1357471-57-8
1357471-57-8 structure
- Name: TJ-M2010-5
- Chemical Name: TJ-M2010-5
- CAS Number: 1357471-57-8
- Molecular Formula: C23H26N4OS
- Molecular Weight: 406.54
- Catalog: Signaling Pathways Immunology/Inflammation MyD88
- Create Date: 2021-12-19 10:59:47
- Modify Date: 2024-01-03 19:55:19
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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].
| Name | TJ-M2010-5 |
|---|
| Description | 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]. |
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| Related Catalog | |
| 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[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: 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[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: Female BalB/c mice (6–8 weeks old) [1] 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). |
| References |
| Molecular Formula | C23H26N4OS |
|---|---|
| Molecular Weight | 406.54 |