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Merck
CN

SML3682

ST2825

≥98% (HPLC), MyD88 dimerization inhibitor, powder

别名:

(2R,4′R,8′aR)-1-[2-[4-[[2-(2,4-Dichlorophenoxy)acetyl]amino]phenyl]acetyl]tetrahydro-6′-oxo-spiro[pyrrolidine-2,7′(6′H)-[2H]pyrrolo[2,1-b][1,3]thiazine]-4′-carboxamide, PAM4-SP19-Beta8-NH2, ST 2825, ST-2825

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关于此项目

经验公式(希尔记法):
C27H28Cl2N4O5S
化学文摘社编号:
分子量:
591.51
UNSPSC Code:
51111800
NACRES:
NA.21
MDL number:
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产品名称

ST2825, ≥98% (HPLC)

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

-10 to -25°C

Quality Level

Biochem/physiol Actions

Orally active peptidomimetic MyD88 homodimerization inhibitor with in vitro and in vivo efficacy against IL-1R and TLR9-dependent processes.
ST2825 is an orally active peptidomimetic of a heptapeptide structure in the MyD88 TIR BB-loop. ST2825 prevents IL-1beta-mediated activation of NF-kappaB by blocking MyD88 homodimerization and thereby the recruitment of IL-1 receptor-associated kinases IRAK1/4. ST2825 at 10 µg/mL completely suppresses 2.5 µg/mL TLR9 ligand ODN 2006-induced B-cell plasma cell differentation and antibodies production from PBMCs. ST2825 inhibits IL-1β-induced IL-6 production in mice (100 & 200 mg/kg p.o. prior to 20 µg/kg IL-1β i.p.) and protects against left ventricular (LV) dilatation and hypertrophy (25 mg/kg/day i.p.) in a murine model of nonreperfused acute myocardial infarction (AMI) in vivo.

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

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历史批次信息供参考:

分析证书(COA)

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Pharmacologic inhibition of myeloid differentiation factor 88 (MyD88) prevents left ventricular dilation and hypertrophy after experimental acute myocardial infarction in the mouse
Journal of Cardiovascular Pharmacology, 55(4), 385-390 (2010)
Hong Yao et al.
International immunopharmacology, 36, 132-141 (2016-05-03)
We previously reported the effects of dioscin against carbon tetrachloride-, acetaminophen- and alcohol-induced acute liver damage. However, its effect on lipopolysaccharide (LPS)-induced inflammatory liver injury remains unknown. In the present work, liver injury in mice and rats was induced by
Pivotal Advance: Inhibition of MyD88 dimerization and recruitment of IRAK1 and IRAK4 by a novel peptidomimetic compound
Journal of Leukocyte Biology, 82(4), 801-810 (2007)
Meng Qi et al.
Pharmacological research, 111, 509-522 (2016-07-20)
We previously reported the potent effect of dioscin against renal ischemia/reperfusion injury, but little is known about the role of dioscin in lipopolysaccharide (LPS)-induced inflammatory kidney injury. The present work aimed to investigate the effects and potential mechanisms of dioscin
Short-term MyD88 inhibition ameliorates cardiac graft rejection and promotes donor-specific hyporesponsiveness of skin grafts in mice
Transplant International : Official Journal of the European Society For Organ Transplantation, 29(8), 941-952 (2016)

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