In vivo effects of a GPR30 antagonist

Nat Chem Biol. 2009 Jun;5(6):421-7. doi: 10.1038/nchembio.168.

Abstract

Estrogen is central to many physiological processes throughout the human body. We have previously shown that the G protein-coupled receptor GPR30 (also known as GPER), in addition to classical nuclear estrogen receptors (ER and ER), activates cellular signaling pathways in response to estrogen. In order to distinguish between the actions of classical estrogen receptors and GPR30, we have previously characterized G-1 (1), a selective agonist of GPR30. To complement the pharmacological properties of G-1, we sought to identify an antagonist of GPR30 that displays similar selectivity against the classical estrogen receptors. Here we describe the identification and characterization of G15 (2), a G-1 analog that binds to GPR30 with high affinity and acts as an antagonist of estrogen signaling through GPR30. In vivo administration of G15 revealed that GPR30 contributes to both uterine and neurological responses initiated by estrogen. The identification of this antagonist will accelerate the evaluation of the roles of GPR30 in human physiology.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • COS Cells
  • Chlorocebus aethiops
  • Estrogens / metabolism
  • Female
  • Humans
  • Ligands
  • Male
  • Mice
  • Mice, Inbred ICR
  • Nuclear Magnetic Resonance, Biomolecular
  • Receptors, Estrogen / metabolism
  • Receptors, Estrogen / physiology*
  • Receptors, G-Protein-Coupled / antagonists & inhibitors*
  • Receptors, G-Protein-Coupled / metabolism
  • Receptors, G-Protein-Coupled / physiology
  • Signal Transduction

Substances

  • Estrogens
  • GPER1 protein, human
  • Ligands
  • Receptors, Estrogen
  • Receptors, G-Protein-Coupled