New calcium channel agonists as potential therapeutics in Lambert-Eaton myasthenic syndrome and other neuromuscular diseases.

Tyler B Tarr, Guillermo Valdomir, Mary Liang, Peter Wipf, Stephen D Meriney

Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Annals of the New York Academy of Sciences 2012 Dec

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Lambert-Eaton myasthenic syndrome (LEMS) causes neuromuscular weakness as a result of an autoimmune attack on the calcium channels that normally regulate chemical transmitter release at the neuromuscular junction. Currently there are limited treatment options for patients with this and other forms of neuromuscular weakness. A novel, first-in-class calcium channel agonist that is selective for the types of voltage-gated calcium channels that regulate transmitter release at neuromuscular synapses has recently been developed. This compound (GV-58) slows deactivation (closing) of the channel, resulting in a large increase in total calcium entry during motor nerve action potential activity. This new calcium channel agonist is currently being evaluated for the treatment of neuromuscular weakness. Potential applications include development as single therapeutics, or for combination treatments. © 2012 New York Academy of Sciences.

Citation

Tyler B Tarr, Guillermo Valdomir, Mary Liang, Peter Wipf, Stephen D Meriney. New calcium channel agonists as potential therapeutics in Lambert-Eaton myasthenic syndrome and other neuromuscular diseases. Annals of the New York Academy of Sciences. 2012 Dec;1275:85-91