Lessons from the drug discovery of lapatinib, a dual ErbB1/2 tyrosine kinase inhibitor

Curr Top Med Chem. 2006;6(5):435-60. doi: 10.2174/156802606776743156.

Abstract

Protein Kinases offer many opportunities for drug intervention points since phosphorylation is the most common post-translational modification. Phosphorylation regulates activity, location, degradation, conformation and the aberrant activity is implicated in many diseases, including cancer, inflammation, cardiovascular and central nervous system diseases. The focus of this review will be on the generation of highly effective signaling inhibitors targeting members of the erbB family of receptor tyrosine kinases, EGFR and ErbB-2, also known as transmembrane Type 1 receptor tyrosine kinases of the HER family of receptors. Ligand binding to the receptor causes a conformational change which activates the tyrosine kinase domain leading to autophosphorylation. This autophosphorylation activates the RAS/mitogen activated protein (MAP) kinase and phosphoinositol-3-kinase (PI3K) pathways leading to a myriad of signaling and cellular activities. Type 1 receptors are over-expressed in a variety of cancers and generally correlate with poor prognosis. For this reason, scientists at GlaxoSmithKline and many others in the scientific community, target the ATP binding site of the intracellular portion of the protein to block the aberrant signaling event. This review intends to cover the lessons learned in the discovery of lapatinib (GW572016, GW2016) by pulling together the various different publications that have been generated in distinct disciplines on aspects of the drug discovery program. Data analyses and correlation of assay data to help with the design of drug like molecules will be included and will demonstrate a break from the traditional focus on absolute potency as a guiding factor in lead compound selection.

Publication types

  • Review

MeSH terms

  • Animals
  • Drug Design*
  • Enzyme Inhibitors / chemical synthesis
  • Enzyme Inhibitors / chemistry
  • Enzyme Inhibitors / pharmacology*
  • ErbB Receptors / antagonists & inhibitors*
  • Humans
  • Lapatinib
  • Molecular Structure
  • Neoplasms / drug therapy*
  • Quinazolines / chemical synthesis
  • Quinazolines / chemistry
  • Quinazolines / pharmacology*
  • Receptor, ErbB-2 / antagonists & inhibitors*
  • Structure-Activity Relationship

Substances

  • Enzyme Inhibitors
  • Quinazolines
  • Lapatinib
  • ErbB Receptors
  • Receptor, ErbB-2