| CAS |
774549-97-2 |
| Chinese Name |
7-氯-4-[4-[(4-氯苯基)磺酰基]-1-哌嗪基]喹啉 |
| English Name |
KM11060 |
| Synonyms |
7-chloro-4-[4-(4-chlorophenyl)sulfonylpiperazin-1-yl]quinoline |
| Molecular Formula |
C19H17Cl2N3O2S |
| Molecular Weight |
422.33 |
| Solubility |
Soluble in DMSO |
| Purity |
≥98% |
| Appearance |
White to off-white Solid |
| Storage |
Powder:-20℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year |
| Delivery Time |
1-2 Days |
| MDL |
MFCD01524977 |
| SMILES |
O=S(N1CCN(C2=CC=NC3=CC(Cl)=CC=C23)CC1)(C4=CC=C(Cl)C=C4)=O |
| InChIKey |
GIEHIZKCIZLXLF-UHFFFAOYSA-N |
| InChI |
InChI=1S/C19H17Cl2N3O2S/c20-14-1-4-16(5-2-14)27(25,26)24-11-9-23(10-12-24)19-7-8-22-18-13-15(21)3-6-17(18)19/h1-8,13H,9-12H2 |
| PubChem CID |
1241327 |
| Target Point |
CFTR |
| Passage |
Membrane Transporter&Ion Channel |
| Background |
KM11060, a novel corrector of F508del-CFTR transport deficiency, corrects F508del-CFTR transport and increases functional CFTR expression at the plasma membrane. |
| Biological Activity |
KM11060 is a corrector of the F508 deletion (F508del)-cystic fibrosis transmembrane conductance regulator (CFTR) trafficking defect. KM11060 can be used for the research of F508del-CFTR processing defect and development of cystic fibrosis research[1]. |
| In 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] |
| Data Literature Source |
[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. |
| Unit |
Bottle |
| Specification |
10mg 10mM*1mL in DMSO |
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