SC-236

Names

[ Name ]:
SC-236

[Synonym ]:
Benzenesulfonamide, 4-[5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-
HMS3262A06
4-[5-(4-Chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-benzenesulfonamide SC-58236
Tracazolate hydrochloride
SC236
4-[5-(4-chorophenyl)-3-(trifluoromethyl)-1H-pyrazole-1-yl]benzenesulfonamide
4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-yl)benzenesulfonamide
4-[5-(4-Chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzenesulfonamide
4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide

Biological Activity

[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].

[Related Catalog]:

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

Research Areas >> Cardiovascular Disease

Signaling Pathways >> Cell Cycle/DNA Damage >> PPAR

Research Areas >> Inflammation/Immunology

Signaling Pathways >> Immunology/Inflammation >> COX

[Target]

COX-2:10 nM (IC50)

COX-1:17.8 μM (IC50)

[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.

[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.

[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.

Chemical & Physical Properties

[ Density]:
1.5±0.1 g/cm3

[ Boiling Point ]:
543.4±60.0 °C at 760 mmHg

[ Molecular Formula ]:
C₁₆H₁₁ClF₃N₃O₂S

[ Molecular Weight ]:
401.791

[ Flash Point ]:
282.4±32.9 °C

[ Exact Mass ]:
401.021271

[ PSA ]:
86.36000

[ LogP ]:
4.32

[ Vapour Pressure ]:
0.0±1.5 mmHg at 25°C

[ Index of Refraction ]:
1.625

Safety Information

[ Symbol ]:

GHS06

[ Signal Word ]:
Danger

[ Hazard Statements ]:
H301

[ Precautionary Statements ]:
P301 + P310

[ RIDADR ]:
UN 2811 6.1 / PGIII

[ HS Code ]:
2935009090

Customs

[ HS Code ]: 2935009090

[ Summary ]:
2935009090 other sulphonamides VAT:17.0% Tax rebate rate:9.0% Supervision conditions:none MFN tariff:6.5% General tariff:35.0%

Articles

Downregulation of sphingosine 1-phosphate (S1P) receptor 1 by dexamethasone inhibits S1P-induced mesangial cell migration.

Biol. Chem. 396 , 803-12, (2015)

Sphingosine 1-phosphate (S1P) is generated by sphingosine kinase (SK)-1 and -2 and acts mainly as an extracellular ligand at five specific receptors, denoted S1P1-5. After activation, S1P receptors re...

Inhibition of COX-1 attenuates the formation of thromboxane A2 and ameliorates the acute decrease in glomerular filtration rate in endotoxemic mice.

Am. J. Physiol. Renal Physiol. 309 , F332-40, (2015)

Thromboxane (Tx) A2 has been suggested to be involved in the development of sepsis-induced acute kidney injury (AKI). Therefore, we investigated the impact of cyclooxygenase (COX)-1 and COX-2 activity...

COX-2 gene dosage-dependent defects in kidney development.

Am. J. Physiol. Renal Physiol. 310 , F1113-22, (2016)

Deletion of cyclooxygenase (COX)-2 causes impairment of kidney development, including hypothrophic glomeruli and cortical thinning. A critical role for COX-2 is seen 4-8 days postnatally. The present ...

Related Compounds

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