93O - First-in-human evaluation of CO-1686, an irreversible, highly selective tyrosine kinase inhibitor of mutations of EGFR (activating and T790M)

Date 27 March 2014
Event ELCC 2014
Session Proffered Papers 1 - Advanced disease with tageted agents
Topics Drug Development
Non-Small-Cell Lung Cancer, Metastatic
Translational Research
Presenter Heather Wakelee
Citation Journal of Thoracic Oncology (2014) 9 (Supplement 9): S7-S52. 10.1097/JTO.0000000000000131
Authors H. Wakelee1, J. Soria2, R. Camidge3, S. Gadgeel4, J. Goldman5, A. Varga2, B. Solomon6, V. Papadimitrakopoulou7, P. Kaur8, L.V. Sequist9
  • 1Thoracic Oncology, Stanford University, 94305 - Stanford/US
  • 2Medical, Institut Gustave Roussy, Villejuif/FR
  • 3Medical, University of Colorado, Denver/US
  • 4Medical, Karmanos Cancer Institute, Detroit/US
  • 5Medical, UCLA, Santa Monica/US
  • 6Department Of Medical Oncology, Peter MacCallum Cancer Centre, Melbourne/AU
  • 7Medical Oncology, MD Anderson Cancer Center, Houston/US
  • 8Clinical, Clovis Oncology, Boulder/US
  • 9Medical, Massachusetts General Hospital, Boston/US



Efficacy of existing EGFR tyrosine kinase inhibitors (TKIs) in NSCLC is limited by emergence of the T790M mutation in approximately 60% of patients, and significant skin rash and diarrhea, caused by wild-type (WT)-EGFR inhibition. CO-1686 is an oral, covalent TKI that targets common activating EGFR mutations and T790M, while sparing WT-EGFR.