PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib

  • Cancer Res. 2007 Dec 15;67(24):11924-32. doi: 10.1158/0008-5472.CAN-07-1885.
Jeffrey A Engelman  1 ,  Kreshnik Zejnullahu ,  Christopher-Michael Gale ,  Eugene Lifshits ,  Andrea J Gonzales ,  Takeshi Shimamura ,  Feng Zhao ,  Patrick W Vincent ,  George N Naumov ,  James E Bradner ,  Irene W Althaus ,  Leena Gandhi ,  Geoffrey I Shapiro ,  James M Nelson ,  John V Heymach ,  Matthew Meyerson ,  Kwok-Kin Wong ,  Pasi A Jänne
Affiliations
  • 1. Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA.
Abstract

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors gefitinib and erlotinib are effective treatments for a subset of non-small cell lung cancers. In particular, cancers with specific EGFR-activating mutations seem to be the most sensitive to these agents. However, despite their initial response, such cancers almost invariably develop resistance. In 50% of such cancers, a secondary EGFR mutation, T790M, has been identified that renders gefitinib and erlotinib ineffective inhibitors of EGFR kinase activity. Thus, there is a clinical need to develop novel EGFR inhibitors that can effectively inactivate T790M-containing EGFR proteins. In this study, we evaluate the effectiveness of a novel compound, PF00299804, an irreversible pan-ERBB inhibitor. The results from these studies show that PF00299804 is a potent inhibitor of EGFR-activating mutations as well as the EGFR T790M resistance mutation both in vitro and in vivo. Additionally, PF00299804 is a highly effective inhibitor of both the wild-type ERBB2 and the gefitinib-resistant oncogenic ERBB2 mutation identified in lung cancers. These preclinical evaluations support further clinical development of PF00299804 for cancers with mutations and/or amplifications of ERBB family members.

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