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Merck
CN
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安全信息

SML3596

Sigma-Aldrich

Losmapimod

≥98% (HPLC)

别名:

6-[5-(Cyclopropylcarbamoyl)-3-fluoro-2-methylphenyl]-N-(2,2-dimethylpropyl)nicotinamide, 6-[5-(cyclopropylcarbamoyl)-3-fluoro-2-methylphenyl]-N-(2,2-dimethylpropyl)pyridine-3-carboxamide, 6-{5-[(cyclopropylamino)carbonyl]-3-fluoro-2-methylphenyl}-N-(2,2-dimethylpropyl)-3-pyridinecarboxamide, CID 11552706, GSK-AHAB, GW856553X, SB 856553

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About This Item

经验公式（希尔记法）:
C22H26FN3O2
CAS号:
585543-15-3
分子量:
383.46
MDL编号:
MFCD16619322
UNSPSC代码:
12352200
NACRES:
NA.77

质量水平

100

方案

≥98% (HPLC)

表单

powder

颜色

white to beige

溶解性

DMSO: 2 mg/mL, clear

储存温度

2-8°C

SMILES字符串

O=C(NCC(C)(C)C)C1=CC=C(C2=C(C)C(F)=CC(C(NC3CC3)=O)=C2)N=C1

InChI

1S/C22H26FN3O2/c1-13-17(9-15(10-18(13)23)21(28)26-16-6-7-16)19-8-5-14(11-24-19)20(27)25-12-22(2,3)4/h5,8-11,16H,6-7,12H2,1-4H3,(H,25,27)(H,26,28)

InChI key

KKYABQBFGDZVNQ-UHFFFAOYSA-N

生化/生理作用

Losmapimod is a potent and selective inhibitor of the p38 mitogen-activated protein kinases (MAPK) family. In SHR-SP rats losmapimod improves survival, endothelial-dependent and -independent vascular relaxation. Also losmapimod attenuates dyslipidemia, hypertension, cardiac remodeling, plasma renin activity (PRA), aldosterone, and interleukin-1 (IL-1 ). Losmapimod produces antidepressant and antipsychotic effects.
Potent and selective inhibitor of the p38 mitogen-activated protein kinases (MAPK) family; p38 inhibitor

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

新产品

历史批次信息供参考:

分析证书(COA)

Lot/Batch Number
0000220790
0000220789
0000213396
0000213396
0000220790

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Inhibition of p38 mitogen-activated protein kinase improves nitric oxide-mediated vasodilatation and reduces inflammation in hypercholesterolemia
Cheriyan J
Circulation, 123, 515-523 (2011)
Nicola M Aston et al.
Journal of medicinal chemistry, 52(20), 6257-6269 (2009-09-24)
p38alpha MAP kinase is a key anti-inflammatory target for rheumatoid arthritis, influencing biosynthesis of pro-inflammatory cytokines TNFalpha and IL-1beta at a translational and transcriptional level. In this paper, we describe how we have optimized a series of novel p38alpha/beta inhibitors

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