KM11060 corrects the F508del-CFTR trafficking defect, also shows inhibition on PDE5 activity.
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产品名称 | CFTR ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Ataluren | ✔ | 98% | |||||||||||||||||
Lumacaftor |
++++
F508del-CFTR, EC50: 0.1 μM |
98% | |||||||||||||||||
CFTR(inh)-172 |
+++
CFTR, Ki: 300 nM |
99%+ | |||||||||||||||||
GlyH-101 |
+
CFTR, Ki: 4.3 μM |
99%+ | |||||||||||||||||
IOWH-032 |
++
CFTR, IC50: 1.01 μM |
99%+ | |||||||||||||||||
Tezacaftor | ✔ | 99%+ | |||||||||||||||||
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 |
描述 | KM11060 is a corrective agent for the F508 deletion (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR), aiming to address the trafficking malfunction associated with this mutation. This compound has applications in researching the F508del-CFTR processing anomaly and contributes to the advancement of cystic fibrosis studies[1]. |
Animal study | In the context of LPS-induced acute lung inflammation, interventions like PSGL-1 (P-selectin glycoprotein ligand-1) or P-selectin blockade, PAF antagonism with WEB2086, or the amendment of mutated CFTR trafficking with KM11060 significantly elevate plasma lipoxin A4 concentrations in F508del compared to wildtype mice, suggesting potential therapeutic strategies[2]. |
计算器 | ||||
存储液制备 | ![]() |
1mg | 5mg | 10mg |
1 mM 5 mM 10 mM |
2.37mL 0.47mL 0.24mL |
11.84mL 2.37mL 1.18mL |
23.68mL 4.74mL 2.37mL |
CAS号 | 774549-97-2 |
分子式 | C19H17Cl2N3O2S |
分子量 | 422.33 |
SMILES Code | O=S(N1CCN(C2=CC=NC3=CC(Cl)=CC=C23)CC1)(C4=CC=C(Cl)C=C4)=O |
MDL No. | MFCD01524977 |
别名 | |
运输 | 蓝冰 |
InChI Key | GIEHIZKCIZLXLF-UHFFFAOYSA-N |
Pubchem ID | 1241327 |
存储条件 |
In solvent -20°C:3-6个月-80°C:12个月 Pure form Keep in dark place, inert atmosphere, room temperature |