TJ-M2010-5
- Product Name
- TJ-M2010-5
- CAS No.
- 1357471-57-8
- Chemical Name
- TJ-M2010-5
- Synonyms
- TJ-M2010-5;TJ-M2010-5, 10 mM in DMSO;3-(4-Benzylpiperazin-1-yl)-N-(4-phenylthiazol-2-yl)propanamide;1-Piperazinepropanamide, 4-(phenylmethyl)-N-(4-phenyl-2-thiazolyl)-;ischemia,MIRI,Anoxia,factor,MyD88,injury,reoxygenation,inhibit,reperfusion,differentiation,Inhibitor,remodeling,myocardial,MyD88,TLR,TJ-M-2010-5,myeloid,TJM20105,TJ M2010 5
- CBNumber
- CB29739857
- Molecular Formula
- C23H26N4OS
- Formula Weight
- 406.54
- MOL File
- 1357471-57-8.mol
TJ-M2010-5 Property
- Density
- 1.232±0.06 g/cm3(Predicted)
- solubility
- DMSO : 100 mg/mL (245.98 mM; Need ultrasonic)
- pka
- 9.36±0.50(Predicted)
- form
- Solid
- color
- Light yellow to yellow
TJ-M2010-5 Chemical Properties,Usage,Production
Uses
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].
Biological Activity
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].
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
[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.
TJ-M2010-5 Preparation Products And Raw materials
Raw materials
Preparation Products
TJ-M2010-5 Suppliers
- Tel
- +1-781-999-5354;
- support@targetmol.com
- Country
- United States
- ProdList
- 39035
- Advantage
- 58