| CAS NO: | 353262-04-1 |
| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| Cas No. | 353262-04-1 |
| 化学名 | 4-(3-(trifluoromethyl)benzyl)-2H-benzo[b][1,4]thiazin-3(4H)-one |
| Canonical SMILES | FC(F)(C1=CC(CN2C3=CC=CC=C3SCC2=O)=CC=C1)F |
| 分子式 | C16H12F3NOS |
| 分子量 | 323.33 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,DMSO:PBS (pH 7.2) (1:1): 0.5 mg/ml,Ethanol: 20 mg/ml |
| 储存条件 | Store at -20℃ |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
| 产品描述 | IC50: 9, 14 and 15 nM for rat, human and mouse erythrocyte KCa3.1 channels, respectively. NS 6180 is a potent KCa3.1 channel blocker. KCa3.1 (the Ca2+-activated K+ channel, encoded by the KCNN4 gene) plays a key role in these processes by participating in the regulation of calcium entry. In vitro: NS6180 blocked cloned human KCa3.1 channels via T250 and V275, while the same amino acid residues conferred sensitivity to triarylmethanes such as like TRAM-34. NS6180 blocked endogenously expressed KCa3.1 channels in human, mouse and rat erythrocytes with similar potencies. Rat and mouse splenocyte proliferation was suppressed NS6180 at submicrolar concentrations, which potently inhibited IL-2 and IFN-g production, exerting smaller effects on IL-4 and TNF-a and no effect on IL-17 production. After induction of colitis, antibody staining exhibited KCa3.1 channels in healthy colon and strong up-regulation in association with infiltrating immune cells [1]. In vivo: Despite poor plasma exposure, NS6180 (3 and 10 mg·kg-1 b.i.d.) abolished colon inflammation and improved body weight gain effectively, just as the standard IBD drug sulfasalazine (300 mg·kg-1 q.d.). The benzothiazinone NS6180 was potent on recombinant and endogenously expressed KCa3.1 channels, selectivity and molecular site of action. Furthermore, the effect of NS6180 characterize its pharmacokinetics on the activity of T-lymphocytes from wild-type and KCa3.1–/– knockout mice and show that it abolishes inflammation in an animal model of IBD [1]. Clinical trial: So far, no clinical study has been conducted. Reference: |
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