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Chemical Compound Review

Melipan     2-methyl-2-[4-(1,2,3,4...

Synonyms: Nafenopin, Nafenopine, Nafenopino, Nafenopinum, TPIA, ...
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Disease relevance of Nafenopin


High impact information on Nafenopin


Chemical compound and disease context of Nafenopin


Biological context of Nafenopin

  • The patterns of cell proliferation induced by these agents were further compared with those induced by a single dose of nafenopin (NAF), a direct mitogen which does not induce liver TNF-alpha messenger RNA (mRNA) [12].
  • However, Nafenopin depressed HTC net population expansion via a suppression of cell death coupled to a more marked inhibition of RDS [13].
  • Role of oxidative stress in age dependent hepatocarcinogenesis by the peroxisome proliferator nafenopin in the rat [14].
  • Prolonged NAF treatment enhanced cell number in normal liver by 25%, while PPF and liver tumors were amplified at least 100-fold [15].
  • Nafenopin also increased FaO cell growth but, surprisingly, retarded the growth of both HTC and RH1 cells [13].

Anatomical context of Nafenopin

  • The responses of a series of rat hepatoma cell lines (FaO, HTC, RH1) to the rodent non-genotoxic hepatocarcinogen and per-oxisome proliferator (PP) Nafenopin were studied to determine if this PP acts with EGF, a naturally occurring liver growth regulator, to perturb the balance between mitosis and apoptosis [13].
  • However, the light microscopic autoradiograms revealed the [35S]sulfate incorporation as follows: azaserine-induced transplantable pancreatic carcinoma greater than nafenopin-induced transplantable pancreatic carcinoma greater than normal pancreas [16].
  • Finally, nafenopin appeared to delay the appearance of gamma-glutamyltranspeptidase activity within the cultured cells [17].
  • A single dose of the peroxisome proliferator (PP) nafenopin (NAF) induced the enzyme predominantly in hepatocytes around the central venules and cell replication mainly in the periportal areas [18].
  • The anti-mouse liver cytosolic epoxide hydrolase antibody was found to precipitate the whole trans-stilbene oxide hydrolase activity also from liver cytosol of nafenopin-treated mice, which indicates the presence of a single cytosolic epoxide hydrolase following induction [19].

Associations of Nafenopin with other chemical compounds

  • The biochemical effects in the livers of male rats of prolonged administration of the experimental hepatocarcinogen nafenopin, a hypolipidemic agent and peroxisome proliferator, were compared to those of another experimental liver carcinogen, phenobarbital, which acts as a neoplasm promoter [20].
  • Therefore, in the present study we evaluated the effect of two potent peroxisome proliferators, nafenopin and WY-14,643, on Kupffer cell activation in vivo [21].
  • In guinea pig hepatocytes transfected with control plasmids and treated with 50 microM nafenopin in the absence or presence of the RXR ligand, 9-cis-retinoic acid (5 microM) gave only a 1.7 +/- 1.5- or 3.3 +/- 1.5-fold induction in CIPCO, respectively [22].
  • Deletion analysis revealed that the responsive region for both DHEA and nafenopin was between -108 and -60 relative to the transcription start site [23].
  • In addition, nafenopin also caused a pronounced and time-dependent increase in palmitoyl-CoA beta-oxidation activity but was found to have only a weak stimulating effect on replicative DNA synthesis (2-fold) when compared to that of epidermal growth factor (6.5-fold) [24].

Gene context of Nafenopin


Analytical, diagnostic and therapeutic context of Nafenopin


  1. Suppression of liver cell apoptosis in vitro by the non-genotoxic hepatocarcinogen and peroxisome proliferator nafenopin. Bayly, A.C., Roberts, R.A., Dive, C. J. Cell Biol. (1994) [Pubmed]
  2. Food restriction eliminates preneoplastic cells through apoptosis and antagonizes carcinogenesis in rat liver. Grasl-Kraupp, B., Bursch, W., Ruttkay-Nedecky, B., Wagner, A., Lauer, B., Schulte-Hermann, R. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  3. Differences in the steady-state levels of c-fos, c-jun and c-myc messenger RNA during mitogen-induced liver growth and compensatory regeneration. Coni, P., Simbula, G., de Prati, A.C., Menegazzi, M., Suzuki, H., Sarma, D.S., Ledda-Columbano, G.M., Columbano, A. Hepatology (1993) [Pubmed]
  4. Hepatocellular carcinomas in acatalasemic mice treated with nafenopin, a hypolipidemic peroxisome proliferator. Reddy, J.K., Rao, S., Moody, D.E. Cancer Res. (1976) [Pubmed]
  5. The repressor protein, Bm3R1, mediates an adaptive response to toxic fatty acids in Bacillus megaterium. Palmer, C.N., Axen, E., Hughes, V., Wolf, C.R. J. Biol. Chem. (1998) [Pubmed]
  6. Malignant tumors in rats fed nafenopin, a hepatic peroxisome proliferator. Reddy, J.K., Rao, M.S. J. Natl. Cancer Inst. (1977) [Pubmed]
  7. Rapid and extensive lethal action of clofibrate on hepatoma cells in vitro. Canuto, R.A., Muzio, G., Maggiora, M., Autelli, R., Barbiero, G., Costelli, P., Bonelli, G., Baccino, F.M. Cell Death Differ. (1997) [Pubmed]
  8. Further evidence that mitogen-induced cell proliferation does not support the formation of enzyme-altered islands in rat liver by carcinogens. Ledda-Columbano, G.M., Columbano, A., Curto, M., Ennas, M.G., Coni, P., Sarma, D.S., Pani, P. Carcinogenesis (1989) [Pubmed]
  9. Activation of c-Ki-ras not detectable in adenomas or adenocarcinomas arising in rat pancreas. Schaeffer, B.K., Zurlo, J., Longnecker, D.S. Mol. Carcinog. (1990) [Pubmed]
  10. No increase of apoptosis in regressing mouse liver after withdrawal of growth stimuli or food restriction. Bursch, W., Wastl, U., Hufnagl, K., Schulte-Hermann, R. Toxicol. Sci. (2005) [Pubmed]
  11. Genotoxic effects of selected peroxisome proliferators. Reisenbichler, H., Eckl, P.M. Mutat. Res. (1993) [Pubmed]
  12. Possible roles of nonparenchymal cells in hepatocyte proliferation induced by lead nitrate and by tumor necrosis factor alpha. Shinozuka, H., Ohmura, T., Katyal, S.L., Zedda, A.I., Ledda-Columbano, G.M., Columbano, A. Hepatology (1996) [Pubmed]
  13. The rodent non-genotoxic hepatocarcinogen Nafenopin and EGF alter the mitosis/apoptosis balance promoting hepatoma cell clonal growth. Gill, J.H., Molloy, C.A., Shoesmith, K.J., Bayly, A.C., Roberts, R.A. Cell Death Differ. (1995) [Pubmed]
  14. Role of oxidative stress in age dependent hepatocarcinogenesis by the peroxisome proliferator nafenopin in the rat. Huber, W., Kraupp-Grasl, B., Esterbauer, H., Schulte-Hermann, R. Cancer Res. (1991) [Pubmed]
  15. Inherent increase of apoptosis in liver tumors: implications for carcinogenesis and tumor regression. Grasl-Kraupp, B., Ruttkay-Nedecky, B., Müllauer, L., Taper, H., Huber, W., Bursch, W., Schulte-Hermann, R. Hepatology (1997) [Pubmed]
  16. Incorporation of [35S]sulfate in normal and neoplastic rat pancreatic acinar cells in relationship to cytodifferentiation. Kanwar, Y.S., Rao, M.S., Longnecker, D.S., Reddy, J.K. Cancer Res. (1984) [Pubmed]
  17. Use of primary cultures of adult rat hepatocytes to investigate mechanisms of action of nafenopin, a hepatocarcinogenic peroxisome proliferator. Bieri, F., Bentley, P., Waechter, F., Stäubli, W. Carcinogenesis (1984) [Pubmed]
