NS-398, a novel non-steroidal anti-inflammatory drug with potent analgesic and antipyretic effects, which causes minimal stomach lesions

Futaki, Nobuko; Yoshikawa, Kensei; Hamasaka, Y; Arai, Iwao; Higuchi, Shohei; Iizuka, Hiroyuki; Otomo, Susumu

doi:10.1016/0306-3623(93)90018-s

Cited by 343 publications

(222 citation statements)

References 4 publications

Supporting

Mentioning

204

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, we examined the effects of COX-2 specific inhibitors, NS-398 79 and JTE-522, 67 on growth of 4 BDC and 1 GBC cell lines in vitro. As described previously in other cancer cell lines, 29,80 these 2 COX-2 selective inhibitors inhibited the proliferation of BDC and GBC cell lines in dose-and time-dependent manner in vitro.…”

Section: Discussionmentioning

confidence: 99%

Differential expression of cyclooxygenase-2 (COX-2) in human bile duct epithelial cells and bile duct neoplasm

et al. 2001

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Differential expression of cyclooxygenase-2 (COX-2) in human bile duct epithelial cells and bile duct neoplasm

et al. 2001

View full text Add to dashboard Cite

show abstract

“…Aspirin was kindly provided by Merck (Rahway, NJ), NS-398 46 was obtained from Cayman Chemical (Ann Arbor, MI), and JTE-522 47 was kindly supplied by Japan Tobacco (Tokyo, Japan). EP receptor selective agonists, ONO-DI-004, ONO-AEI-257, ONO-AE-248, and ONO-AEI-329, 39 were kindly supplied from Ono Pharmaceutical Co., Osaka, Japan.…”

Section: Drugsmentioning

confidence: 99%

“…A COX-2 selective inhibitor, NS-398 46 or JTE522, 47 was suspended in 5% gum Arabic at a concentration of 6 mg/ml and was orally administered (0.05 ml/10 g body weight, 30 mg/kg, twice a day) to the WT mice. For vehicle control mice, distilled water with 5% gum Arabic was administered orally (0.05 ml/10 g body weight, twice a day).…”

mentioning

confidence: 99%

Recruitment of a Prostaglandin E Receptor Subtype, EP3-Expressing Bone Marrow Cells Is Crucial in Wound-Induced Angiogenesis

Kamoshita

Ikeda

Fujita

et al. 2006

The American Journal of Pathology

View full text Add to dashboard Cite

E-type prostaglandins have been reported to be proangiogenic in vivo. Thus, we examined prostaglandin receptor signaling relevant to wound-induced angiogenesis. Full-thickness skin wounds were created on the backs of mice, and angiogenesis in wound granulation tissues was estimated. Wound closure and re-epithelization in EP3 receptor knockout mice (EP3 ؊/؊ ) were significantly delayed compared with their wild-type (WT) mice, whereas those in EP1 ؊/؊ , EP2 ؊/؊ , and EP4 ؊/؊ were not delayed. Wound-induced angiogenesis estimated with CD31 immunohistochemistry in EP3 ؊/؊ mice was significantly inhibited compared with that in WT mice. Immunoreactive vascular endothelial growth factor (VEGF) in wound granulation tissues in EP3 ؊/؊ mice was markedly less than that in WT mice. Wound closure in WT mice was delayed significantly by VEGF neutralizing antibody compared with control IgG. Wound-induced angiogenesis and wound closure were significantly suppressed in EP3 ؊/؊ bone marrow transplantation mice compared with those in WT bone marrow transplantation mice. These were accompanied with the reductions in accumulation of VEGF-expressing cells in wound granulation tissues and in mobilization of VEGF receptor 1-expressing leukocytes in peripheral circulation. These results indicate that the recruitment of EP3-expressing cells to wound granulation tissues is critical for surgical wound healing and angiogenesis via up-regulation of VEGF. (Am J Pathol

show abstract

“…The aspirin was a gift from Merck (Rahway, New Jersey); and NS-398 (N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide) (Futaki et al, 1993) was purchased from Cayman Chemical (Ann Arbor, Michigan). The mofezolac ([3,4-di(4-methoxyphenyl)-5-isoxazolyl] acetic acid) (Kitamura et al, 2002) was a gift from Yoshitomi Pharmaceutical Corporation.…”

Section: Chemicals and Other Materialsmentioning

confidence: 99%

COX-2/VEGF-Dependent Facilitation of Tumor-Associated Angiogenesis and Tumor Growth in vivo

Yoshida

Aoki

Hayashi

et al. 2003

Laboratory Investigation

View full text Add to dashboard Cite

SUMMARY: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. S-180 tumor growth in the subcutaneous tissues was also suppressed by aspirin, COX-2 selective inhibitors, and the VEGF antibody, but not by the COX-1 inhibitor. These results demonstrate that the inhibition of the COX-2/VEGF-dependent pathway was effective in tumor-associated angiogenesis, tumor growth, and tumor metastasis. (Lab Invest 2003, 83:1385-1394.

show abstract

NS-398, a novel non-steroidal anti-inflammatory drug with potent analgesic and antipyretic effects, which causes minimal stomach lesions

Cited by 343 publications

References 4 publications

Differential expression of cyclooxygenase-2 (COX-2) in human bile duct epithelial cells and bile duct neoplasm

Differential expression of cyclooxygenase-2 (COX-2) in human bile duct epithelial cells and bile duct neoplasm

Recruitment of a Prostaglandin E Receptor Subtype, EP3-Expressing Bone Marrow Cells Is Crucial in Wound-Induced Angiogenesis

COX-2/VEGF-Dependent Facilitation of Tumor-Associated Angiogenesis and Tumor Growth in vivo

Contact Info

Product

Resources

About