Targeting JNK for therapeutic benefit: from junk to gold?

Nat Rev Drug Discov. 2003 Jul;2(7):554-65. doi: 10.1038/nrd1132.


The c-Jun NH(2)-terminal kinases (JNKs) phosphorylate and activate members of the activator protein-1 (AP-1) transcription factor family and other cellular factors implicated in regulating altered gene expression, cellular survival and proliferation in response to cytokines and growth factors, noxious stimuli and oncogenic transformation. Because these events are commonly associated with the pathogenesis of a number of human diseases, the potential of JNK inhibitors as therapeutics has attracted considerable interest. Here we discuss the evidence supporting the application of JNK inhibitors in inflammatory, vascular, neurodegenerative, metabolic and oncological diseases in humans, and describe the present status of drug discovery targeting JNK.

Publication types

  • Review

MeSH terms

  • Animals
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / metabolism
  • Drug Design
  • Enzyme Inhibitors / pharmacology
  • Enzyme Inhibitors / therapeutic use*
  • Humans
  • Inflammation / drug therapy
  • Inflammation / immunology
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors*
  • Mitogen-Activated Protein Kinases / physiology
  • Neoplasms / drug therapy
  • Neoplasms / metabolism
  • Neurodegenerative Diseases / drug therapy
  • Neurodegenerative Diseases / etiology
  • Obesity / drug therapy
  • Obesity / metabolism
  • Signal Transduction
  • T-Lymphocytes / immunology


  • Enzyme Inhibitors
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases