SEATTLE, June 20, 2012 /PRNewswire/ -- Cell Therapeutics, Inc. ("CTI") (NASDAQ and MTA: CTIC), a company focused on translating science into novel cancer therapies, today announced that it is re-aligning its resources and re-prioritizing its product development pipeline to focus on the launch of Pixuvri in the EU and accelerate the advancement of pacritinib, CTI's recently-acquired, highly-selective JAK 2 inhibitor, into phase III clinical trials. As a result, CTI's operating burn rate will be reduced from an average of $6.5 million per month to an average of $4.5 million per month.
"In-market research across the five largest EU markets confirms significant physician interest in product adoption in the target patient population. With the potential to generate meaningful Pixuvri® product sales, coupled with the recent acquisition of pacritinib and investigator interest in participating in its pivotal studies, we believe that focusing our resources on the Pixuvri launch and accelerating the start of pacritinib phase III studies is the best deployment of our limited resources to build near-term shareholder value," said James A. Bianco, M.D., Chief Executive Officer of CTI.
"We are re-evaluating the tostedostat phase III clinical trial design and are considering both studies in a refractory setting and in front line treatment," said Steven E. Benner, M.D., M.H.S, CMO of CTI. "With two ongoing phase II investigator-sponsored trials examining the activity of combining tosedostat with hypomethylating agents (HMAs), we should have adequate data to make an evidence-based decision on the trial design with the highest probability of both regulatory and commercial success by early next year."
About Pixuvri (pixantrone)Pixuvri is a novel aza-anthracenedione with unique structural and physio-chemical properties. Unlike related compounds, Pixuvri forms stable DNA adducts and in preclinical models has superior anti-lymphoma activity compared to related compounds. Pixuvri was structurally designed so that it cannot bind iron and perpetuate oxygen radical production or form a long-lived hydroxyl metabolite -- both of which are the putative mechanisms for anthracycline-induced acute and chronic cardiotoxicity. These novel pharmacologic properties allow Pixuvri to be administered to patients with near maximal lifetime exposure to anthracyclines without unacceptable rates of cardiotoxicity, and, because Pixuvri is not a vesicant, allow it to be safely delivered via a peripheral intravenous catheter.
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