TJ-M2010-5 是一种 MyD88 抑制剂，可与 MyD88 的 TIR 结构域结合以干扰其同源二聚化和 TLR/MyD88 信号通路。TJ-M2010-5 可用于心肌缺血/再灌注损伤（MIRI）的研究。
货号:ajcx35534
CAS:1357471-57-8
分子式:C23H26N4OS
分子量：406.54
溶解度:DMSO : 100 mg/mL (245.98 mM; Need ultrasonic)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

TJ-M2010-5 is a MyD88 inhibitor that binds to the TIR domain of MyD88 to interfere with its homodimerization, and the TLR/MyD88 signal pathway[1][2]. TJ-M2010-5 can be used for the research of myocardial ischemia/reperfusion injury (MIRI)[2].

TJ-M2010-5 (40 µM) inhibits MyD88 homodimerization in transfected HEK293 cells in a concentration-dependent manner and suppresses MyD88 signaling in LPS (100 ng/mL)-responsive RAW 264.7 cells in vitro[1].TJ-M2010-5 (5-30 μM) prevents B cell proliferation and induces B cells apoptosis after stimulation with R848 (500 ng/mL)[3].

TJ-M2010-5 treatment statistically significantly reduces AOM/DSS-induced colitis and completely prevented CAC development with less related body mass loss, results in 0% mortality of treated mice, decreases cell proliferation, and increased apoptosis in colon tissue in a 10-week CAC mouse model[1].TJ-M2010-5 statistically significantly decreases TNF-α, IL-6, G-CSF, MIP-1β, IL-11, IL-17A, IL-22, and IL-23 serum concentrations in mice at both two and seven weeks postinduction, as well as TGF-β1 serum levels at seven weeks postinduction[1].

[1]. Lin Xie, et al. Targeting of MyD88 Homodimerization by Novel Synthetic Inhibitor TJ-M2010-5 in Preventing Colitis-Associated Colorectal Cancer. J Natl Cancer Inst. 2015 Dec 28;108(4):djv364.
[2]. Yan Miao,et al. Inhibition of MyD88 by a novel inhibitor reverses two-thirds of the infarct area in myocardial ischemia and reperfusion injury.Am J Transl Res. 2020 Sep 15;12(9):5151-5169.