ARIAD Pharmaceuticals, Inc.’s (ARIA) shares slipped 40.7% on Oct 18, 2013 following the company’s announcement of the discontinuation of a phase III EPIC (Evaluation of Ponatinib versus Imatinib in Chronic Myeloid Leukemia) study on Iclusig. On Oct 21, shares however gained marginally to close at $2.94. We note that ARIAD shares slipped approximately 66% on Oct 9, 2013 to close at $5.83 following the company’s announcement that the U.S. Food and Drug Administration (:FDA) has placed a partial clinical hold on enrolling new patients in studies on Iclusig due to safety issues. Since the start of the month shares have plummeted approximately 84%.
ARIAD discontinued the phase III EPIC study, in which Iclusig was being compared to Novartis’ (NVS) Gleevec in patients with newly diagnosed chronic myeloid leukemia (:CML). The decision was taken in the wake of arterial thrombotic events observed in patients treated with Iclusig. The randomized (1:1), two-arm, multicenter EPIC study was supposed to evaluate 500 patients of at least 18 years of age. The primary endpoint of the study was major molecular response at 1 year of treatment.
Iclusig, a tyrosine kinase inhibitor (:TKI), launched in the U.S. in Jan 2013, is currently marketed by ARIAD for treating adults suffering from CML, and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), who are resistant or intolerant to TKI therapy. ARIAD recorded Iclusig sales of $13.9 million in the second quarter of 2013.
In Jul 2013, ARIAD gained EU approval for Iclusig for a couple of indications. The first indication is the treatment of chronic phase, accelerated phase or blast phase CML in adults who do not respond to or cannot tolerate Sprycel or Tasigna. It is also approved for treating patients in whom Gleevec is not appropriate as a subsequent treatment. The second indication covers the treatment of Ph+ ALL in adults unresponsive to Sprycel. It also includes patients for whom Gleevec is not clinically appropriate. Iclusig is also approved for patients who have the T315I mutation.