TJ-M2010-5_product_DataBase

Bioactivity	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].
Invitro	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]. Cell Viability Assay[3] Cell Line:
In Vivo	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]. Animal Model:
Name	TJ-M2010-5
CAS	1357471-57-8
Formula	C23H26N4OS
Molar Mass	406.54
Appearance	Solid
Transport	Room temperature in continental US; may vary elsewhere.
Storage	4°C, protect from light, stored under nitrogen *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)
Reference	[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.

PeptideDB

TJ-M2010-5

CAS: 1357471-57-8 F: C23H26N4OS W: 406.54