Lead optimization of a dihydropyrrolopyrimidine inhibitor against phosphoinositide 3-kinase (PI3K) to improve the phenol glucuronic acid conjugation

Bioorg Med Chem Lett. 2013 Feb 1;23(3):673-8. doi: 10.1016/j.bmcl.2012.11.112. Epub 2012 Dec 3.

Abstract

Our lead compound for a phosphoinositide 3-kinase (PI3K) inhibitor (1) was metabolically unstable because of rapid glucuronidation of the phenol moiety. Based on structure-activity relationship (SAR) information and a FlexSIS docking simulation score, aminopyrimidine was identified as a bioisostere of phenol. An X-ray structure study revealed a hydrogen bonding pattern of aminopyrimidine derivatives. Finally, aminopyrimidine derivatives 33 showed strong tumor growth inhibition against a KPL-4 breast cancer xenograft model in vivo.

MeSH terms

  • Animals
  • Breast Neoplasms / drug therapy
  • Cell Line, Tumor
  • Crystallography, X-Ray
  • Enzyme Activation / drug effects
  • Female
  • Glucuronic Acid / chemistry*
  • Humans
  • Hydrogen Bonding
  • Inhibitory Concentration 50
  • Mice
  • Molecular Structure
  • Phenols / chemistry*
  • Phosphoinositide-3 Kinase Inhibitors*
  • Pyrimidines / chemical synthesis*
  • Pyrimidines / chemistry
  • Pyrimidines / pharmacology
  • Pyrroles / chemical synthesis*
  • Pyrroles / chemistry
  • Pyrroles / pharmacology
  • Structure-Activity Relationship
  • Xenograft Model Antitumor Assays

Substances

  • Phenols
  • Phosphoinositide-3 Kinase Inhibitors
  • Pyrimidines
  • Pyrroles
  • pyrrolopyrimidine
  • Glucuronic Acid