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SC-236

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Identification

Generic Name
SC-236
DrugBank Accession Number
DB14059
Background

SC-236 is a potent, selective, orally active inhibitor of cyclooxygenase-2 (COX-2) 12 that has been studied in cancer therapy 3, lower back pain 4, and inflammation 1, 2,11, 5.

Type
Small Molecule
Groups
Experimental, Investigational
Structure
3D
Similar Structures
Weight
Average: 401.79
Monoisotopic: 401.02126
Chemical Formula
C16H11ClF3N3O2S
Synonyms
Not Available
External IDs
  • SC 236
  • SC-236
  • SC236
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Pharmacology

Indication

Not Available

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Pharmacodynamics

Not Available

Mechanism of action

This drug is a selective inhibitor of the COX-2 enzyme 2, 3. COX-2 is expressed in the brain, in the kidney, in bone, and likely in the female reproductive system 14. Its expression at other sites is increased during inflammation, experimentally, in response to mitogenic stimuli. Growth factors, phorbol esters, and interleukin (IL)-1 stimulate the expression of COX-2 in fibroblasts, while endotoxin serves the same function in monocytes/macrophages 14.

SC-236 works also directly through suppressing the nuclear translocation of RelA/p65, a transcription factor. SC-236 directly targets proteins that facilitate the nuclear translocation of NF-κB, an inflammatory signaling pathway 2, 8.

TargetActionsOrganism
ACyclooxygenase 2
inhibitor
Canis lupus familiaris
AProstaglandin G/H synthase 2
inhibitor
Humans
ANuclear factor NF-kappa-B complex
inhibitor
Humans
Absorption

Not Available

Volume of distribution

Not Available

Protein binding

Not Available

Metabolism
Not Available
Route of elimination

Not Available

Half-life

Long plasma half-life 6.

Clearance

Not Available

Adverse Effects
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Toxicity

Not Available

Pathways
Not Available
Pharmacogenomic Effects/ADRs
Not Available

Interactions

Drug Interactions
This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
DrugInteraction
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interactions in your software
AbacavirSC-236 may decrease the excretion rate of Abacavir which could result in a higher serum level.
AbciximabThe risk or severity of bleeding and hemorrhage can be increased when SC-236 is combined with Abciximab.
AcebutololSC-236 may decrease the antihypertensive activities of Acebutolol.
AceclofenacThe risk or severity of adverse effects can be increased when Aceclofenac is combined with SC-236.
AcemetacinThe risk or severity of adverse effects can be increased when Acemetacin is combined with SC-236.
Food Interactions
Not Available

Categories

Drug Categories
Classification
Not classified
Affected organisms
Not Available

Chemical Identifiers

UNII
9HGW1H8S2M
CAS number
170569-86-5
InChI Key
NSQNZEUFHPTJME-UHFFFAOYSA-N
InChI
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)
IUPAC Name
4-[5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzene-1-sulfonamide
SMILES
NS(=O)(=O)C1=CC=C(C=C1)N1N=C(C=C1C1=CC=C(Cl)C=C1)C(F)(F)F

