KM 11060

A F508del-CFTR corrector

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10mg

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货号: ajci14070
CAS: 774549-97-2
别名: 7-氯-4-[4-[(4-氯苯基)磺酰基]-1-哌嗪基]喹啉
分子式: C19H17Cl2N3O2S
分子量: 422.33
纯度: >98%
溶解度: DMF: 5 mg/ml,DMSO: 2 mg/ml,Ethanol: 0.5 mg/ml
储存: Store at RT
库存: 现货

Background

KM11060 is a novel corrector of the F508del-CFTR trafficking defect.Target: CFTRin vitro: Small-molecule correctors such as KM11060 may serve as useful pharmacological tools in studies of the F508del-CFTR processing defect and in the development of cystic fibrosis therapeutics. KM11060 rescues F508del-CFTR trafficking in cultured cells and native epithelial tissues. KM11060 partially corrects F508del-CFTR processing and increases surface expression to 75% of that observed in cells incubated at low temperature. Up to 50% of the F508del-CFTR in cells treated with KM11060 was complex-glycosylated, indicating passage through the Golgi. KM11060 as a promising compound for further development of CF therapeutics. [1]in vivo: In LPS-induced acute lung inflammation, blockade of PSGL-1 (P-selectin glycoprotein ligand-1) or P-selectin, antagonism of PAF by WEB2086, or correction of mutated CFTR trafficking by KM11060 could significantly increase plasma lipoxin A4 levels in F508del relevant to wildtype mice. [2]

参考文献:
[1]. Robert R, et al. Structural analog of sildenafil identified as a novel corrector of the F508del-CFTR trafficking defect. Mol Pharmacol. 2008 Feb;73(2):478-89.
[2]. Wu H, et al. Lipoxin A4 and platelet activating factor are involved in E. coli or LPS-induced lung inflammation in CFTR-deficient mice. PLoS One. 2014 Mar 26;9(3):e93003.