:121. doi: 10.3389/fphar.2016.00121

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Copyright © 2016 Imbrici, Liantonio, Camerino, De Bellis, Camerino, Mele, Giustino, Pierno, De Luca, Tricarico, Desaphy and Conte.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pharmacogenetics of myotonic sodium channel mutants. (A,B) Representative sodium current traces from hNav1.4 WT channels and myotonic G1306E mutants recorded in transfected cells at steady-state before and during application of mexiletine at 0.1 and 10 Hz stimulation frequencies. (C) Concentration-effect relationships for mexiletine on WT and G1306E, fitted to a first-order binding function. (D,E) Effects of flecainide on sodium currents in the same conditions as in (A,B). (F) Concentration-effect relationships for flecainide on WT and G1306E. The G1306E mutation impairs mexiletine inhibition, while leaving flecainide affinity unchanged. Consequently, patients carrying G1306E, who suffer form a severe form of myotonia, obtained significant improvement by shifting treatment from mexiletine to flecainide.