Identification of 3-substituted-6-(1-(1H-[1,2,3]triazolo[4,5-b]pyrazin-1-yl)ethyl)quinoline derivatives as highly potent and selective mesenchymal-epithelial transition factor (c-Met) inhibitors via metabolite profiling-based structural optimization

Eur J Med Chem. 2017 Jul 7:134:147-158. doi: 10.1016/j.ejmech.2017.03.085. Epub 2017 Apr 4.

Abstract

c-Met/HGF signaling pathway plays an important role in cancer progression, and it was considered to be related to poor prognosis and drug resistance. Based on metabolite profiling of (S)-7-fluoro-6-(1-(6-(1-methyl-1H-pyrazol-4-yl)-1H-imidazo[4,5-b]pyrazin-1-yl)ethyl)quinoline (1), a series of 2-substituted or 3-substituted-6-(1-(1H-[1,2,3]triazolo[4,5-b]pyrazin-1-yl)ethyl)quinoline derivatives was rationally designed and evaluated. Most of the 3-substituted derivatives not only exhibited potent activities in both enzymatic and cellular assays, but also were stable in liver microsomes among different species (human, rat and monkey). SAR investigation revealed that introducing of N-methyl-1H-pyrazol-4-yl group at the 3-position of quinoline moiety is beneficial to improve the inhibitory potency, especially in the cellular assays. The influence of fluorine atom at 7-position or 5, 7-position of quinoline moiety and substituents at the 6-position of triazolo[4,5-b]pyrazine core on overall activity is not very significant. Racemate 14, an extremely potent and exquisitely selective c-Met inhibitor, demonstrated favorable pharmacokinetic properties in rats, no significant AO metabolism, and effective tumor growth inhibition in c-Met overexpressed NSCLC (H1993 cell line) and gastric cancer (SNU-5 cell line) xenograft models. Docking analysis indicated that besides the typical interactions of most selective c-Met inhibitors, the intramolecular halogen bond and additional hydrogen bond interactions with kinase are beneficial to the binding. These results may provide deep insight into potential structural modifications for developing potent c-Met inhibitors.

Keywords: 3-Substituted quinolines; Docking study; Metabolism; SAR; Triazolopyrazine; c-Met.

MeSH terms

  • Animals
  • Carcinoma, Non-Small-Cell Lung / drug therapy
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Cell Line, Tumor
  • Female
  • Gastric Mucosa / metabolism
  • Haplorhini
  • Humans
  • Lung / drug effects
  • Lung / metabolism
  • Lung Neoplasms / drug therapy
  • Lung Neoplasms / metabolism
  • Male
  • Mice, Inbred BALB C
  • Mice, Nude
  • Molecular Docking Simulation
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Protein Kinase Inhibitors / chemistry*
  • Protein Kinase Inhibitors / pharmacokinetics
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use*
  • Proto-Oncogene Proteins c-met / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-met / metabolism
  • Pyrazines / chemistry
  • Pyrazines / pharmacokinetics
  • Pyrazines / pharmacology
  • Pyrazines / therapeutic use
  • Quinolines / chemistry*
  • Quinolines / pharmacokinetics
  • Quinolines / pharmacology
  • Quinolines / therapeutic use*
  • Rats
  • Rats, Sprague-Dawley
  • Stomach / drug effects
  • Stomach Neoplasms / drug therapy
  • Stomach Neoplasms / metabolism

Substances

  • Protein Kinase Inhibitors
  • Pyrazines
  • Quinolines
  • Proto-Oncogene Proteins c-met