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. TJ-M2010-5 can be used for the research of myocardial ischemia/reperfusion injury (MIRI) . In Vitro 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. ?\nTJ-M2010-5 (5-30 μM) prevents B cell proliferation and induces B cells apoptosis after stimulation with R848 (500 ng/mL). MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell Line: Purified B cells Concentration: 0 μM, 5 μM, 10 μM, 20 μM and 30 μM Incubation Time: 48 hours Result: Inhibited the viability of B cells with or without the stimulation of CD40L. 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 . ?\nTJ-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 . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Female BalB/c mice (6–8 weeks old) Dosage: 50 mg/kg Administration: Treated i.p. daily beginning two days before the first dextran sodium sulfate (DSS) administration throughout a 10-week observation period. Result: Significantly prevented inflammation/CAC-related body weight loss and mortality (0% vs 53% in the control group). Form:Solid