SML1551
GV-58
≥97% (HPLC)
别名:
(2R)-2-[[6-[[(5-Methyl-2-thienyl)methyl]amino]-9-propyl-9H-purin-2-yl]amino]-1-butanol
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选择尺寸
关于此项目
经验公式（希尔记法）:
C18H26N6OS
化学文摘社编号:
分子量:
374.50
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
InChI
1S/C18H26N6OS/c1-4-8-24-11-20-15-16(19-9-14-7-6-12(3)26-14)22-18(23-17(15)24)21-13(5-2)10-25/h6-7,11,13,25H,4-5,8-10H2,1-3H3,(H2,19,21,22,23)/t13-/m1/s1
SMILES string
CCCN1C2=NC(N[C@H](CC)CO)=NC(NCC3=CC=C(C)S3)=C2N=C1
InChI key
DPTXJOUVBMUSGY-CYBMUJFWSA-N
assay
≥97% (HPLC)
form
powder
storage condition
desiccated
color
white to beige
solubility
DMSO: 20 mg/mL, clear
storage temp.
−20°C
Quality Level
Biochem/physiol Actions
GV-58 is a roscovitine analog that retains the ability to prolong the open state of calcium channels, but unlike roscovitine, is inactive against Cdk activity. GV-58 is a selective agonist of N-type and P/Q type calcium channels, which are critical to the triggering of neurotransmitter release at the neuromuscular junction. GV-58 has been studied as a possible therapeutic agent in a mouse model of Lambert-Eaton myasthenic syndrome (LEMS). The EC50 values for activation of N-, P/Q- and L- type calcium channels are 6.8, 9.9 and >100 μM, respectively.
GV-58 is a selective agonist of N-type and P/Q type calcium channels.
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Bryan J Black et al.
Frontiers in cellular neuroscience, 11, 304-304 (2017-10-17)
Motor neurons are the site of action for several neurological disorders and paralytic toxins, with cell bodies located in the ventral horn (VH) of the spinal cord along with interneurons and support cells. Microelectrode arrays (MEAs) have emerged as a
Brett J Hilton et al.
Neuron, 110(1), 51-69 (2021-10-28)
Axons in the adult mammalian central nervous system fail to regenerate after spinal cord injury. Neurons lose their capacity to regenerate during development, but the intracellular processes underlying this loss are unclear. We found that critical components of the presynaptic
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