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

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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

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Hazard and Precautionary Statements (GHS)

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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

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TJ-M2010-5 Suppliers

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1357471-57-8, TJ-M2010-5Related Search:

TJ-M2010-5

ischemia,MIRI,Anoxia,factor,MyD88,injury,reoxygenation,inhibit,reperfusion,differentiation,Inhibitor,remodeling,myocardial,MyD88,TLR,TJ-M-2010-5,myeloid,TJM20105,TJ M2010 5

3-(4-Benzylpiperazin-1-yl)-N-(4-phenylthiazol-2-yl)propanamide

1-Piperazinepropanamide, 4-(phenylmethyl)-N-(4-phenyl-2-thiazolyl)-

TJ-M2010-5, 10 mM in DMSO

1357471-57-8