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Key Documents

PZ0106

Sigma-Aldrich

SC-236

≥98% (HPLC)

Synonym(s):

4-[5-(4-Chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-benzenesulfonamide, SC-58236

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About This Item

Empirical Formula (Hill Notation):
C16H11ClF3N3O2S
CAS Number:
Molecular Weight:
401.79
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

Assay

≥98% (HPLC)

form

powder

color

white to off-white

solubility

DMSO: >20 mg/mL

storage temp.

2-8°C

SMILES string

NS(=O)(=O)c1ccc(cc1)-n2nc(cc2-c3ccc(Cl)cc3)C(F)(F)F

InChI

1S/C16H11ClF3N3O2S/c17-11-3-1-10(2-4-11)14-9-15(16(18,19)20)22-23(14)12-5-7-13(8-6-12)26(21,24)25/h1-9H,(H2,21,24,25)

InChI key

NSQNZEUFHPTJME-UHFFFAOYSA-N

Application

SC-236 has been used as a COX-2 inhibitor to study its effects on the mechano-reflex in rats.

Biochem/physiol Actions

SC-236 exhibits anti-tumor activity in gastric cancer cells by modulating activator protein-1 (AP-1) expression and by blocking the anchorage-independent cell growth. It also exhibits a protective effect against cartilage damage by minimizing the inflammation and pain in osteoarthritis. It is also reported to treat allergic inflammation.
SC-236 is a cyclooxygenase-2 (COX-2) inhibitor.

Pictograms

Skull and crossbones

Signal Word

Danger

Hazard Statements

Hazard Classifications

Acute Tox. 3 Oral

Storage Class Code

6.1C - Combustible, acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Hae-Kyoung Kim et al.
International archives of allergy and immunology, 171(1), 61-70 (2016-11-14)
Cytosolic phospholipase A2 (cPLA2) plays a key role in the development of late-phase anaphylaxis. L-Glutamine (Gln), a nonessential amino acid, has anti-inflammatory activity via inhibiting cPLA2. We used a penicillin-induced murine model of anaphylaxis, and late-phase anaphylaxis was quantified by
Patrick Slattery et al.
American journal of physiology. Renal physiology, 310(10), F1113-F1122 (2016-03-18)
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 study was aimed at answering whether different COX-2 gene dosage and partial pharmacological
Valerie P O'Brien et al.
Nature microbiology, 2, 16196-16196 (2016-11-01)
Recurrent bacterial infections are a significant burden worldwide, and prior history of infection is often a significant risk factor for developing new infections. For urinary tract infection (UTI), a history of two or more episodes is an independent risk factor
Manuel Meurer et al.
Pflugers Archiv : European journal of physiology, 470(11), 1691-1703 (2018-07-22)
Endotoxemia-related acute kidney injury (AKI) is associated with increased formation of prostaglandins, which may serve as a compensatory mechanism to maintain renal function. We hypothesized that an increase of renal EP2 or EP4 receptors and/or a downregulation of renal EP1
B R Silva et al.
European journal of pharmacology, 814, 87-94 (2017-08-07)
In this work, we hypothesized that cyclooxygenase (COX) activity can be regulated by nitric oxide (NO) and hydrogen peroxide (H

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