JTE522 - CAS 180200-68-4
Category: Inhibitor
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Molecular Formula:
C16H19FN2O3S
Molecular Weight:
338.4
COA:
Inquire
Targets:
COX
Description:
JTE522, a selective COX-2 inhibitor, can induce apoptosis and inhibit cell proliferation in human endometrial cancer cell line RL95-2 cells and to explore the molecular mechanisms.
Synonyms:
4-(4-cyclohexyl-2-methyl-1,3-oxazol-5-yl)-2-fluorobenzenesulfonamide; 4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide; JTE 522; JTE-522
Storage:
Store in a cool and dry place (or refer to the Certificate of Analysis).
MSDS:
Inquire
Boiling Point:
500.6±60.0 ℃ at 760 Torr
Melting Point:
166-167 ℃
Density:
1.294±0.06 g/cm3
InChIKey:
MIMJSJSRRDZIPW-UHFFFAOYSA-N
InChI:
1S/C16H19FN2O3S/c1-10-19-15(11-5-3-2-4-6-11)16(22-10)12-7-8-14(13(17)9-12)23(18,20)21/h7-9,11H,2-6H2,1H3,(H2,18,20,21)
Canonical SMILES:
CC1=NC(=C(O1)C2=CC(=C(C=C2)S(=O)(=O)N)F)C3CCCCC3
1.JTE-522, a cyclooxygenase-2 inhibitor, is an effective chemopreventive agent against rat experimental liver fibrosis1.
Yamamoto H;Kondo M;Nakamori S;Nagano H;Wakasa K;Sugita Y;Chang-De J;Kobayashi S;Damdinsuren B;Dono K;Umeshita K;Sekimoto M;Sakon M;Matsuura N;Monden M Gastroenterology. 2003 Aug;125(2):556-71.
BACKGROUND & AIMS: ;The aim of this study was to assess the effects of cyclooxygenase (COX)-2 inhibition on rat experimental liver fibrogenesis.;METHODS: ;We investigated the inhibitory effects of a selective COX-2 inhibitor, JTE-522, on liver fibrosis induced by a choline-deficient, l-amino acid-defined diet (CDAA). Inhibitory effect was also tested in a second model of thioacetamide (TAA)-induced liver fibrosis.;RESULTS: ;CDAA induced liver fibrosis and preneoplastic foci at 12 weeks and cirrhosis at 36 weeks. Hepatocellular carcinoma was noted in 13 of 15 rats (87%). JTE-522 significantly inhibited fibrosis and development of preneoplastic lesions in a dose-dependent manner and completely inhibited generation of cirrhosis and hepatocellular carcinoma at both low and high doses (10 and 30 mg/kg body wt/day, respectively). JTE-522 administrated only from 12 weeks to 36 weeks also prevented cirrhosis and formation of hepatocellular carcinoma. JTE-522 itself did not cause local or systemic gross or histopathologic changes at 36 weeks. Mechanistic studies indicated that the CDAA model displayed up-regulation of several biomarkers, including COX-2, arachidonate metabolite (prostaglandin E(2)), serum aspartate aminotransferase, and c-myc expression.
2.Prostacyclin synthase gene transfer modulates cyclooxygenase-2-derived prostanoid synthesis and inhibits neointimal formation in rat balloon-injured arteries.
Yamada M;Numaguchi Y;Okumura K;Harada M;Naruse K;Matsui H;Ito T;Hayakawa T Arterioscler Thromb Vasc Biol. 2002 Feb 1;22(2):256-62.
Previous studies have shown that prostacyclin (PGI(2)) synthase (PCS) gene transfer inhibits neointimal formation in balloon-injured arteries. However, the role of each cyclooxygenase (COX) isoform in this healing mechanism remains unknown. We hypothesized that overexpression of PCS may modulate COX-2-mediated prostaglandin (PG) metabolism. That is to say, excessive PGH(2) derived from COX-2 after balloon injury may be converted into PGI(2) rather than PGE(2) or thromboxane (TX) A(2) by overexpressed PCS. We examined the expression of COX isoforms and evaluated the role of COX-2 with regard to the effects of PCS gene transfer by using 4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide (JTE-522), a selective COX-2 inhibitor. Rats were divided into 4 groups in conjunction with PCS gene transfer and JTE-522 treatment. The PCS gene (30 microg) was transfected into rat balloon-injured arteries by a lipotransfection method. JTE-522 (30 mg/kg per day) was administered for 14 days after balloon injury. Immunohistochemical analysis demonstrated marked COX-2 expression on the neointima. PCS gene transfer markedly inhibited neointimal formation, but JTE-522 reversed this beneficial effect.
3.COX-2/VEGF-dependent facilitation of tumor-associated angiogenesis and tumor growth in vivo.
Yoshida S;Amano H;Hayashi I;Kitasato H;Kamata M;Inukai M;Yoshimura H;Majima M Lab Invest. 2003 Oct;83(10):1385-94.
Nonsteroidal anti-inflammatory drugs are known to suppress the occurrence and progression of malignancies such as colorectal cancers. However, the precise mechanism of these actions remains unknown. We have evaluated the role of an inducible cyclo-oxygenase (COX-2) in tumor-associated angiogenesis and tumor growth, and identified the downstream molecules involved using a ddy mouse model of sponge angiogenesis, which mimics tumor angiogenesis and is COX-2 and vascular endothelial growth factor (VEGF) dependent. In this model, VEGF expression was down-regulated by selective COX-2 inhibition with NS-398. To find out the involvement of COX-2/VEGF pathway in tumor-associated angiogenesis, we estimated angiogenesis occurring around implanted Millipore chambers containing sarcoma-180 (S-180) cells or Lewis lung carcinoma cells. Daily oral administration of NS-398 or of aspirin, a nonselective COX inhibitor, suppressed angiogenesis seen around the Millipore chambers. S-180 cells implanted in ddy mice formed substantial tumors with extensive angiogenesis markedly suppressed by aspirin and COX-2 inhibitors NS-398 and JTE522, but not by mofezolac, an inhibitor of constitutive COX-1. Tumor-associated angiogenesis was also significantly suppressed by a neutralizing antibody against VEGF.
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CAS 180200-68-4 JTE522

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