References

General References
  1. Kim SJ, Jeong HJ, Moon PD, Myung NY, Kim MC, Kang TH, Lee KM, Park RK, So HS, Kim EC, An NH, Um JY, Kim HM, Hong SH: 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. doi: 10.1016/j.lfs.2007.06.027. Epub 2007 Sep 5. [Article]
  2. Kim SJ, Jeong HJ, Choi IY, Lee KM, Park RK, Hong SH, Kim HM: Cyclooxygenase-2 inhibitor SC-236 [4-[5-(4-chlorophenyl)-3-(trifluoromethyl)-1-pyrazol-1-l] benzenesulfonamide] suppresses nuclear factor-kappaB activation and phosphorylation of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase, and c-Jun N-terminal kinase in human mast cell line cells. J Pharmacol Exp Ther. 2005 Jul;314(1):27-34. doi: 10.1124/jpet.104.082792. Epub 2005 Mar 22. [Article]
  3. Wong BC, Jiang XH, Lin MC, Tu SP, Cui JT, Jiang SH, Wong WM, Yuen MF, Lam SK, Kung HF: Cyclooxygenase-2 inhibitor (SC-236) suppresses activator protein-1 through c-Jun NH2-terminal kinase. Gastroenterology. 2004 Jan;126(1):136-47. [Article]
  4. Deleo TA, Hashizume H, Rutkowski MD, Weinstein TN: Cyclooxygenase-2 inhibitor SC-236 attenuates mechanical allodynia following nerve root injury in rats. J Orthop Res. 2000 Nov;18(6):977-82. doi: 10.1002/jor.1100180618. [Article]
  5. Jiang XH, Lam SK, Lin MC, Jiang SH, Kung HF, Slosberg ED, Soh JW, Weinstein IB, Wong BC: Novel target for induction of apoptosis by cyclo-oxygenase-2 inhibitor SC-236 through a protein kinase C-beta(1)-dependent pathway. Oncogene. 2002 Sep 5;21(39):6113-22. doi: 10.1038/sj.onc.1205778. [Article]
  6. Penning TD, Talley JJ, Bertenshaw SR, Carter JS, Collins PW, Docter S, Graneto MJ, Lee LF, Malecha JW, Miyashiro JM, Rogers RS, Rogier DJ, Yu SS, AndersonGD, Burton EG, Cogburn JN, Gregory SA, Koboldt CM, Perkins WE, Seibert K, Veenhuizen AW, Zhang YY, Isakson PC: 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. [Article]
  7. Dai Y, Wang WH: Non-steroidal anti-inflammatory drugs in prevention of gastric cancer. World J Gastroenterol. 2006 May 14;12(18):2884-9. [Article]
  8. Wong BC, Jiang Xh, Fan XM, Lin MC, Jiang SH, Lam SK, Kung HF: Suppression of RelA/p65 nuclear translocation independent of IkappaB-alpha degradation by cyclooxygenase-2 inhibitor in gastric cancer. Oncogene. 2003 Feb 27;22(8):1189-97. doi: 10.1038/sj.onc.1206234. [Article]
  9. Randall E. Harris (2002). COX-2 Blockade in Cancer Prevention and Therapy. Humana Press.
  10. Luka Milas, K. K Ang, C. Nieder (2003). Modification of Radiation Response: Cytokines, Growth Factors, and Other Biological Targets (Medical Radiology). Springer.
  11. Comparative Protection against Liver Inflammation and Fibrosis by a Selective Cyclooxygenase-2 Inhibitor and a Nonredox-Type 5-Lipoxygenase Inhibitor [Link]
  12. SC-236 [Link]
  13. Enhancement of Tumor Response to -Radiation by an Inhibitor of Cyclooxygenase-2 Enzyme [Link]
  14. Overview of selective COX-2 inhibitors [Link]
ChemSpider
8041499
BindingDB
50057527
ChEMBL
CHEMBL282093
ZINC
ZINC000000600558
MSDS
Download (72.3 KB)

Clinical Trials

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Pharmacoeconomics

Manufacturers
Not Available
Packagers
Not Available
Dosage Forms
Not Available
Prices
Not Available
Patents
Not Available

Properties

State
Solid
Experimental Properties
PropertyValueSource
water solubilityinsoluble MSDS
Predicted Properties
PropertyValueSource
Water Solubility0.004 mg/mLALOGPS
logP4.51ALOGPS
logP4.1Chemaxon
logS-5ALOGPS
pKa (Strongest Acidic)10.6Chemaxon
pKa (Strongest Basic)-0.44Chemaxon
Physiological Charge0Chemaxon
Hydrogen Acceptor Count3Chemaxon
Hydrogen Donor Count1Chemaxon
Polar Surface Area77.98 Å2Chemaxon
Rotatable Bond Count4Chemaxon
Refractivity92 m3·mol-1Chemaxon
Polarizability35.2 Å3Chemaxon
Number of Rings3Chemaxon
Bioavailability1Chemaxon
Rule of FiveYesChemaxon
Ghose FilterYesChemaxon
Veber's RuleNoChemaxon
MDDR-like RuleNoChemaxon
Predicted ADMET Features
Not Available

Spectra

Mass Spec (NIST)
Not Available
Spectra
SpectrumSpectrum TypeSplash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSsplash10-0udi-0000900000-bc0b3ecc07476da16bfa
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSsplash10-0udi-0000900000-eff4dcc980556f22265c
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSsplash10-001i-9000400000-14f0fb71bfe47a48abf1
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSsplash10-0udi-0001900000-8d1f734a33675cee47fb
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSsplash10-001i-9000000000-0325ebaf0b61b7f5c12d
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSsplash10-0udi-0229000000-47b7059bc736b28e33ed
Predicted 1H NMR Spectrum1D NMRNot Applicable
Predicted 13C NMR Spectrum1D NMRNot Applicable
Chromatographic Properties
Collision Cross Sections (CCS)
Not Available

