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Chemical Compound Review

MF-tricyclic     3-(3,4-difluorophenyl)-4-(4...

Synonyms: MF Tricyclic, CHEMBL18264, AG-E-11766, SureCN2159864, CHEBI:121704, ...
 
 
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Disease relevance of MF Tricyclic

 

High impact information on MF Tricyclic

  • RESULTS: MF-Tricyclic and Sulindac reduced the relative risk of development of esophageal cancer by 55% (95% confidence interval [CI] = 43%-66%, P < 0.008) and by 79% (95% CI = 68%-87%, P < 0.001), respectively, compared with controls [1].
  • A selective COX-2 inhibitor was administered either acutely [NS398; 100 mg/kg, i.p.] on day 14 or chronically in chow [MF. tricyclic; 0.015%, p.o.] from day 6 to day 14 after tumor implantation [5].
  • Apc+/-Msh2-/- mice treated with MF-tricyclic had significantly fewer small-bowel polyps (mean +/- SD, 178 +/- 29) compared with mice on sulindac (278 +/- 80), or control diet (341 +/- 43; P < 0.001) [2].
  • Both MF-tricyclic and sulindac further increased blood pressure and albuminuria in mREN2 rats [6].
  • Renal effects of a selective cyclooxygenase-2 (COX-2) inhibitor [MF-Tricyclic; 3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl)phenyl)-2-(5H)-furanone] were studied in control and volume-depleted conscious dogs [7].
 

Associations of MF Tricyclic with other chemical compounds

 

Analytical, diagnostic and therapeutic context of MF Tricyclic

  • RESULTS: In vivo COX-2 inhibition, unexpectedly increased viral load: in the CMV-infected animals viral load was 2.58 +/- 1.0 in the nontreated group, 4.74 +/- 1.38 in the group treated with 12 mg/kg/day MF-tricyclic, and 6.51 +/- 1.64 in the group treated with 24 mg/kg/day MF-tricyclic (p trend = 0.050) [3].

References

  1. Chemoprevention of esophageal adenocarcinoma by COX-2 inhibitors in an animal model of Barrett's esophagus. Buttar, N.S., Wang, K.K., Leontovich, O., Westcott, J.Y., Pacifico, R.J., Anderson, M.A., Krishnadath, K.K., Lutzke, L.S., Burgart, L.J. Gastroenterology (2002) [Pubmed]
  2. Suppression of intestinal polyps in Msh2-deficient and non-Msh2-deficient multiple intestinal neoplasia mice by a specific cyclooxygenase-2 inhibitor and by a dual cyclooxygenase-1/2 inhibitor. Lal, G., Ash, C., Hay, K., Redston, M., Kwong, E., Hancock, B., Mak, T., Kargman, S., Evans, J.F., Gallinger, S. Cancer Res. (2001) [Pubmed]
  3. Effects of MF-tricyclic, a selective cyclooxygenase-2 inhibitor, on atherosclerosis progression and susceptibility to cytomegalovirus replication in apolipoprotein-E knockout mice. Rott, D., Zhu, J., Burnett, M.S., Zhou, Y.F., Zalles-Ganley, A., Ogunmakinwa, J., Epstein, S.E. J. Am. Coll. Cardiol. (2003) [Pubmed]
  4. MF tricyclic and sulindac retard tumor formation in an animal model. Dvory-Sobol, H., Kazanov, D., Liberman, E., Birkenfeld, S., Bulvik, B., Luk, P., Leshno, M., Arber, N. Int. J. Cancer (2006) [Pubmed]
  5. Simultaneous reduction in cancer pain, bone destruction, and tumor growth by selective inhibition of cyclooxygenase-2. Sabino, M.A., Ghilardi, J.R., Jongen, J.L., Keyser, C.P., Luger, N.M., Mach, D.B., Peters, C.M., Rogers, S.D., Schwei, M.J., de Felipe, C., Mantyh, P.W. Cancer Res. (2002) [Pubmed]
  6. Cardiovascular and renal effects of cyclooxygenase inhibition in transgenic rats harboring mouse renin-2 gene (TGR[mREN2]27). Cheng, Z.J., Finckenberg, P., Louhelainen, M., Merasto, S., Tikkanen, I., Vapaatalo, H., Mervaala, E.M. Eur. J. Pharmacol. (2003) [Pubmed]
  7. Differential effect of a selective cyclooxygenase-2 inhibitor versus indomethacin on renal blood flow in conscious volume-depleted dogs. Black, S.C., Brideau, C., Cirino, M., Belley, M., Bosquet, J., Chan, C.C., Rodger, I.W. J. Cardiovasc. Pharmacol. (1998) [Pubmed]
 
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