Lambert–Eaton myasthenic syndrome: from clinical characteristics

Lambert-Eaton Myasthenic Syndrome – Zero To Finals

We developed a novel calcium (Ca2+) channel agonist that is selective for N- and P/Q-type Ca2+ channels, which are the Ca2+ channels that regulate transmitter release at most synapses. We have shown that this new molecule (GV-58) slows the deactivation of channels, resulting in a large increase in presynaptic Ca2+ entry during activity. GV-58 was developed as a modification of ( R )-roscovitine, which was previously shown to be a Ca2+ channel agonist, in addition to its known cyclin-dependent kinase activity. In comparison with the parent molecule, ( R )-roscovitine, GV-58 has a ∼20-fold less potent cyclin-dependent kinase antagonist effect, a ∼3- to 4-fold more potent Ca2+ channel agonist effect, and ∼4-fold higher efficacy as a Ca2+ channel agonist. We have further evaluated GV-58 in a passive transfer mouse model of Lambert–Eaton myasthenic syndrome and have shown that weakened Lambert–Eaton myasthenic syndrome-model neuromuscular synapses are significantly strengthened following exposure to GV-58. This new Ca2+ channel agonist has potential as a lead compound in the development of new therapeutic approaches to a variety of disorders that result in neuromuscular weakness.

Evaluation of a Novel Calcium Channel Agonist for Therapeutic

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Lambert-Eaton Myasthenic Syndrome: A Very Rare and Tortuously

Solved 2. Lambert Eaton Myasthenic Syndrome (LEMS) is an

Lambert–Eaton myasthenic syndrome: from clinical characteristics

P/Q-type calcium channel antibodies, Lambert–Eaton myasthenic

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What is Lambert-Eaton syndrome? - Quora

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