480060
坏死抑制剂，IM-54
The Necrosis Inhibitor, IM-54, also referenced under CAS 861891-50-1, selectively blocks oxidative stress-induced necrotic cell death. This small molecule/inhibitor is primarily used for Cancer applications.
别名:
坏死抑制剂，IM-54, 2-（1H-吲哚-3-基）-3-戊基氨基-马来酰亚胺
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关于此项目
经验公式（希尔记法）:
C19H23N3O2
化学文摘社编号:
分子量:
325.40
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
产品名称
坏死抑制剂，IM-54, The Necrosis Inhibitor, IM-54, also referenced under CAS 861891-50-1, selectively blocks oxidative stress-induced necrotic cell death. This small molecule/inhibitor is primarily used for Cancer applications.
SMILES string
N1(C(=O)C(=C(C1=O)c2c3c([n](c2)C)cccc3)NCCCCC)C
InChI
1S/C19H23N3O2/c1-4-5-8-11-20-17-16(18(23)22(3)19(17)24)14-12-21(2)15-10-7-6-9-13(14)15/h6-7,9-10,12,20H,4-5,8,11H2,1-3H3
InChI key
SGLOMINNEBLJFF-UHFFFAOYSA-N
assay
≥95% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
color
yellow-orange
solubility
methanol: 10 mg/mL
DMSO: 100 mg/mL
shipped in
ambient
storage temp.
2-8°C
Quality Level
相关类别
Biochem/physiol Actions
主要靶标
阻断氧化应激诱导的坏死性细胞死亡
阻断氧化应激诱导的坏死性细胞死亡
产物不与ATP竞争。
可逆：否
细胞可渗透性：具有
靶标IC50：（〜3 µM可防止暴露于100 µM H₂O₂的HL60细胞中〜50%的细胞死亡）。
Disclaimer
毒性：标准处理（A）
General description
一种可渗透细胞的单吲哚马来酰亚胺化合物，可选择性阻断氧化应激诱导的坏死性细胞死亡（〜3 µM Im-54可防止暴露于100 µM H2O2的HL60细胞中〜50%的细胞死亡）。不提供针对依托泊苷（目录号341205）诱导的凋亡的保护或显示抗氧化剂特性。即使在浓度高为50µM时，也不会影响S6K1和PKC同工酶的激酶活性。
Other Notes
Dodo, K., et al. 2005.Bioorg.Med. Chem. Lett.15, 3114.
Packaging
用惰性气体包装
Preparation Note
复溶后，等分并冷冻保存（-20°C）。贮备液在-20°C下可稳定保存至多6个月。
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Toria Tomasek et al.
Biochemical and biophysical research communications, 556, 199-206 (2021-04-14)
Circulating cell-free hemoglobin (CFH) contributes to endothelial injury in several inflammatory and hemolytic conditions. We and others have shown that CFH causes increased endothelial permeability, but the precise mechanisms of CFH-mediated endothelial barrier dysfunction are not fully understood. Based on
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