Selective inhibition of Src SH2 by a novel thiol-targeting tricarbonyl-modified inhibitor and mechanistic analysis by (1)H/(13)C NMR spectroscopy

Bioorg Med Chem Lett. 2001 Jul 9;11(13):1665-9. doi: 10.1016/s0960-894x(01)00269-4.

Abstract

Detailed analysis of Src SH2 binding by peptides containing a novel tricarbonyl-modified pTyr moiety is described. We envisaged that Src SH2 selectivity might be obtained by exploiting the thiol group of Cys188 present in the pTyr binding pocket of the protein at the betaC3 position. Peptidyl as well as non-peptidyl compounds 1-4 possessing a 4-alpha,beta-diketoester-modified pTyr mimic exhibited micromolar affinity to Src SH2. Furthermore, these tricarbonyl compounds were selective for Src SH2 to the extent they showed no significant affinity for either Cys188Ser or Cys188Ala Src SH2 mutants. Upon closer examination of the binding of these tricarbonyls to Src SH2 using NMR of 13C-labeled compounds (6a, 6b, and 6c), we found that after the initial binding event the molecule disproportionated in a 'retro-Claisen' fashion to provide benzoic acid 16 and, following hydrolysis of the methyl ester 17, the hemiketal adduct of glyoxalic acid 18.

MeSH terms

  • Carbon Isotopes
  • Enzyme Inhibitors / chemistry
  • Enzyme Inhibitors / pharmacology*
  • Nuclear Magnetic Resonance, Biomolecular
  • Protons
  • Sulfhydryl Compounds / metabolism*
  • src Homology Domains*
  • src-Family Kinases / antagonists & inhibitors*
  • src-Family Kinases / chemistry

Substances

  • Carbon Isotopes
  • Enzyme Inhibitors
  • Protons
  • Sulfhydryl Compounds
  • src-Family Kinases