  18. Peroxisomal enzyme induction uncoupled from enhanced DNA synthesis in putative preneoplastic liver foci of rats treated with a single dose of the peroxisome proliferator nafenopin. Grasl-Kraupp, B., Huber, W., Timmermann-Trosiener, I., Schulte-Hermann, R. Carcinogenesis (1993) [Pubmed]
  19. Organ distribution of epoxide hydrolases in cytosolic and microsomal fractions of normal and nafenopin-treated male DBA/2 mice. Waechter, F., Bentley, P., Bieri, F., Muakkassah-Kelly, S., Stäubli, W., Villermain, M. Biochem. Pharmacol. (1988) [Pubmed]
  20. Effects of the hepatocarcinogen nafenopin, a peroxisome proliferator, on the activities of rat liver glutathione-requiring enzymes and catalase in comparison to the action of phenobarbital. Furukawa, K., Numoto, S., Furuya, K., Furukawa, N.T., Williams, G.M. Cancer Res. (1985) [Pubmed]
  21. Peroxisome proliferators activate Kupffer cells in vivo. Bojes, H.K., Thurman, R.G. Cancer Res. (1996) [Pubmed]
  22. Addition of peroxisome proliferator-activated receptor alpha to guinea pig hepatocytes confers increased responsiveness to peroxisome proliferators. Macdonald, N., Holden, P.R., Roberts, R.A. Cancer Res. (1999) [Pubmed]
  23. Regulation of CYP2C11 by dehydroepiandrosterone and peroxisome proliferators: identification of the negative regulatory region of the gene. Ripp, S.L., Falkner, K.C., Pendleton, M.L., Tamasi, V., Prough, R.A. Mol. Pharmacol. (2003) [Pubmed]
  24. Long-term maintenance of hepatocytes in primary culture in the presence of DMSO: further characterization and effect of nafenopin, a peroxisome proliferator. Muakkassah-Kelly, S.F., Bieri, F., Waechter, F., Bentley, P., Stäubli, W. Exp. Cell Res. (1987) [Pubmed]
  25. Role for tumor necrosis factor alpha receptor 1 and interleukin-1 receptor in the suppression of mouse hepatocyte apoptosis by the peroxisome proliferator nafenopin. West, D.A., James, N.H., Cosulich, S.C., Holden, P.R., Brindle, R., Rolfe, M., Roberts, R.A. Hepatology (1999) [Pubmed]
  26. The peroxisome proliferator class of non-genotoxic hepatocarcinogens synergize with epidermal growth factor to promote clonal expansion of initiated rat hepatocytes. James, N.H., Roberts, R.A. Carcinogenesis (1994) [Pubmed]
  27. Tumour necrosis factor alpha (TNF alpha) suppresses apoptosis and induces DNA synthesis in rodent hepatocytes: a mediator of the hepatocarcinogenicity of peroxisome proliferators? Rolfe, M., James, N.H., Roberts, R.A. Carcinogenesis (1997) [Pubmed]
  28. Increased plasma clearance rate of thyroxine despite decreased 5'-monodeiodination: study with a peroxisome proliferator in the rat. Kaiser, C.A., Seydoux, J., Giacobino, J.P., Girardier, L., Burger, A.G. Endocrinology (1988) [Pubmed]
  29. The rodent non-genotoxic hepatocarcinogen nafenopin suppresses apoptosis preferentially in non-cycling hepatocytes but also elevates CDK4, a cell cycle progression factor. Gill, J.H., Brickell, P., Dive, C., Roberts, R.A. Carcinogenesis (1998) [Pubmed]
  30. Induction of cytosolic and microsomal epoxide hydrolases by the hypolipidaemic compound nafenopin in the mouse liver. Waechter, F., Bieri, F., Stäubli, W., Bentley, P. Biochem. Pharmacol. (1984) [Pubmed]
  31. Hepatobiliary elimination of the peroxisome proliferator nafenopin by conjugation and subsequent ATP-dependent transport across the canalicular membrane. Jedlitschky, G., Leier, I., Böhme, M., Buchholz, U., Bar-Tana, J., Keppler, D. Biochem. Pharmacol. (1994) [Pubmed]
  32. Nafenopin causes protein kinase C-mediated serine phosphorylation and loss of function of connexin 32 protein in rat hepatocytes without aberrant expression or localization. Elcock, F.J., Deag, E., Roberts, R.A., Chipman, J.K. Toxicol. Sci. (2000) [Pubmed]
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