A diphenylmethane derivative selective for the anti-estrogen binding site may help define its biological role

Biochem Biophys Res Commun. 1984 Oct 15;124(1):244-9. doi: 10.1016/0006-291x(84)90943-4.


By employing as a probe the new compound, N,N-diethyl-2-[(4-phenyl-methyl)-phenoxy]-ethanamine X HC1 (N,N-DPPE), which preferentially binds the anti-estrogen binding site, it is demonstrated that this site appears to contribute to the growth inhibitory action of tamoxifen on MCF-7 human breast cancer cells, even at lower concentrations of this anti-estrogen (1 X 10(-7) M to 1 X 10(-6) M) at which the major effect is clearly mediated via estrogen receptor. The combination of N,N-DPPE and tamoxifen is additive and this effect is not abolished by 17 beta-estradiol. This suggests that the anti-estrogen binding site is not simply a passive reservoir for binding tamoxifen, but may itself mediate the cytotoxic effects of specific ligands.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Cell Division / drug effects
  • Cell Line
  • Female
  • Humans
  • Kinetics
  • Phenyl Ethers / pharmacology*
  • Receptors, Drug*
  • Receptors, Estrogen / metabolism*
  • Tamoxifen / metabolism*
  • Tamoxifen / pharmacology


  • Phenyl Ethers
  • Receptors, Drug
  • Receptors, Estrogen
  • Tamoxifen
  • tesmilifene