4-(5-(4-氯苯基)-3-(三氟甲基)-1H-

生物活性靶点体外研究体内研究 4-(5-(4-氯苯基)-3-(三氟甲基)-1H- 试剂级价格

CAS号:170569-86-5
英文名:4-[5-(4-CHLOROPHENYL)-3-(TRIFLUOROMETHYL)-1H-PYRAZOL-1-YL]BENZENESULFONAMIDE
中文名:4-(5-(4-氯苯基)-3-(三氟甲基)-1H-
CBNumber:CB3243082
分子式:C16H11ClF3N3O2S
分子量:401.79
MOL File:Mol file

4-(5-(4-氯苯基)-3-(三氟甲基)-1H-化学性质

熔点 :146-148°C
沸点 :543.4±60.0 °C(Predicted)
密度 :1.54±0.1 g/cm3(Predicted)
储存条件 :2-8°C
溶解度 :DMSO: >20mg/mL
形态 :powder
酸度系数(pKa) :9.66±0.10(Predicted)
颜色 :white to off-white

安全信息

危险品标志 :T
危险类别码 :25
安全说明 :45
危险品运输编号 :UN 2811 6.1 / PGIII
WGK Germany :3

4-(5-(4-氯苯基)-3-(三氟甲基)-1H-性质、用途与生产工艺

生物活性 SC-236 是具有口服活性的 COX-2 特异性抑制剂 (对 COX-1 的 IC50 值为 10 nM)和 PPARγ 激动剂。SC-236 可通过 c-Jun 氨基端抑制激活蛋白-1 (AP-1) 活性。SC-236在小鼠模型中通过抑制 ERK 的磷酸化发挥抗炎作用。
靶点

COX-2

10 nM (IC ₅₀ )

COX-1

17.8 μM (IC ₅₀ )

体外研究

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.

体内研究

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.