SEATTLE and SINGAPORE, April 19, 2012 /PRNewswire/ -- Cell Therapeutics, Inc.("CTI") (Nasdaq and MTA: CTIC) and S*BIO Pte Ltd announced today that the companies have entered into an asset purchase agreement pursuant to which CTI would acquire world-wide rights to S*BIO's pacritinib, a highly selective JAK2 inhibitor. Pacritinib is an oral JAK2 (Janus Associated Kinase 2) selective inhibitor that has demonstrated encouraging clinical benefit in phase 1 and 2 clinical studies in patients with primary myelofibrosis (MF) or MF secondary to other myeloproliferative neoplasms (MPN). Pacritinib has orphan drug designation in the U.S. and Europe for myelofibrosis.
"JAK2 dysregulation is associated with a broad range of difficult-to-treat illnesses, including cancers and autoimmune diseases, and is one of the most exciting potential new targets in cancer therapy today," said James A. Bianco, M.D., CEO of Cell Therapeutics, Inc. "We believe a highly selective JAK2 inhibitor that also inhibits the JAK2 clonal mutation (JAK2V617F) offers a distinct biological and clinical advantage over marketed or development stage compounds which are non-selective inhibitors of the JAK pathway. We believe that the lack of suppression of red blood cell and platelet formation seen with pacritinib has the potential to satisfy a medical need not currently addressed with existing non-selective JAK1/JAK2 inhibitors."
"The acquisition of pacritinib is aligned with our strategy of becoming a leader in the treatment of blood related cancers and disorders. We are looking forward to build on the progress made by S*BIO," Bianco continued. "With Pixuvri approaching approval and launch in the EU, and tosedostat and pacritinib entering phase 3 our late stage portfolio addresses a full complement of blood related cancers ranging from MPN to MDS, leukemia and lymphoma."
"JAK inhibitors are a very exciting new class of targeted agents that provide effective treatment in a previously difficult to treat disease called myelofibrosis," stated Srdan Verstovsek, M.D., Ph.D., Associate Professor, Department of Leukemia, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas and Executive Committee Member, International Working Group for Myelofibrosis. "Pacritinib is a highly specific JAK2 inhibitor that does not appear to cause suppression of platelets or red blood cells as seen with other treatments, while reducing enlarged spleen and improving disease related debilitating symptoms in patients with myelofibrosis. I am looking forward to working with Cell Therapeutics in developing this agent for patients with myelofibrosis who present with low blood counts or develop them on therapy."
"We are most impressed with CTI's experienced team and believe that they are the ideal company to further develop pacritinib, S*BIO's most advanced program," commented Ms. Tamar Howson, S*BIO's CEO. S*BIO is a privately-held biotechnology company focused on the research and clinical development of novel targeted small molecule drugs for the treatment of cancer with leading programs around kinases and histone deacetylases (HDAC). S*BIO has strong links with a network of medical oncologists in Asia Pacific and its investors include Bio*One Capital a subsidiary of EDBI, Aravis Ventures, Mitsui Ventures and other international funds.
Pursuant to the terms of the agreement, CTI will make an upfront payment of $15 million and issue $15 million shares of unregistered preferred stock convertible into common stock in CTI. The agreement also includes regulatory success- and sales-based milestone payments, as well as single digit royalties on net sales. CTI will be solely responsible for development and commercialization activities of pacritinib worldwide. The agreement will be subject to satisfaction of certain closing conditions. The terms of the agreement will be provided in more detail in a Form 8-K to be filed with the U.S. Securities and Exchange Commission.
About Janus Associated Kinase (JAK)
The JAK family of enzymes are a central component in signal transduction pathways, which are critical to normal blood cell growth and development as well as inflammatory cytokine expression and immune responses. When dysregulated by activating mutations, uncontrolled blood cell growth can occur accompanied by inflammation and immune system activation contributing to disease manifestations in MPN. Autoimmune diseases such as psoriasis and rheumatoid arthritis also have activation of this pathway and JAK inhibitors are in development for these disorders. In addition, activation of the JAK2 pathway and the related FLT3 pathway (whether by activating mutations or other causes) is frequently associated with leukemia, and lymphoma. Pacritinib inhibits both JAK2 and FLT3 suggesting potential use in treating such blood related cancers.
Myelofibrosis is a stem cell-derived clonal myeloproliferative disease frequently associated with a mutation in the JAK2 gene (JAK2V617F). Inhibition of JAK1/ JAK2 has recently been shown to lead to clinical benefit in patients with advanced MF and platelet counts of 100,000 or higher at study entry, resulting in the first JAK1/JAK2 inhibitor to be approved for patients with advanced MF. The approved JAK inhibitor is not selective for JAK2 but inhibits both JAK1 and JAK2. While effective in reducing patients symptoms associated with MF, JAK1/JAK2 inhibitors frequently cause suppression of platelets and red blood cells, often leading to a need for red blood cell transfusions. Pacritinib may offer an advantage over other JAK inhibitors by having less bone marrow suppression. Such agents may also lead to a modification of the underlying disease process by selectively affecting the malignant clone expressing JAK2V617F.
About Myeloproliferative Neoplasms (MPN)