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500363-63-3

中文名稱 化合物 T12260
英文名稱 NSC117079
CAS 500363-63-3
分子式 C20H15N3O7S2
分子量 473.48
MOL 文件 500363-63-3.mol
更新日期 2026/03/06 10:49:55
500363-63-3 結(jié)構(gòu)式 500363-63-3 結(jié)構(gòu)式

基本信息

中文別名
化合物 T12260
英文別名
NSC117079
NSC-117079,NSC117079
2-Anthracenesulfonic acid, 1-amino-4-[[3-(aminosulfonyl)phenyl]amino]-9,10-dihydro-9,10-dioxo-

物理化學(xué)性質(zhì)

密度1.696±0.06 g/cm3(Predicted)
儲(chǔ)存條件-20°C儲(chǔ)存
溶解度DMSO: 50 mg/mL (105.60 mM)
酸度系數(shù)(pKa)-1.19±0.20(Predicted)
形態(tài)Solid
顏色Pale purple to purple

安全數(shù)據(jù)

危險(xiǎn)性符號(hào)(GHS)有害 (GHS07)
GHS07
警示詞警告
危險(xiǎn)性描述H302-H315-H319-H335
防范說(shuō)明P261-P305+P351+P338
化合物 T12260價(jià)格(試劑級(jí))
報(bào)價(jià)日期產(chǎn)品編號(hào)產(chǎn)品名稱CAS號(hào)包裝價(jià)格
2026/06/05HY-19819化合物 T12260
NSC117079
500363-63-31 mg863元
2026/06/05HY-19819化合物 T12260
NSC117079
500363-63-35mg1600元
2026/06/05HY-19819化合物 T12260
NSC117079
500363-63-310mM * 1mLin DMSO1667元

常見問(wèn)題列表

生物活性
NSC117079是新型的 PHLPP 抑制劑。
靶點(diǎn)

PHLPP

體外研究

NSC-117079 at 30 μM induces neutrophil adhesion to plated fibrinogen from 9.0±2.4% to 27.0±8.0% and enhanced neutrophil adhesion caused by 50 ng/mL GM-CSF from 22.9±6.0% to 47.6±10.9%. Neutrophil adhesion is followed by neutrophil transendothelial migration. Results suggest that PHLPP inhibitor NSC-117079 is effective in preventing Akt from dephosphorylation in neutrophils, and Akt phosphatase PHLPP serves to attenuate neutrophil adhesion but not migration.

體內(nèi)研究

A single intraarticular injection of the Phlpp inhibitor NSC117079 attenuates mechanical allodynia and slows articular cartilage degradation in joints with a destabilized meniscus. Animals treated with the Phlpp inhibitor seven weeks after injury maintain normal activity levels, while those in the control group travel shorter distances and are less active three months after the joint injury. NSC117079 also increases production of cartilage extracellular matrix components (glycosaminoglycans and aggrecan) in over 90% of human articular cartilage explants from osteoarthritis patients and increased phosphorylation of Phlpp1 substrates (AKT2, ERK1/2 and PKC) in human articular chondrocytes.

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