TJ-M2010-5

Research use only, not for human use.

TJ-M2010-5 is a MyD88 inhibitor that binds to the TIR domain to interfere with its homodimerization and suppress MyD88 signaling. TJ-M2010-5 can be used in myocardial ischemia/reperfusion injury studies.

TJ-M2010-5 is a MyD88 inhibitor that binds to the TIR domain to interfere with its homodimerization and suppress MyD88 signaling. TJ-M2010-5 can be used in myocardial ischemia/reperfusion injury studies.(In Vitro):TJ-M2010-5 (0 μM, 5 μM, 10 μM, 20 μM and 30 μM) prevents B cell proliferation and induces B cells apoptosis after stimulation with R848 (500 ng/mL).(In Vivo):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. In a 10-week CAC mouse model, TJ-M2010-5 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.

Cell Viability Assay Cell 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.

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).

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Immunology/Inflammation

MyD88

inflammation

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1357471-57-8

406.54

C23H26N4OS

>98% (HPLC)

In Vitro:?DMSO : 100 mg/mL (245.98 mM)

O=C(NC1=NC(C2=CC=CC=C2)=CS1)CCN3CCN(CC4=CC=CC=C4)CC3

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(-20℃)

With Ice Pack

≥ 2 years