位置:首页 > 产品库 > ICCB-19 hydrochloride
立即咨询
咨询类型:
     
*姓名:
*电话:
*单位:
Email:
*留言内容:
请详细说明您的需求。
*验证码:
 
ICCB-19 hydrochloride
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
ICCB-19 hydrochloride图片
规格:98%
分子量:291.84
包装与价格:
包装价格(元)
5mg询价
10mg询价
25mg询价
50mg询价
100mg询价

ICCB-19 hydrochloride 是一种 TRADD (TNFRSF1A associated via death domain) 抑制剂。ICCB-19 hydrochloride 与 TRADD (TRADD-N) 的 N 端结构域结合,破坏其与 TRADD-C 和 TRAF2 的结合。ICCB-19 hydrochloride 是 RIPK1 激酶活性的间接抑制剂。ICCB-19 hydrochloride 有效诱导自噬 (autophagy) 和长寿命蛋白质的降解。
货号:ajcx34096
CAS:1803605-68-6
分子式:C12H22ClN3OS
分子量:291.84
溶解度:DMSO : 83.33 mg/mL (285.53 mM; Need ultrasonic)
纯度:98%
存储:Store at -20°C
库存:现货

Background:

ICCB-19 hydrochloride is a TRADD (TNFRSF1A associated via death domain) inhibitor. ICCB-19 hydrochloride binds with N-terminal domain of TRADD (TRADD-N), disrupting its binding to both TRADD-C and TRAF2. ICCB-19 hydrochloride is indirect inhibitor of RIPK1 kinase activity. ICCB-19 hydrochloride effectively induces autophagy and the degradation of long-lived proteins[1].

ICCB-19 inhibits Bortezomib-induced apoptosis and RIPK1-dependent apoptosis (RDA) with an IC50 of about 1 μM[1]. ICCB-19 has no effect on mTOR. ICCB-19 (10 μM) treatment of cells increases the levels of DsRed-FYVE dots and the lipid kinase activity of VPS34[1]. ICCB-19 (10 μM) promotes autophagy via K63-linked ubiquitination of beclin 1 mediated by E3 ubiquitin ligases cIAP1 and cIAP2 and the adaptor TRAF2[1]. ICCB-19 (10 μM) reduces the rapid activation of RIPK1 in complex I induced by TNF. Treatment with ICCB-19 increases recruitment of TRADD, HOIP, and A20, but not RIPK1, to complex I[1].

ICCB-19 reduces inflammatory responses in Tradd-/- mice. ICCB-19 reduces expression of the TNF-induced inflammatory target gene products, NOS and COXII27, and of inflammatory cytokines in cells stimulated with pathogen-associated molecular patterns[1].

[1]. Daichao Xu, et al. Modulating TRADD to restore cellular homeostasis and inhibit apoptosis. Nature. 2020 Nov;587(7832):133-138.

 
 
维奥蛋白资源库 - 中文蛋白资源 CopyRight © 2010-2024