Clovis Oncology Announces Enrollment Of First Patient In First Human Study Of Oral EGFR Mutant-Selective Inhibitor CO-1686

Clovis Oncology, Inc. (Nasdaq: CLVS) announced today that the first clinical study of CO-1686 has commenced with the dosing of the first patient at a U.S. study site. CO-1686 is a novel, oral, targeted covalent inhibitor of epidermal growth factor receptor (EGFR) mutations currently being studied for the treatment of non-small cell lung cancer (NSCLC).

The dose escalation portion of the Phase I/II study is being conducted at 5 sites in the U.S. and Europe, and the Company intends to initiate a parallel Phase I/II study in Asia during the third quarter of 2012. Following the establishment of the appropriate dose, Clovis intends to study CO-1686 in an expansion cohort of NSCLC patients who have failed EGFR-directed therapy, such as Tarceva ^® or Iressa ^®, and have developed the T790M mutation, which is the dominant resistance mechanism to Tarceva and Iressa. Clovis is developing a companion diagnostic in collaboration with Roche Molecular Systems, Inc. to identify patients with the T790M mutation.

“While the development of EGFR tyrosine kinase inhibitor therapy for NSCLC patients with EGFR mutations has been a major advance, resistance develops after about a year and is a major obstacle lung oncologists face in the clinic each day,” said Lecia Sequist, Thoracic Medical Oncologist at Massachusetts General Cancer Center, Assistant Professor of Medicine at Harvard Medical School and an investigator in the study. “At the current time, there are no approved standard treatments available for patients with the T790M resistance mutation. Better solutions to this problem are desperately needed.”

“CO-1686 is the first covalent inhibitor to enter the clinic designed to target both the activating mutations of EGFR and the resistance mutation T790M, and we are committed to working with our investigators to rapidly develop this compound,” said Patrick J. Mahaffy, president and CEO of Clovis Oncology. “As has been presented at scientific meetings, CO-1686 is highly potent against these mutations of EGFR, including T790M, while sparing wild-type EGFR, and we are pleased to seek confirmation of these characteristics in patients.”

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