170569-86-5
170569-86-5 結(jié)構(gòu)式
基本信息
4-(5-(4-氯苯基)-3-(三氟甲基)-1H-吡唑-1-基)苯磺酰胺
SC-58236
SC 236 - SC 58236
4-[5-(4-CHLOROPHENYL)-3-(TRIFLUOROMETHYL)PYRAZOL-1-YL]BENZENESULFONAMIDE
4-[5-(4-CHLOROPHENYL)-3-(TRIFLUOROMETHYL)-1H-PYRAZOL-1-YL]BENZENESULFONAMIDE
Benzenesulfonamide, 4-[5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-
物理化學(xué)性質(zhì)
| 報(bào)價(jià)日期 | 產(chǎn)品編號(hào) | 產(chǎn)品名稱 | CAS號(hào) | 包裝 | 價(jià)格 |
| 2024/08/19 | HY-W010983 | 4-(5-(4-氯苯基)-3-(三氟甲基)-1H- SC-236 | 170569-86-5 | 5mg | 800元 |
| 2024/08/19 | HY-W010983 | 4-(5-(4-氯苯基)-3-(三氟甲基)-1H- SC-236 | 170569-86-5 | 10mM * 1mLin DMSO | 880元 |
| 2024/08/19 | HY-W010983 | 4-(5-(4-氯苯基)-3-(三氟甲基)-1H- SC-236 | 170569-86-5 | 10mg | 1200元 |
常見問題列表
|
COX-2 10 nM (IC 50 ) |
COX-1 17.8 μM (IC 50 ) |
SC-236 (15 μM, 30 min) suppresses the side effects of NSAIDs and prevented inflammation in vECs subjected to ALSS.
SC-236 significantly induces PPARγ expression in HSCs and acted as a potent PPARγ agonist in a luciferase-reporter trans-activation assay.
SC-236 strongly inhibits, in a time- and concentration-dependent manner, macrophage
viability.
SC-236, either alone or in combination with 15d-PGJ2, induced a marked pro-apoptotic effect in HSCs in culture.
SC-236 mediates antitumor effect by modulation of AP-1-signaling pathway.
Western Blot Analysis
| Cell Line: | vECs. |
| Concentration: | 15 μM |
| Incubation Time: | 30 min. |
| Result: | Showd significant reduction in COX-2 level and increase in IκBα level, thus preventing ALSS-induced NFκB activation and inflammation in vECs. |
Western Blot Analysis
| Cell Line: | COS 7 cells. |
| Concentration: | 3 and 10 μM. |
| Incubation Time: | 18 h (combined with 15d-PGJ 2 ). |
| Result: | Acted in a concentration-dependent manner as a PPARγ agonist. |
SC-236 (6 mg/kg, gavage) exhibits anti-fibrotic properties in CCl4- treated animals.
| Animal Model: | Seventy-six male adult Wistar rats weighing 200-220 g (CCl 4 -treated). |
| Dosage: | 6 mg/kg. |
| Administration: | Orally, 3 times per week. |
| Result: |
A marked induction of COX-2 protein expression was detected by immunohistochemistry in the liver of CCl4-treated rats.
Significantly reduced the degree of liver fibrosis. Dramatically suppressed α-SMA expression in CCl4-treated rats. |