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Merck
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重要文件

SML1551

Sigma-Aldrich

GV-58

≥97% (HPLC)

同義詞:

(2R)-2-[[6-[[(5-Methyl-2-thienyl)methyl]amino]-9-propyl-9H-purin-2-yl]amino]-1-butanol

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About This Item

經驗公式(希爾表示法):
C18H26N6OS
CAS號碼:
分子量::
374.50
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77
暫時無法取得訂價和供貨情況

品質等級

化驗

≥97% (HPLC)

形狀

powder

儲存條件

desiccated

顏色

white to beige

溶解度

DMSO: 20 mg/mL, clear

儲存溫度

−20°C

SMILES 字串

CCCN1C2=NC(N[C@H](CC)CO)=NC(NCC3=CC=C(C)S3)=C2N=C1

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

InChI 密鑰

DPTXJOUVBMUSGY-CYBMUJFWSA-N

生化/生理作用

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.

象形圖

Exclamation mark

訊號詞

Warning

危險聲明

危險分類

Eye Irrit. 2 - Skin Irrit. 2

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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分析證明 (COA)

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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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