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Chemical Compound Review

Tocris-0760     4-[(5,5,8,8-tetramethyl-6,7...

Synonyms: CHEMBL69367, SureCN726740, AM-580, CD-336, AG-K-25670, ...
 
 
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Disease relevance of Am 580

  • The multiplicity of colon tumors in the group fed Am-55P and the incidences of nephroblastomas with ACA or Am-580 were decreased as compared with the control values, but the other chemicals had no modifying effects on tumor development in any organs [1].
 

High impact information on Am 580

  • Moreover, physiologic concentrations of glucocorticoids efficiently antagonized LCL growth inhibition induced by 13-cis-RA; 9-cis-RA; all-trans-RA; and Ro 40-6055, an RA alpha receptor (RAR alpha) selective agonist [2].
  • The effects of Am 580, CD417, and CD437, three synthetic retinoids selective for the RARs subtypes RARalpha, RARbeta, and RARgamma, respectively, were also investigated [3].
  • When pregnant hamsters were given an oral bolus of CD 336 or CD 135 during the early primitive streak stage of gestation, these retinoids proved 60-100 times more potent teratogens than all-trans-retinoic acid [4].
  • The RARalpha agonist, Ro 40-6055 also strongly downregulated these proteins although did not produce an equivalent decrease in S-phase cells [5].
  • Their rank order for inhibitory potency was Re 80 > Am 580 > Am 80, the ID50 values being 6.3, 23 and 28 pmol/egg, respectively [6].
 

Biological context of Am 580

  • Treatment with the selective RARalpha agonist Ro 40-6055 completely mimicked the effects of ATRA on growth and transactivation of a betaRAREx2-luciferase reporter construct, while RARbeta- and gamma-specific analogues were ineffective [7].
 

Associations of Am 580 with other chemical compounds

 

Gene context of Am 580

  • Application of 114 nmol of Am 80, Am 81, Am 580, Am 590, Am 68, Sa 80, or Ch 55, 10 min before 11.4 nmol of teleocidin, resulted in 76.7%, 82.0%, 76.2%, 28.3%, 48.4%, 58.6%, and 85.1% inhibition of ODC induction, respectively [10].

References

  1. Modifying effects of 1'-acetoxychavicol acetate (ACA) and the novel synthetic retinoids Re-80, Am-580 and Am-55P in a two-stage carcinogenesis model in female rats. Orita, S., Hirose, M., Takahashi, S., Imaida, K., Ito, N., Shudo, K., Ohigashi, H., Murakami, A., Shirai, T. Toxicologic pathology. (2004) [Pubmed]
  2. Glucocorticoids promote the proliferation and antagonize the retinoic acid-mediated growth suppression of Epstein-Barr virus-immortalized B lymphocytes. Quaia, M., Zancai, P., Cariati, R., Rizzo, S., Boiocchi, M., Dolcetti, R. Blood (2000) [Pubmed]
  3. Evidence for the involvement of both retinoic acid receptor- and retinoic X receptor-dependent signaling pathways in the induction of tissue transglutaminase and apoptosis in the human myeloma cell line RPMI 8226. Joseph, B., Lefebvre, O., Méreau-Richard, C., Danzé, P.M., Belin-Plancot, M.T., Formstecher, P. Blood (1998) [Pubmed]
  4. Receptor-selective retinoid agonists and teratogenic activity. Willhite, C.C., Dawson, M.I., Reichert, U. Drug Metab. Rev. (1996) [Pubmed]
  5. Differential regulation of protein expression, growth and apoptosis by natural and synthetic retinoids. Christine Pratt, M.A., Niu, M., White, D. J. Cell. Biochem. (2003) [Pubmed]
  6. Three novel synthetic retinoids, Re 80, Am 580 and Am 80, all exhibit anti-angiogenic activity in vivo. Oikawa, T., Okayasu, I., Ashino, H., Morita, I., Murota, S., Shudo, K. Eur. J. Pharmacol. (1993) [Pubmed]
  7. Retinoic acid receptor alpha mediates growth inhibition by retinoids in human colon carcinoma HT29 cells. Nicke, B., Kaiser, A., Wiedenmann, B., Riecken, E.O., Rosewicz, S. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
  8. Retinoids induce lumen morphogenesis in mammary epithelial cells. Montesano, R., Soulié, P. J. Cell. Sci. (2002) [Pubmed]
  9. Effects of retinoids on the production of tumour necrosis factor-alpha and nitric oxide by lipopolysaccharide-stimulated rat Kupffer cells in vitro: evidence for participation of retinoid X receptor signalling pathway. Motomura, K., Sakai, H., Isobe, H., Nawata, H. Cell Biochem. Funct. (1997) [Pubmed]
  10. Inhibition of ornithine decarboxylase induction by retinobenzoic acids in relation to their binding affinities to cellular retinoid-binding proteins. Takagi, K., Suganuma, M., Kagechika, H., Shudo, K., Ninomiya, M., Muto, Y., Fujiki, H. J. Cancer Res. Clin. Oncol. (1988) [Pubmed]
 
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