ARIAD Presents New Preclinical Data Showing AP26113 Inhibits Clinically Relevant Mutants of ALK and ROS1 Business Wire CAMBRIDGE, Mass. & WASHINGTON -- April 10, 2013 ARIAD Pharmaceuticals, Inc. (NASDAQ: ARIA) today 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. About ARIAD ARIAD Pharmaceuticals, Inc., headquartered in Cambridge, Massachusetts and Lausanne, Switzerland, is an integrated global oncology company focused on transforming the lives of cancer patients with breakthrough medicines. ARIAD is working on new medicines to advance the treatment of various forms of chronic and acute leukemia, lung cancer and other difficult-to-treat cancers. ARIAD utilizes computational and structural approaches to design small-molecule drugs that overcome resistance to existing cancer medicines. For additional information, visit http://www.ariad.comor follow ARIAD on Twitter (@ARIADPharm). This press release contains “forward-looking statements” including, but not limited to, updates on preclinical developments for our product candidates. Forward-looking statements are based on management's expectations and are subject to certain factors, risks and uncertainties that may cause actual results, outcome of events, timing and performance to differ materially from those expressed or implied by such statements. These risks and uncertainties include, but are not limited to, preclinical data and early-stage clinical data that may not be replicated in later-stage clinical studies, the costs associated with our research, development, manufacturing and other activities, the conduct, timing and results of pre-clinical and clinical studies of our product candidates, the adequacy of our capital resources and the availability of additional funding, and other factors detailed in the Company's public filings with the U.S. Securities and Exchange Commission. The information contained in this press release is believed to be current as of the date of original issue. The Company does not intend to update any of the forward-looking statements after the date of this document to conform these statements to actual results or to changes in the Company's expectations, except as required by law. Contact: ARIAD Pharmaceuticals For Investors Kendra Adams, 617-503-7028 Kendra.email@example.com or For Media Liza Heapes, 617-621-2315 Liza.firstname.lastname@example.org
ARIAD Presents New Preclinical Data Showing AP26113 Inhibits Clinically Relevant Mutants of ALK and ROS1
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