SMILES string
[Cl-].[Cl-].Clc1c(cccc1)CNCC2CCC(CC2)CNCc3c(cccc3)Cl.[H+].[H+]
InChI
1S/C22H28Cl2N2.2ClH/c23-21-7-3-1-5-19(21)15-25-13-17-9-11-18(12-10-17)14-26-16-20-6-2-4-8-22(20)24;;/h1-8,17-18,25-26H,9-16H2;2*1H
InChI key
NRVIEWRSGDDWHP-UHFFFAOYSA-N
description
RTECS - GU7025000
assay
≥95% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, desiccated (hygroscopic)
color
white
solubility
DMSO: 20 mg/mL, water: 20 mg/mL
shipped in
ambient
Quality Level
相关类别
General description
一种细胞可渗透的两亲性二胺,作为胆固醇生物合成和酯化的有效抑制剂并表现出致畸性。特异性阻断7-脱氢胆固醇还原酶(Δ7-甾醇还原酶;DHC)活性,IC50=13 nM。据报道在大鼠胚胎发生过程中破坏音猬因子(Shh)信号传导。还报道了在成纤维细胞中诱导酸性鞘磷脂酶活性的快速和不可逆的降低。
一种细胞可渗透的两亲性二胺,可阻断胆固醇生物合成和酯化。特异性阻断7-脱氢胆固醇还原酶(Δ7-甾醇还原酶)活性,IC50=13 nM。音猬因子信号传导和致畸性研究中的重要工具。还报道了在成纤维细胞中诱导酸性鞘磷脂酶活性的快速和不可逆的降低。
Biochem/physiol Actions
主要靶标
7-脱氢胆固醇还原酶(δ7-甾醇还原酶)
7-脱氢胆固醇还原酶(δ7-甾醇还原酶)
产物不与ATP竞争。
可逆:否
细胞可渗透性:是
靶标IC50:13 nM阻断7-脱氢胆固醇还原酶(δ7-甾醇还原酶)活性
Packaging
用惰性气体包装
Preparation Note
复溶后,等分并冷冻(-20°C)。储备液在-20°C条件下可稳定保存3个月。
Other Notes
Gofflot, F., et al. 2001.Dev.Dyn.220, 99.
Cooper, M.K., et al. 1998.Science280, 1603.
Incardona, J.P., et al. 1998.Development125, 3553.
Moebius, F.F., et al. 1998.Proc.Natl.Acad.Sci. USA95, 1899.
Yoshida, Y. 1985.J. Biochem.98, 1669.
Kraml, M., et al. 1964.Biochem.Biophys.Res. Commun.15, 455.
Cooper, M.K., et al. 1998.Science280, 1603.
Incardona, J.P., et al. 1998.Development125, 3553.
Moebius, F.F., et al. 1998.Proc.Natl.Acad.Sci. USA95, 1899.
Yoshida, Y. 1985.J. Biochem.98, 1669.
Kraml, M., et al. 1964.Biochem.Biophys.Res. Commun.15, 455.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
毒性:有害 & 致癌/致畸性(E)
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Oral
存储类别
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
wgk
WGK 3
Qi Sun et al.
Communications biology, 6(1), 1108-1108 (2023-11-02)
Recent findings have shown that fatty acid metabolism is profoundly involved in ferroptosis. However, the role of cholesterol in this process remains incompletely understood. In this work, we show that modulating cholesterol levels changes vulnerability of cells to ferroptosis. Cholesterol
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