Pharmacological characterization of a new, orally active and potent allosteric metabotropic glutamate receptor 1 antagonist, 4-[1-(2-fluoropyridin-3-yl)-5-methyl-1H-1,2,3-triazol-4-yl]-N-isopropyl-N-methyl-3,6-dihydropyridine-1(2H)-carboxamide (FTIDC)

J Pharmacol Exp Ther. 2007 Jun;321(3):1144-53. doi: 10.1124/jpet.106.116574. Epub 2007 Mar 14.

Abstract

A highly potent and selective metabotropic glutamate receptor (mGluR) 1 antagonist, 4-[1-(2-fluoropyridin-3-yl)-5-methyl-1H-1,2, 3-triazol-4-yl]-N-isopropyl-N-methyl-3,6-dihydropyridine-1(2H)-carboxamide (FTIDC), is described. FTIDC inhibits, with equal potency, l-glutamate-induced intracellular Ca(2+) mobilization in Chinese hamster ovary cells expressing human, rat, or mouse mGluR1a. The IC(50) value of FTIDC is 5.8 nM for human mGluR1a and 6200 nM for human mGluR5. The maximal response in agonist concentration-response curves was reduced in the presence of higher concentrations of FTIDC, suggesting the inhibition in a noncompetitive manner. FTIDC at 10 microM showed no agonistic, antagonistic, or positive allosteric modulatory activity toward mGluR2, mGluR4, mGluR6, mGluR7, or mGluR8. FTIDC did not displace [(3)H]l-quisqualate binding to human mGluR1a, indicating FTIDC is an allosteric antagonist. Studies using chimeric and mutant receptors of mGluR1 showed that transmembrane (TM) domains 4 to 7, especially Phe801 in TM6 and Thr815 in TM7, play pivotal roles in the antagonism of FTIDC. FTIDC inhibited the constitutive activity of mGluR1a, suggesting that FTIDC acts as an inverse agonist of mGluR1a. Intraperitoneally administered FTIDC inhibited face-washing behavior elicited by a group I mGluR agonist, (S)-3,5-dihydroxyphenylglycine in mice at doses that did not produce motor impairment. Oral administration of FTIDC also inhibited the face-washing behavior. FTIDC is a highly potent and selective allosteric mGluR1 antagonist and a compound having oral activity without species differences in its antagonistic activity on recombinant human, mouse, and rat mGluR1. FTIDC could therefore be a valuable tool for elucidating the functions of mGluR1 not only in rodents but also in humans.

MeSH terms

  • Animals
  • Benzimidazoles / pharmacology
  • Binding, Competitive
  • CHO Cells
  • Calcium Signaling / drug effects
  • Cell Line
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Cricetinae
  • Cricetulus
  • Dose-Response Relationship, Drug
  • Glutamic Acid / pharmacology
  • Humans
  • Inositol Phosphates / metabolism
  • Male
  • Mice
  • Mice, Inbred ICR
  • Molecular Structure
  • Motor Activity / drug effects
  • Naphthalenes / pharmacology
  • Point Mutation
  • Quisqualic Acid / pharmacology
  • Rats
  • Receptors, Metabotropic Glutamate / agonists
  • Receptors, Metabotropic Glutamate / antagonists & inhibitors*
  • Receptors, Metabotropic Glutamate / genetics
  • Receptors, Metabotropic Glutamate / metabolism
  • Thiazoles / pharmacology
  • Transfection
  • Triazoles / chemistry
  • Triazoles / metabolism
  • Triazoles / pharmacology*

Substances

  • 4-(1-(2-fluoropyridin-3-yl)-5-methyl-1H-1,2,3,-triazol-4-yl)-N-isopropyl-N-methyl-3,6-dihydropyridine-1(2H)-carboxamide
  • 6-amino-N-cyclohexyl-N,3-dimethylthiazolo(3,2-a)benzimidazole-2-carboxamide
  • BAY36-7620
  • Benzimidazoles
  • Inositol Phosphates
  • Naphthalenes
  • Receptors, Metabotropic Glutamate
  • Thiazoles
  • Triazoles
  • metabotropic glutamate receptor type 1
  • Glutamic Acid
  • Quisqualic Acid