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Chemical Compound Review

AGN-PC-00BLBM     5-(4-fluorophenyl)-1-(4...

Synonyms: CHEMBL274990, SureCN214120, CHEBI:8983, Curator_000018, CHEBI:116866, ...
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Disease relevance of C11705


High impact information on C11705

  • Serum IL-6 and paw IL-6 mRNA levels were also reduced to near normal levels by SC-58125 [5].
  • Two specific COX-2 inhibitors, SC-58125 and NS 398, also, in a dose-dependent manner, attenuate baseline and type alpha transforming growth factor-stimulated mitogenesis, although PG levels are decreased > 90% at all concentrations of inhibitor tested [6].
  • The IL-1beta-induced increase in the release of PGH2 by HUVECs was suppressed by the COX-2-selective inhibitor SC-58125 and correlated with both COX-2 expression and PGIS inactivation [7].
  • A new class of compounds has recently been developed (SC-58125) that have a high degree of selectivity for the inducible form of cyxlooxygenase (COX-2) over the constitutive form (COX-1) [8].
  • SC-58125 moderately induced apoptosis and inhibited growth on soft agar at higher concentrations than were required for SC-560 [3].

Biological context of C11705

  • Substitutions of COX-1 sequences in COX-2 at the mouth of the active site of COX-2 did not change the selectivity of SC-58125 [8].
  • When cells were preincubated with inhibitors to allow time-dependent inhibition prior to arachidonic acid stimulation, NS-398, CGP 28238, L-745,337, SC-58125 all behaved as potent (IC50 = 1-30 nM) and selective inhibitors of PGHS-2, in contrast to indomethacin, flurbiprofen or diclofenac which are potent inhibitors of enzymes [9].
  • We conclude that SC-58125 primarily exerts a cytostatic effect in vivo, which is likely to be mediated through inhibition of progression through the G(2)/M phase of the cell cycle [10].
  • Cell proliferation ((3)H-thymidine uptake) was significantly inhibited by NS-398 and SC-58125, the EP(1) antagonist SC-51322, AH6809 (EP(1)/EP(2) antagonist), and the EP(4) antagonist AH23848B, but was not affected by exogenous PGE(2) [11].

Anatomical context of C11705

  • 4. SC-58125 did not significantly affect leukocyte infiltration into the airpouch at any dose tested (up to 10 mg kg(-1)) [12].
  • In both cell lines [3H]thymidine incorporation stimulated by serum was inhibited by the COX-2 inhibitor SC-58125, but not by the COX-1 inhibitor VSA [13].

Associations of C11705 with other chemical compounds


Gene context of C11705

  • Additional rats received Pio (10 for 3 days and intravenous SC-58125 [a cyclooxygenase-2 (COX-2) inhibitor] or SC-560 (a COX-1 inhibitor) 15 min before ischemia [19].
  • Unstimulated and stimulated cells were exposed to the specific COX-1 inhibitor valerylsalicylic acid (VSA) and the COX-2 inhibitors NS-398 and SC-58125 [20].
  • The effects of serum on proliferation were then evaluated in the presence of the COX-1 inhibitor, valerylsalicyclic acid (VSA), the COX-2 inhibitor, SC-58125, or indomethacin [13].
  • SC-58125, a selective inhibitor of COX-2, has a potent apoptosis inducing effect [13].
  • Low concentrations of indomethacin and valerylsalicylic acid (VSA) were evaluated as cyclooxygenase-1 inhibitors and their effects compared with the effects of a specific cyclooxygenase-2 inhibitor, SC-58125 [21].

Analytical, diagnostic and therapeutic context of C11705

  • These results indicate that aberrant expression of PGHS-2 in epidermal tumors may be a relevant target for prevention of epidermal cancer development in experimental animals and that the PGHS-2-specific inhibitor SC-58125, which is a potent inhibitor of tumor promotion in mouse skin, may be important for cancer chemoprevention in humans as well [4].
  • A cyclooxygenase-2 inhibitor (SC-58125) blocks growth of established human colon cancer xenografts [10].


