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经验公式(希尔记法):
C21H26N2O7
化学文摘社编号:
分子量:
418.44
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
SMILES string
[N+](=O)([O-])c1cc(ccc1)C2C(=C(NC(=C2C(=O)OCCOC)C)C)C(=O)OC(C)C
InChI
1S/C21H26N2O7/c1-12(2)30-21(25)18-14(4)22-13(3)17(20(24)29-10-9-28-5)19(18)15-7-6-8-16(11-15)23(26)27/h6-8,11-12,19,22H,9-10H2,1-5H3
InChI key
UIAGMCDKSXEBJQ-UHFFFAOYSA-N
description
Merck USA index - 14, 6551
assay
>98% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
color
yellow
solubility
DMSO: 25 mg/mL, methanol: soluble
shipped in
ambient
Quality Level
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General description
An L-type Ca2+ channel blocker. Enhances memory in old or brain-damaged animals. Ameliorates experimental diabetic neuropathy in streptozotocin-induced diabetic rats. Also reported to block TNF-α and LPS-induced iNOS activity (IC50 = 36 pM) in mouse astroglial cells.
Biochem/physiol Actions
Cell permeable: no
Primary Target
L-type Ca2+ channel blocker
L-type Ca2+ channel blocker
Product does not compete with ATP.
Reversible: no
Target IC50: 36 pM blocking TNF-α and LPS-induced iNOS activity in mouse astroglial cells
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Other Notes
Zhu, D., et al. 1999. Life. Sci.65, PL 221.
Marchetti, C. and Usai, C. 1996. Neurosci. Lett. 207, 77.
Kappelle, A.C., et al. 1994. Br. J. Pharmacol.111, 887.
Weiss, J.H., et al. 1994. J. Neurochem. 62, 372.
Kappelle, A.C., et al. 1993. Br. J. Pharmacol.108, 780.
Marchetti, C. and Usai, C. 1996. Neurosci. Lett. 207, 77.
Kappelle, A.C., et al. 1994. Br. J. Pharmacol.111, 887.
Weiss, J.H., et al. 1994. J. Neurochem. 62, 372.
Kappelle, A.C., et al. 1993. Br. J. Pharmacol.108, 780.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Harmful & Carcinogenic / Teratogenic (E)
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Ariel Caviedes et al.
Cell death & disease, 12(1), 4-4 (2021-01-09)
Cell death by glutamate excitotoxicity, mediated by N-methyl-D-aspartate (NMDA) receptors, negatively impacts brain function, including but not limited to hippocampal neurons. The NF-κB transcription factor (composed mainly of p65/p50 subunits) contributes to neuronal death in excitotoxicity, while its inhibition should
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