| Bioactivity | GV-58 is a novel N- and P/Q-type calcium (Ca2+) channel agonist with EC50s of 7.21 and 8.81 μM, respectively. GV-58 slows the deactivation of channels, resulting in a large increase in presynaptic Ca2+ entry during activity. GV-58 can be used in lambert-eaton myasthenic syndrome (LEMS) research[1][2][3]. | ||||||||||||
| Invitro | GV-58 (50 μM; 30 min) restores function in LEMS passive transfer neuromuscular junction[1]. Cell Viability Assay[1] Cell Line: | ||||||||||||
| Name | GV-58 | ||||||||||||
| CAS | 1402821-41-3 | ||||||||||||
| Formula | C18H26N6OS | ||||||||||||
| Molar Mass | 374.50 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Tarr TB, et al. Evaluation of a novel calcium channel agonist for therapeutic potential in Lambert-Eaton myasthenic syndrome. J Neurosci. 2013 Jun 19;33(25):10559-67. [2]. Tarr TB, et al. Complete reversal of Lambert-Eaton myasthenic syndrome synaptic impairment by the combined use of a K+ channel blocker and a Ca2+ channel agonist. J Physiol. 2014 Aug 15;592(16):3687-96. [3]. Meriney SD, et al. Lambert-Eaton myasthenic syndrome: mouse passive-transfer model illuminates disease pathology and facilitates testing therapeutic leads. Ann N Y Acad Sci. 2018 Jan;1412(1):73-81. |