  1. Decreased susceptibility to renovascular hypertension in mice lacking the prostaglandin I2 receptor IP. Fujino, T., Nakagawa, N., Yuhki, K., Hara, A., Yamada, T., Takayama, K., Kuriyama, S., Hosoki, Y., Takahata, O., Taniguchi, T., Fukuzawa, J., Hasebe, N., Kikuchi, K., Narumiya, S., Ushikubi, F. J. Clin. Invest. (2004) [Pubmed]
  2. Cyclooxygenase-2 Inhibition Attenuates Antibody Responses against Human Papillomavirus-Like Particles. Ryan, E.P., Malboeuf, C.M., Bernard, M., Rose, R.C., Phipps, R.P. J. Immunol. (2006) [Pubmed]
  3. Gene modulation by Cox-1 and Cox-2 specific inhibitors in human colorectal carcinoma cancer cells. Bottone, F.G., Martinez, J.M., Alston-Mills, B., Eling, T.E. Carcinogenesis (2004) [Pubmed]
  4. Localization of prostaglandin H synthase isoenzymes in murine epidermal tumors: suppression of skin tumor promotion by inhibition of prostaglandin H synthase-2. Müller-Decker, K., Kopp-Schneider, A., Marks, F., Seibert, K., Fürstenberger, G. Mol. Carcinog. (1998) [Pubmed]
  5. Selective inhibition of cyclooxygenase (COX)-2 reverses inflammation and expression of COX-2 and interleukin 6 in rat adjuvant arthritis. Anderson, G.D., Hauser, S.D., McGarity, K.L., Bremer, M.E., Isakson, P.C., Gregory, S.A. J. Clin. Invest. (1996) [Pubmed]
  6. Epidermal growth factor receptor activation induces nuclear targeting of cyclooxygenase-2, basolateral release of prostaglandins, and mitogenesis in polarizing colon cancer cells. Coffey, R.J., Hawkey, C.J., Damstrup, L., Graves-Deal, R., Daniel, V.C., Dempsey, P.J., Chinery, R., Kirkland, S.C., DuBois, R.N., Jetton, T.L., Morrow, J.D. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  7. Rate of vasoconstrictor prostanoids released by endothelial cells depends on cyclooxygenase-2 expression and prostaglandin I synthase activity. Camacho, M., López-Belmonte, J., Vila, L. Circ. Res. (1998) [Pubmed]
  8. A single amino acid difference between cyclooxygenase-1 (COX-1) and -2 (COX-2) reverses the selectivity of COX-2 specific inhibitors. Gierse, J.K., McDonald, J.J., Hauser, S.D., Rangwala, S.H., Koboldt, C.M., Seibert, K. J. Biol. Chem. (1996) [Pubmed]
  9. Characterization of autocrine inducible prostaglandin H synthase-2 (PGHS-2) in human osteosarcoma cells. Wong, E., DeLuca, C., Boily, C., Charleson, S., Cromlish, W., Denis, D., Kargman, S., Kennedy, B.P., Ouellet, M., Skorey, K., O'Neill, G.P., Vickers, P.J., Riendeau, D. Inflamm. Res. (1997) [Pubmed]
  10. A cyclooxygenase-2 inhibitor (SC-58125) blocks growth of established human colon cancer xenografts. Williams, C.S., Sheng, H., Brockman, J.A., Armandla, R., Shao, J., Washington, M.K., Elkahloun, A.G., DuBois, R.N. Neoplasia (2001) [Pubmed]
  11. Effects of selective PGE(2) receptor antagonists in esophageal adenocarcinoma cells derived from Barrett's esophagus. Piazuelo, E., Jim??nez, P., Strunk, M., Santander, S., Garc??a, A., Esteva, F., Lanas, A. Prostaglandins Other Lipid Mediat. (2006) [Pubmed]
  12. Limited anti-inflammatory efficacy of cyclo-oxygenase-2 inhibition in carrageenan-airpouch inflammation. Wallace, J.L., Chapman, K., McKnight, W. Br. J. Pharmacol. (1999) [Pubmed]
  13. The effect of selective cyclooxygenase inhibitors on intestinal epithelial cell mitogenesis. Erickson, B.A., Longo, W.E., Panesar, N., Mazuski, J.E., Kaminski, D.L. J. Surg. Res. (1999) [Pubmed]
  14. Arachidonic acid and nonsteroidal anti-inflammatory drugs induce conformational changes in the human prostaglandin endoperoxide H2 synthase-2 (cyclooxygenase-2). Smith, T., McCracken, J., Shin, Y.K., DeWitt, D. J. Biol. Chem. (2000) [Pubmed]
  15. Role of NF-kappaB in the antiproliferative effect of endothelin-1 and tumor necrosis factor-alpha in human hepatic stellate cells. Involvement of cyclooxygenase-2. Gallois, C., Habib, A., Tao, J., Moulin, S., Maclouf, J., Mallat, A., Lotersztajn, S. J. Biol. Chem. (1998) [Pubmed]
  16. Cyclooxygenase-2 and synthesis of PGE2 in human bronchial smooth-muscle cells. Viganò, T., Habib, A., Hernandez, A., Bonazzi, A., Boraschi, D., Lebret, M., Cassina, E., Maclouf, J., Sala, A., Folco, G. Am. J. Respir. Crit. Care Med. (1997) [Pubmed]
  17. Cyclooxygenase metabolites mediate glomerular monocyte chemoattractant protein-1 formation and monocyte recruitment in experimental glomerulonephritis. Schneider, A., Harendza, S., Zahner, G., Jocks, T., Wenzel, U., Wolf, G., Thaiss, F., Helmchen, U., Stahl, R.A. Kidney Int. (1999) [Pubmed]
  18. Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E(2) production. Candelario-Jalil, E., Akundi, R.S., Bhatia, H.S., Lieb, K., Appel, K., Muñoz, E., Hüll, M., Fiebich, B.L. J. Neuroimmunol. (2006) [Pubmed]
  19. Myocardial protection by pioglitazone, atorvastatin, and their combination: mechanisms and possible interactions. Ye, Y., Lin, Y., Atar, S., Huang, M.H., Perez-Polo, J.R., Uretsky, B.F., Birnbaum, Y. Am. J. Physiol. Heart Circ. Physiol. (2006) [Pubmed]
  20. The role of selective cyclooxygenase isoforms in human intestinal smooth muscle cell stimulated prostanoid formation and proliferation. Longo, W.E., Erickson, B., Panesar, N., Mazuski, J.E., Robinson, S., Kaminski, D.L. Mediators of inflammation. (1998) [Pubmed]
  21. The role of cyclooxygenase-1 and cyclooxygenase-2 in lipopolysaccharide and interleukin-1 stimulated enterocyte prostanoid formation. Longo, W.E., Damore, L.J., Mazuski, J.E., Smith, G.S., Panesar, N., Kaminski, D.L. Mediators of inflammation. (1998) [Pubmed]
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