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SC-236

  Cat. No.:  DC21629   Featured
Chemical Structure
170569-86-5
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More than 5000 active chemicals with high quality for research!
Field of application
SC-236 (SC58236) is a potent, selective, orally active inhibitor of COX-2 with IC50 of 10 nM.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 170569-86-5
Chemical Name: 4-[5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-benzenesulfonamide
Synonyms: SC236;SC58236;SC 236
SMILES: O=S(C1=CC=C(N2N=C(C(F)(F)F)C=C2C3=CC=C(Cl)C=C3)C=C1)(N)=O
Formula: C16H11ClF3N3O2S
M.Wt: 401.79
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: SC-236 is an orally active COX-2 specific inhibitor (IC50 = 10 nM) and a PPARγ agonist. SC-236 suppresses activator protein-1 (AP-1) through c-Jun NH2-terminal kinase. SC-236 exerts anti-inflammatory effects by suppressing phosphorylation of ERK in a murine model[1][2][3][4][5].
Target: COX-2:10 nM (IC50) COX-1:17.8 μM (IC50)
In Vivo: SC-236 (6 mg/kg, gavage) exhibits anti-fibrotic properties in CCl4- treated animals[2]. Animal Model: Seventy-six male adult Wistar rats weighing 200-220 g (CCl4-treated)[2]. 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.
In Vitro: SC-236 (15 μM, 30 min) suppresses the side effects of NSAIDs and prevented inflammation in vECs subjected to ALSS[1]. SC-236 significantly induces PPARγ expression in HSCs and acted as a potent PPARγ agonist in a luciferase-reporter trans-activation assay[2]. SC-236 strongly inhibits, in a time- and concentration-dependent manner, macrophageviability[2]. SC-236, either alone or in combination with 15d-PGJ2, induced a marked pro-apoptotic effect in HSCs in culture[2]. SC-236 mediates antitumor effect by modulation of AP-1-signaling pathway[3]. Western Blot Analysis[1] 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[2] Cell Line: COS 7 cells. Concentration: 3 and 10 μM. Incubation Time: 18 h (combined with 15d-PGJ2). Result: Acted in a concentration-dependent manner as a PPARγ agonist.
References: [1]. Shao-Yu Fang, et al. Reduction in MicroRNA-4488 Expression Induces NFκB Translocation in Venous Endothelial Cells Under Arterial Flow. Cardiovasc Drugs Ther. 2020 Sep 9. [2]. Anna Planagumà, et al. The selective cyclooxygenase-2 inhibitor SC-236 reduces liver fibrosis by mechanisms involving non-parenchymal cell apoptosis and PPARgamma activation. FASEB J. 2005 Jul;19(9):1120-2. [3]. Benjamin Chun-Yu Wong, et al. Cyclooxygenase-2 inhibitor (SC-236) suppresses activator protein-1 through c-Jun NH2-terminal kinase. Gastroenterology. 2004 Jan;126(1):136-47. [4]. Su-Jin Kim, et al. The COX-2 inhibitor SC-236 exerts anti-inflammatory effects by suppressing phosphorylation of ERK in a murine model. Life Sci. 2007 Aug 23;81(11):863-72. [5]. T D Penning, et al. Synthesis and biological evaluation of the 1,5-diarylpyrazole class of cyclooxygenase-2 inhibitors: identification of 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benze nesulfonamide (SC-58635, celecoxib). J Med Chem. 1997 Apr 25;40(9):1347-65.
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