ARIAD Pharmaceuticals, Inc. (ARIA)
ARIAD ESMO Investor Call
October 1, 2012 8:00 am ET
Maria E. Cantor – Senior Vice President, Corporate Affairs
Harvey J. Berger – Chairman and Chief Executive Officer
Scott N. Gettinger – Associate Professor of Medicine, Yale School of Medicine
Frank G. Haluska – Chief Medical Officer and Senior Vice President, Clinical R&D
Timothy P. Clackson – President of Research and Development and Chief Scientific Officer
Michael J. Yee – RBC Capital Markets
Matthew Harrison - UBS Securities LLC
Cory Kasimov – JPMorgan
Jim Birchenough – BMO Capital Markets
Joel D. Sendek – Stifel, Nicolaus & Co., Inc.
Phil Nadeau – Cowen & Co. LLC
Ying Huang – Barclays Capital, Inc.
Howard Liang – Leerink Swann LLC
Mike King – Dawson James Securities, Inc
Ryan S. Martins – Lazard Capital Markets LLC
Ling Wang – Summer Street Research Partners
Y. Katherine Xu – William Blair & Co. LLC
Echo Yinghui He - Maxim Group Securities
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At this time, I’d like to introduce Ms. Maria Cantor, ARIAD’s Senior Vice President Corporate Communications and Investor Relations. Please go ahead ma’am.
Maria E. Cantor
Good morning and welcome to ARIAD’s investor call and webcast. This morning we will review the clinical data presented Saturday at the 2012 Congress of the European Society for Medical Oncology from an ongoing Phase 1/2 study of our investigational tyrosine-kinase inhibitor, AP26113 in patients with advanced non-small cell lung cancer. You can access the presentation slides that we will review this morning by going to the investor page of ARIAD’s website www.ariad.com and clicking on the link to this morning’s webcast.
Joining me for this call are Dr. Harvey Berger, our Chairman and Chief Executive Officer; Dr. Tim Clackson, our President of Research and Development and Chief Scientific Officer; and Dr. Frank Haluska, our Senior Vice President for Clinical Research and Chief Medical Officer. Also joining us today is Scott Gettinger, Associate Professor of Medicine at Yale School of Medicine and an investigator in the Phase 1/2 study.
Before we get started, I’d like to state that during this call, we will be making forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements are subject to factors, risks and uncertainties such as those detailed in our filings with the U.S. Securities and Exchange Commission that may cause actual results to differ materially from the results expressed or implied by such statements.
Now, I’d like to turn the call over to Dr. Berger for opening remarks.
Harvey J. Berger
Thank you very much Maria, and good morning everyone. We’re very pleased to have the opportunity to update you on the clinical data’s that were presented this weekend from our ongoing Phase 1/2 trial of 113 in patients with advanced non-small cell lung cancer. We believe this study provides compelling clinical evidence of the anti-tumor activity of 113 at multiple dose levels in patients with ALK+ lung cancer, as well as initial clinical evidence of anti-tumor activity in patients with EGFR+ lung cancer.
During Saturday’s oral presentation at the ESMO meeting, Dr. Scott Gettinger detailed the findings to date from the Phase 1 dose escalation portion of the ongoing Phase 1/2 trial. We are very fortunate today to have Dr. Gettinger with us this morning to review the data and answer your questions about 113, about lung cancer, and about various new investigational treatment options for lung cancer.
As Maria noted earlier, the slide that Dr. Gettinger is about to present are available on the investor page of ARIAD’s website. Let me now hand the call over to him, to present the data and his perspectives on the key findings. Dr. Gettinger?
Scott N. Gettinger
Thank you Harvey. And it's my pressure today to talk to you about this Phase 1/2 Study of AP26113 and to share with you some of the findings today.
As you may know, the most exciting development in lung cancer over the last decade has been the identification of key driver molecular events in some of our patients with lung cancer, that are targetable with some of these newer oral tyrosine-kinase inhibitors. The first one that we heard about back in 2004 is the EGFR mutation, which lends itself to treatment with Tarceva, a small molecule inhibitor of the EGFR.
And back in 2003, 2004 we saw some dramatic responses in a trial evaluating an agent called gefitinib, and when we went back, we looked at that tissue from some of the patients we found this EGFR mutation. We then heard about an ALK rearrangement in a patient with lung cancer in 2007, and within a few short years crizotinib, small molecule inhibitor of ALK was developed and approved in the United States and Europe for treatment, based upon very high response rate similar to what we see with Tarceva, and patients with EGFR mutant disease.
Recently, we've heard about the ROS1 translocation and patients who have tumors driven by this molecular event into response as well to crizotinib as patients who have ALK rearranged lung cancer. So the problem with these wonderful drugs is that inevitably patients develop resistance, usually that happens within ten to twelve months. We’ve learned a bit about mechanisms of resistance in patients who have EGFR mutant lung cancer that has become resistant to either erlotinib or gefitinib medications now used to treat these patients. We’ve found that roughly 50% of them will be found to harbor a second EGFR mutation, known as the T790M mutation. And if the tumor harbors this, the effects of Tarceva are limited in these patients or gefitinib.
For patients with ALK rearranged lung cancer who develop resistance to crizotinib, we see similar mutations in ALK although at a lower frequency. And for patients with ROS1 translocations, we’re just beginning to treat them with crizotinib and by doing that repeat biopsies on our patients which I think most academic oncologists are dedicated to, we’re going to learn about mechanisms of resistance in that population as well.