Targets

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Details1. Cyclooxygenase 2
Kind
Protein
Organism
Canis lupus familiaris
Pharmacological action
Yes
Actions
Inhibitor
General Function
Not Available
Specific Function
enzyme binding
Gene Name
PTGS2
Uniprot ID
Q8SPQ9
Uniprot Name
Cyclooxygenase 2
Molecular Weight
68974.625 Da
References
  1. Nonsteroidal Antiinflammatory Drugs and a Selective Cyclooxygenase 2 Inhibitor Uncouple Mitochondria in Intact Cells [Link]
  2. The COX-2 inhibitor SC-236 exerts anti-inflammatory effects by suppressing phosphorylation of ERK in a murine model [Link]
  3. A cyclooxygenase-2 (COX-2) inhibitor compared with dexamethasone in a survival study of rats with intracerebral 9L gliosarcomas [File]
Details2. Prostaglandin G/H synthase 2
Kind
Protein
Organism
Humans
Pharmacological action
Yes
Actions
Inhibitor
General Function
Dual cyclooxygenase and peroxidase in the biosynthesis pathway of prostanoids, a class of C20 oxylipins mainly derived from arachidonate ((5Z,8Z,11Z,14Z)-eicosatetraenoate, AA, C20:4(n-6)), with a particular role in the inflammatory response (PubMed:11939906, PubMed:16373578, PubMed:19540099, PubMed:22942274, PubMed:26859324, PubMed:27226593, PubMed:7592599, PubMed:7947975, PubMed:9261177). The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes (PubMed:16373578, PubMed:22942274, PubMed:26859324, PubMed:27226593, PubMed:7592599, PubMed:7947975, PubMed:9261177). This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons (PubMed:16373578, PubMed:22942274, PubMed:26859324, PubMed:27226593, PubMed:7592599, PubMed:7947975, PubMed:9261177). Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins (PubMed:11939906, PubMed:19540099). In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids (PubMed:27642067). Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response (PubMed:22942274). Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols (PubMed:11034610, PubMed:11192938, PubMed:9048568, PubMed:9261177). Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation (PubMed:12391014). Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) (PubMed:12391014). As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 (PubMed:21206090). In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection (PubMed:26236990). In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) (PubMed:22068350, PubMed:26282205). Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity). During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
Specific Function
enzyme binding
Gene Name
PTGS2
Uniprot ID
P35354
Uniprot Name
Prostaglandin G/H synthase 2
Molecular Weight
68995.625 Da
References
  1. Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]
Details3. Nuclear factor NF-kappa-B complex (Protein Group)
Kind
Protein group
Organism
Humans
Pharmacological action
Yes
Actions
Inhibitor
General Function
NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. In a non-canonical activation pathway, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. The NF-kappa-B heterodimeric RelB-p52 complex is a transcriptional activator. The NF-kappa-B p52-p52 homodimer is a transcriptional repressor. NFKB2 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p100 and generation of p52 by a cotranslational processing. The proteasome-mediated process ensures the production of both p52 and p100 and preserves their independent function. p52 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. p52 and p100 are respectively the minor and major form; the processing of p100 being relatively poor. Isoform p49 is a subunit of the NF-kappa-B protein complex, which stimulates the HIV enhancer in synergy with p65. In concert with RELB, regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-BMAL1 heterodimer
Specific Function
DNA-binding transcription activator activity, RNA polymerase II-specific
Components:
NameUniProt ID
Nuclear factor NF-kappa-B p100 subunitQ00653
Nuclear factor NF-kappa-B p105 subunitP19838
Transcription factor p65Q04206
References
  1. Wong BC, Jiang Xh, Fan XM, Lin MC, Jiang SH, Lam SK, Kung HF: Suppression of RelA/p65 nuclear translocation independent of IkappaB-alpha degradation by cyclooxygenase-2 inhibitor in gastric cancer. Oncogene. 2003 Feb 27;22(8):1189-97. doi: 10.1038/sj.onc.1206234. [Article]
  2. Kim SJ, Jeong HJ, Choi IY, Lee KM, Park RK, Hong SH, Kim HM: Cyclooxygenase-2 inhibitor SC-236 [4-[5-(4-chlorophenyl)-3-(trifluoromethyl)-1-pyrazol-1-l] benzenesulfonamide] suppresses nuclear factor-kappaB activation and phosphorylation of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase, and c-Jun N-terminal kinase in human mast cell line cells. J Pharmacol Exp Ther. 2005 Jul;314(1):27-34. doi: 10.1124/jpet.104.082792. Epub 2005 Mar 22. [Article]
  3. Cyclooxygenase-2 Inhibitor SC-236 [4-[5-(4-Chlorophenyl)-3-(trifluoromethyl)-1-pyrazol-1-l] Benzenesulfonamide] Suppresses Nuclear Factor-κB Activation and Phosphorylation of p38 Mitogen-Activated Protein Kinase, Extracellular Signal-Regulated Kinase, and c-Jun N-Terminal Kinase in Human Mast Cell Line Cells [Link]

Drug created at June 14, 2018 19:34 / Updated at August 26, 2024 19:22