Novel compounds reducing IRS-1 serine phosphorylation for treatment of diabetes

Laura Simon-Szabó, Márton Kokas, Zoltán Greff, Sándor Boros, Péter Bánhegyi, Lilián Zsákai, Csaba Szántai-Kis, T. Vántus, J. Mandl, G. Bánhegyi, István Vályi-Nagy, L. Őrfi, Axel Ullrich, M. Csala, G. Kéri

Research output: Contribution to journalArticle

8 Citations (Scopus)


Activation of various interacting stress kinases, particularly the c-Jun N-terminal kinases (JNK), and a concomitant phosphorylation of insulin receptor substrate 1 (IRS-1) at serine 307 play a central role both in insulin resistance and in β-cell dysfunction. IRS-1 phosphorylation is stimulated by elevated free fatty acid levels through different pathways in obesity. A series of novel pyrido[2,3-d]pyrimidin-7-one derivatives were synthesized as potential antidiabetic agents, preventing IRS-1 phosphorylation at serine 307 in a cellular model of lipotoxicity and type 2 diabetes.

Original languageEnglish
Pages (from-to)424-428
Number of pages5
JournalBioorganic and Medicinal Chemistry Letters
Issue number2
Publication statusPublished - Jan 15 2016


  • c-Jun N-terminal kinase
  • IRS-1 phosphorylation
  • Lipotoxicity
  • Pyrido[2,3-d]pyrimidin
  • Type 2 diabetes

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Molecular Biology
  • Molecular Medicine
  • Organic Chemistry
  • Drug Discovery
  • Pharmaceutical Science

Fingerprint Dive into the research topics of 'Novel compounds reducing IRS-1 serine phosphorylation for treatment of diabetes'. Together they form a unique fingerprint.

  • Cite this