- ￥340 - 3790
- Solarbio
- 北京
- IK0080
- 2025年10月10日
企业认证
相关产品推荐更多 >
万千商家帮你免费找货
0 人在求购买到急需产品
- 详细信息
- 文献和实验
- 技术资料
- 保存条件：
Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 保质期：
Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 英文名：
KM11060
- 库存：
现询
- 供应商：
北京索莱宝科技有限公司
- CAS号：
774549-97-2
- 规格：
100mg/50mg/25mg/5mg/10mg
| 规格： | 100mg | 产品价格： | ￥3790.0 |
|---|---|---|---|
| 规格： | 50mg | 产品价格： | ￥2190.0 |
| 规格： | 25mg | 产品价格： | ￥1190.0 |
| 规格： | 5mg | 产品价格： | ￥340.0 |
| 规格： | 10mg | 产品价格： | ￥590.0 |
| 基本信息 | |
| CAS | No.774549-97-2 |
| 中文名称 | 7-氯-4-[4-[(4-氯苯基)磺酰基]-1-哌嗪基]C9H7N |
| 英文名称 | KM11060 |
| 别名 | 7-chloro-4-[4-(4-chlorophenyl)sulfonylpiperazin-1-yl]quinoline |
| 分子式 | C19H17Cl2N3O2S |
| 分子量 | 422.33 |
| 溶解性 | Soluble in DMSO |
| 纯度 | ≥98% |
| 外观(性状) | White to off-white Solid |
| 货期 | 1-2个工作日 |
| 储存条件 | Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year |
| 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 |
| 靶点 | CFTR |
| 通路 | Membrane Transporter&Ion Channel |
| 背景说明 | KM11060是F508del-CFTR转运缺陷的新型校正剂,可校正F508del-CFTR转运,增加质膜上功能性CFTR表达。 |
| 生物活性 | 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] |
| 细胞实验 | 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] |
| 数据来源文献 | [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. |
| 单位 | 瓶 |
风险提示：丁香通仅作为第三方平台，为商家信息发布提供平台空间。用户咨询产品时请注意保护个人信息及财产安全，合理判断，谨慎选购商品，商家和用户对交易行为负责。对于医疗器械类产品，请先查证核实企业经营资质和医疗器械产品注册证情况。
文献和实验梯度（浓度差）（表4-1）、驱动相应离子经过当时开放的细胞膜上特殊离子通道的跨膜扩散，是心肌细胞跨膜电位形成的主要基础，只是由于心肌细胞膜上具有数目较多的离子通道，跨膜电位形成机制中涉及的离子流远比骨骼肌要复杂得多。在电生理学中，电流的方向以正离子在膜两侧的流动方向来命名，正离子外流或负离子内流称外向电流，正离子内流或负离子外流称内向电流。外向电流导致膜内电位向负电性转化，促使膜复极，内向电流导致膜内电位向正电性转化，促使膜除极。 表4-1 心肌细胞中各种主要离子的浓度及平衡电位值
0SoyuWjNKRFlNUuWkgaZA/ixqklm1l/vs6zKrdWyls+m9KIAfxdyEH7qTTSO9buLMbM/QIp9V38iSQ5IxN83EoFIkt9INGNeEYGIQEQgInDgIiCC15AJQlqEs5nul4a0aY8uecHee8mHbYhMC9I6U631iTA27ef3PGQTJ44TEa5bK2YQIqcF/aREMeuyj6imCuKBWetVfhDNotNU2TD3S4srLbIYp+yBIc0ik05ma1ba0W2f/9yX7J//5dv20qpN9tX//hX7zg//j
atS1S/3CjjEmCD04y7twlaWbvWLdC8dXvKVqmN0aNGolOXrjh6+BCOnzydpMRuIldL/949YWRkhG07diZoTlyZCTCBlCcgXGtFdtp8+fIleTBxdFulSmW4kPGqsP0IK6oUF+Tc2bNJProN64//pn8CrPlI/3uYLCuoULkqnlPcDTOz+jh4+CiuXrqItes3JEnwENlpx4wagZw5c2LLNqtkmSd3wgSYQPISEHYeySF4iFnlypULV65c
技术资料暂无技术资料 索取技术资料
