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WEHI-345
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。
WEHI-345图片
CAS NO:1354825-58-3
包装与价格:
包装价格(元)
1mg电议
5mg电议
10mg电议
25mg电议

产品介绍
WEHI-345 是一种有效的选择性 RIPK2 激酶抑制剂,IC50 为 0.13 μM,可延迟 RIPK2 泛素化和 NF-κB 在寡聚化结构域 (NOD) 刺激下的激活。
Cas No.1354825-58-3
别名N-[2-[4-氨基-3-(4-甲基苯基)-1H-吡唑并[3,4-D]嘧啶-1-基]-2-甲基丙基]-4-吡啶甲酰胺
化学名N-[2-[4-amino-3-(4-methylphenyl)-1H-pyrazolo[3,4-d]pyrimidin-1-yl]-2-methylpropyl]-4-pyridinecarboxamide
Canonical SMILESCC(C=C1)=CC=C1C2=NN(C(C)(C)CNC(C3=CC=NC=C3)=O)C4=NC=NC(N)=C42
分子式C22H23N7O
分子量401.5
溶解度DMF: 2 mg/ml,DMSO: 2 mg/ml,Ethanol: slightly soluble
储存条件Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

WEHI-345 is a potent and selective RIPK2 kinase inhibitor with an IC50 of 0.13 μM, which delays RIPK2 ubiquitylation and NF-κB activation on oligomerization domain (NOD) stimulation[1].

WEHI-345 (500 nM; Raw 267.4 cells) is able to inhibit MDP-induced autophosphorylation activity of RIPK2 in cells[1].WEHI-345 (500 nM; 0 hour, 2 hours, 4 hours, 8 hours; BMDMs or THP-1 cells) potently blocks MDP-induced transcription of the inflammatory mediators TNF and interleukin-6 (IL-6) in bone marrow-derived macrophages (BMDMs). In THP-1 cells, WEHI-345 reduces mRNA levels of NF-kB targets such as TNF, IL-8, IL-1b and A20[1].

WEHI-345 (20 mg/kg; intraperitoneal injection; twice daily; for 6 days; C57BL/6 male mice) treatment reduces disease score, inflammatory infiltrate, histological score and recruitment of dendritic cells to the site of inflammation. And improves body weight and reduces cytokine and chemokine levels, indicating an overall improvement of the condition in experimental autoimmune encephalomyelitis (EAE)-induced wild-type C57Bl/6 mice[1].

References:
[1]. Nachbur U, et al. A RIPK2 inhibitor delays NOD signalling events yet prevents inflammatory cytokine production. Nat Commun. 2015 Mar 17;6:6442.