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Increased sodium channel use-dependent inhibition by a new potent analogue of tocainide greatly enhances in vivo antimyotonic activity.
Neuropharmacology
February 2017
Section of Pharmacology, Department of Biomedical Sciences and Human Oncology, University of Bari Aldo Moro, 70126 Bari, Italy. Electronic address:
Article Synopsis
- Mexiletine is the primary treatment for myotonia, but many patients experience issues with its effectiveness or side effects, highlighting the need for new treatment options.
- Recent studies identified new derivatives of tocainide, To040 and To042, which showed significantly greater potency in blocking sodium channels compared to existing medications and could be effective antimyotonic agents.
- The compound To042 demonstrated good safety and efficacy profiles, being 120 times more potent than mexiletine in laboratory settings, suggesting it could be a valuable candidate for future clinical trials in treating myotonia and related disorders.
Anesthetic-Receptor Relationship Status: It's Complicated.
Anesthesiology
December 2016
From M. Jenkins Medical Communications, LLC, Atlanta, Georgia (M.A.J.); and Departments of Anesthesiology and Pharmacology, Emory University School of Medicine, Atlanta, Georgia (A.J.).
Indoxacarb, Metaflumizone, and Other Sodium Channel Inhibitor Insecticides: Mechanism and Site of Action on Mammalian Voltage-Gated Sodium Channels.
Pestic Biochem Physiol
July 2013
Insecticide Toxicology Laboratory, Department of Entomology, Cornell University, Geneva, NY 14456.
Sodium channel inhibitor (SCI) insecticides were discovered almost four decades ago but have only recently yielded important commercial products (eg., indoxacarb and metaflumizone). SCI insecticides inhibit sodium channel function by binding selectively to slow-inactivated (non-conducting) sodium channel states.
View Article and Find Full Text PDFBisphenol A binds to the local anesthetic receptor site to block the human cardiac sodium channel.
PLoS One
April 2013
Institute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Bavaria, Germany.
Bisphenol A (BPA) has attracted considerable public attention as it leaches from plastic used in food containers, is detectable in human fluids and recent epidemiologic studies link BPA exposure with diseases including cardiovascular disorders. As heart-toxicity may derive from modified cardiac electrophysiology, we investigated the interaction between BPA and hNav1.5, the predominant voltage-gated sodium channel subtype expressed in the human heart.
View Article and Find Full Text PDFMolecular Insights into the Local Anesthetic Receptor within Voltage-Gated Sodium Channels Using Hydroxylated Analogs of Mexiletine.
Front Pharmacol
October 2012
Section of Pharmacology, Department of Pharmacobiology, Faculty of Pharmacy, University of Bari Bari, Italy.
We previously showed that the β-adrenoceptor modulators, clenbuterol and propranolol, directly blocked voltage-gated sodium channels, whereas salbutamol and nadolol did not (Desaphy et al., 2003), suggesting the presence of two hydroxyl groups on the aromatic moiety of the drugs as a molecular requisite for impeding sodium channel block. To verify such an hypothesis, we synthesized five new mexiletine analogs by adding one or two hydroxyl groups to the aryloxy moiety of the sodium channel blocker and tested these compounds on hNav1.
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