Improving the Armamentarium of PI3K Inhibitors with Isoform-Selective Agents: A New Light in the Darkness

Cancer Discov. 2017 Jul;7(7):666-669. doi: 10.1158/2159-8290.CD-17-0500.

Abstract

<b/> Excitement and drug-development efforts aimed at targetable genetic aberrations in the PI3K/AKT/mTOR pathway have declined due to the limited clinical performance of these inhibitors as monotherapies. New, more isoform-selective treatments, such as taselisib, promise to both expand the therapeutic window and increase efficacy. Cancer Discov; 7(7); 666-9. ©2017 AACR.See related article by Juric et al., p. 704.

Publication types

  • Comment

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Humans
  • Imidazoles / therapeutic use*
  • Molecular Targeted Therapy*
  • Neoplasms / drug therapy*
  • Neoplasms / epidemiology
  • Neoplasms / genetics
  • Oxazepines / therapeutic use*
  • Phosphoinositide-3 Kinase Inhibitors
  • Protein Isoforms / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Signal Transduction / drug effects*
  • TOR Serine-Threonine Kinases

Substances

  • 2-(3-(2-(1-isopropyl-3-methyl-1H-1,2-4-triazol-5-yl)-5,6-dihydrobenzo(f)imidazo(1,2-d)(1,4)oxazepin-9-yl)-1H-pyrazol-1-yl)-2-methylpropanamide
  • Antineoplastic Agents
  • Imidazoles
  • Oxazepines
  • Phosphoinositide-3 Kinase Inhibitors
  • Protein Isoforms
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases