KM11060

Research use only, not for human use.

A potent corrector of the F508del-CFTR trafficking defect that partially restores F508del trafficking and increases maturation significantly in BHK cells.

A potent corrector of the F508del-CFTR trafficking defect that partially restores F508del trafficking and increases maturation significantly in BHK cells (10 nM for 24 h or 10 uM for 2 h); also can significantly increase plasma lipoxin A4 levels in F508del relevant to wildtype mice.

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.

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.

KM 11060 | KM-11060

Apoptosis

CFTR

CFTR

Endocrinology

——

774549-97-2

422.3282

C19H17Cl2N3O2S

>98% (HPLC)

10 mM in DMSO

O=S(N1CCN(C2=CC=NC3=CC(Cl)=CC=C23)CC1)(C4=CC=C(Cl)C=C4)=O

Quinoline, 7-chloro-4-[4-[(4-chlorophenyl)sulfonyl]-1-piperazinyl]-

(-20℃)

With Ice Pack

≥ 2 years