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Necrosulfonamide

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产品名称: Necrosulfonamide
产品型号: GOY-Y2638
产品展商: 谷研
产品文档: 无相关文档
发布时间:2023-04-28

简单介绍

Necrosulfonamide≥ 46.1mg/mL in DMSO


Necrosulfonamide  的详细介绍

性能参数

产品名称

Necrosulfonamide

规格

10mg 50mg

货号

GOY-Y2638

 含量

>98.00%

CAS

432531-71-0

别名

N/A

 

 

化学名

(E)-N-[4-[[(3-Methoxy-2-pyrazinyl)amino]sulfonyl]phenyl]-3-(5-nitro-2-thienyl)-2-propenamide

分子式

C18H15N5O6S2

分子量

分子量 461.47

溶解度

≥ 46.1mg/mL in DMSO

储存条件

Store at -20°C

General tips

 

用途

仅供科研

价格

电询

详细内容

Necrosulfonamide (NSA) is a pharmacological inhibitor of mixed lineage kinase-like protein (MLKL) [1]. NSA is potent in protecting necrotic/necroptotic death of human HT-29 with an IC50 value of 124 nM [2].

MLKL, a functional RIP3 substrate, can bind to RIP3 through its kinase-like domain but it lacks kinase activity. MLKL can be phosphorylated by RIP3 at the T357 and S358 sites [3].

Treatment with NSA alone did not rescue cell death, while NSA significantly enhanced the protection of zVAD.fmk against BV6/5AC-induced cell death. In the same line, knockdown of MLKL did not significantly protect cells against BV6/5AC cotreatment in the absence of zVAD.fmk [1]. In the Dox-treated HeLa cells, NSA inhibited necrosis. With a higher level of RIP3, the allosteric inhibition of necrostatin-1 on RIP1 was overcome by cells. In contrast, NSA still efficiently prevented necrosis under this condition. Consistently, knockdown of MLKL also blocked necrosis. Under necrosis-inducing conditions, the presence of NSA made tubular mitochondrial morphology remain normal. Consistently the mitochondrial morphological changes were also prevented by the knockdown of MLKL [4]. Even at 5 μM concentration, NSA had no effect on the apoptosis induced by TNF-α plus Smac mimetic in non-RIP3-expressing Panc-1 cells. In the presence of NSA, the discrete RIP3 punctae were detected but failed to enlarge. That meant NSA blocked necrosis at a specific step in the necrosis pathway [3].

Pharmacological treatment with NSA delayed cone degeneration [5].

 

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