Tyrphostins I: synthesis and biological activity of protein tyrosine kinase inhibitors

J Med Chem. 1989 Oct;32(10):2344-52. doi: 10.1021/jm00130a020.

Abstract

A novel class of low molecular weight protein tyrosine kinase inhibitors is described. These compounds constitute a systematic series of molecules with a progressive increase in affinity toward the substrate site of the EGF receptor kinase domain. These competitive inhibitors also effectively block the EGF-dependent autophosphorylation of the receptor. The potent EGF receptor kinase blockers examined were found to competitively inhibit the homologous insulin receptor kinase at 10(2)-10(3) higher inhibitor concentrations in spite of the significant homology between these protein tyrosine kinases. These results demonstrate the ability to synthesize selective tyrosine kinase inhibitors. The most potent EGF receptor kinase inhibitors also inhibit the EGF-dependent proliferation of A431/clone 15 cells with little or no effect on EGF independent cell growth. These results demonstrate the potential use of protein tyrosine kinase inhibitors as selective antiproliferative agents for proliferative diseases caused by the hyperactivity of protein tyrosine kinases. We have suggested the name "tyrphostins" for this class of antiproliferative compounds which act as protein tyrosine kinase blockers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Benzylidene Compounds / chemical synthesis*
  • Benzylidene Compounds / pharmacology
  • Carcinoma, Squamous Cell
  • Cell Division / drug effects
  • Cell Line
  • Epidermal Growth Factor / pharmacology
  • ErbB Receptors / drug effects
  • ErbB Receptors / metabolism
  • Humans
  • Kinetics
  • Molecular Structure
  • Nitriles / chemical synthesis*
  • Nitriles / pharmacology
  • Phosphorylation
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Structure-Activity Relationship

Substances

  • Benzylidene Compounds
  • Nitriles
  • Epidermal Growth Factor
  • ErbB Receptors
  • Protein-Tyrosine Kinases