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ARIAD Presents Data for Investigational Inhibitor

Published: Thursday, April 11, 2013
Last Updated: Thursday, April 11, 2013
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New preclinical data showing AP26113 inhibits clinically relevant mutants of ALK and ROS1.

ARIAD Pharmaceuticals, Inc. announced the presentation of preclinical data on AP26113, an investigational inhibitor of anaplastic lymphoma kinase (ALK), epidermal growth factor receptor (EGFR), and c-ros oncogene 1 (ROS1), at the American Association for Cancer Research (AACR) Annual Meeting 2013, in Washington.

The study, “AP26113 possesses pan-inhibitory activity versus crizotinib-resistant ALK mutants and oncogenic ROS1 fusions,” shows that AP26113 inhibits clinically relevant crizotinib-resistant ALK mutants and oncogenic ROS1 fusions recently identified in patients with non-small cell lung cancer (NSCLC).

The research conducted by ARIAD scientists was determined using cell lines harboring crizotinib-resistant mutant forms of ALK and oncogenic ROS1 fusions, tested in both in vitro studies and mouse-disease models.

“This preclinical research demonstrates that AP26113 inhibits all nine clinically identified crizotinib-resistant ALK mutations, at plasma concentrations we know to be clinically achievable,” said Timothy P. Clackson, Ph.D., president of research and development and chief scientific officer at ARIAD. “Some of these mutations were also shown to be resistant to additional ALK inhibitors other than crizotinib. This supports the potential of AP26113 to offer a pan-ALK inhibitor profile.”

AP26113 was also shown to inhibit ROS1 fusions as potently as it inhibits ALK, to retain activity against the gatekeeper mutation of ROS1, and to substantially suppress the outgrowth of resistant ROS1 cells in a mutation assay, all at clinically achievable plasma concentrations. These data suggest that AP26113 may be able to avoid the emergence of drug-resistant mutants in NSCLC patients with these oncogenic gene fusions.

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