480073
Necrosulfonamide
≥95% (HPLC), solid, MLKL inhibitor, Calbiochem®
别名:
MLKL抑制剂，Necrosulfonamide
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关于此项目
经验公式（希尔记法）:
C18H15N5O6S2
化学文摘社编号:
分子量:
461.47
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
产品名称
MLKL抑制剂，Necrosulfonamide, MLKL Inhibitor, Necrosulfonamide, CAS 432531-71-0, is a cell-permeable inhibitor that covalently modifies Cys88 and blocks human MLKL adaptor function.
SMILES string
[S](=O)(=O)(Nc3ncc[n+H]c3OC)c1ccc(cc1)\N=C(/[O-])\C=C\c2[s]c(cc2)[N+](=O)[O-]
InChI
1S/C18H15N5O6S2/c1-29-18-17(19-10-11-20-18)22-31(27,28)14-6-2-12(3-7-14)21-15(24)8-4-13-5-9-16(30-13)23(25)26/h2-11H,1H3,(H,19,22)(H,21,24)/b8-4+
InChI key
FNPPHVLYVGMZMZ-XBXARRHUSA-N
assay
≥95% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
color
dark yellow
solubility
DMSO: 100 mg/mL
shipped in
ambient
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
主靶
人 MLKL
人 MLKL
可逆：否
细胞可渗透性：具有
Disclaimer
毒性：标准处理（A）
General description
一种细胞渗透性丙烯酰胺化合物。可通过迈克尔加成作用共价修饰Cys86以抑制人类（不抑制鼠类）MLKL接头。抑制人HT-29（使用药物对抗20 ng/mL TNF-&alpha/100 nM Smac类似物/20 µM Z-VAD-诱导死亡的IC50分别为124 nM和2 µM）和FADD-null Jurkat培养物（0.5 µM NSA或10 µM Nec-1对200 ng/mL TNF-&alpha-诱导死亡有80%保护作用）的坏死/坏死性凋亡时,效力强于RIP1抑制剂Nec-1（货号480065）。即使在浓度高达5 µM的情况下，也不能有效抑制鼠的坏死/坏死性凋亡或人RIP3-null Panc-1细胞的凋亡。与通过抑制RIP1-RIP3相互作用防止坏死体形成的Nec-1不同， MLKL抑制MLKL-RIP1-RIP3坏死体复合物与下游效应子相互作用。
Other Notes
Dunai, Z.A., et al. 2012.PLoS One7, e41945.
Sun, L., et al. 2012.Cell 148, 213.
Sun, L., et al. 2012.Cell 148, 213.
Packaging
用惰性气体包装
Preparation Note
仅使用新鲜的DMSO进行溶解。
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
Jialin Dai et al.
Cell death & disease, 11(4), 282-282 (2020-04-26)
Mixed-lineage kinase domain-like protein (MLKL) is known as the terminal executor of necroptosis. However, its function outside of necroptosis is still not clear. Herein, we demonstrate that MLKL promotes vascular inflammation by regulating the expression of adhesion molecules ICAM1, VCAM1
Andre L Samson et al.
Nature communications, 11(1), 3151-3151 (2020-06-21)
Mixed lineage kinase domain-like (MLKL) is the terminal protein in the pro-inflammatory necroptotic cell death program. RIPK3-mediated phosphorylation is thought to initiate MLKL oligomerization, membrane translocation and membrane disruption, although the precise choreography of events is incompletely understood. Here, we
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