The Quest for Orally Available Selective Estrogen Receptor Degraders (SERDs)

ChemMedChem. 2020 Nov 18;15(22):2072-2097. doi: 10.1002/cmdc.202000473. Epub 2020 Oct 27.

Abstract

Estrogen receptor-alpha (ERα) is the target of endocrine therapies for the treatment of more than 70 % of ERα-positive breast cancers. Selective estrogen receptor degraders (SERDs) antagonize estrogen binding and target the receptor for degradation, representing the last line of treatment for resistant metastatic breast cancer patients. However, the clinical efficacy of the lone clinically approved SERD (Fulvestrant) is limited by its poor oral bioavailability. Recently, several analogues of GW5638, an acrylic acid-based ERα ligand developed by Glaxo Research Institute in 1994, have been reported as promising orally bioavailable SERDs. Some of these compounds are currently in clinical trials, while various other structurally novel SERDs have also been reported by pharma as well as academic research groups. This review provides a critical analysis of the recent developments in orally available SERDs, with a focus on the structure-activity relationships, binding interactions and pharmacokinetic properties of these compounds.

Keywords: anti-tumor agents; cancer; drug design; medicinal chemistry; structure-activity relationships.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Administration, Oral
  • Antineoplastic Agents / administration & dosage
  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology*
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Cell Proliferation / drug effects
  • Estrogen Antagonists / administration & dosage
  • Estrogen Antagonists / chemistry
  • Estrogen Antagonists / pharmacology*
  • Estrogen Receptor alpha / antagonists & inhibitors*
  • Estrogen Receptor alpha / metabolism
  • Female
  • Humans
  • Molecular Structure

Substances

  • Antineoplastic Agents
  • ESR1 protein, human
  • Estrogen Antagonists
  • Estrogen Receptor alpha