Gilead Sciences, Inc. (Nasdaq: GILD) and YM BioSciences Inc. (NYSE MKT: YMI, TSX: YM) announced today that the companies have signed a definitive agreement under which Gilead will acquire YM for U.S.$2.95 per share in cash. The transaction has received the unanimous approval of YM’s Board of Directors, and values YM at approximately U.S.$510 million, with YM reporting C$125.5 million in cash and cash equivalents as of September 30, 2012. Gilead plans to fund the acquisition with cash on hand. The transaction is expected to close in the first quarter of 2013.
YM’s lead drug candidate, CYT387, is an orally-administered, once-daily, selective inhibitor of the Janus kinase (JAK) family, specifically JAK1 and JAK2. The JAK enzymes have been implicated in a number of disorders including myeloproliferative diseases, inflammatory disorders and certain cancers. YM has reported positive results from a Phase 1/2 clinical trial of CYT387 in 166 patients with myelofibrosis, a life-threatening myeloproliferative disease. Pending completion of the acquisition, Gilead intends to initiate a pivotal Phase 3 clinical trial of CYT387 in myelofibrosis in the second half of 2013.
“This acquisition represents an opportunity to add a complementary clinical program in the area of hematologic cancers to our growing oncology portfolio,” said Norbert W. Bischofberger, PhD, Gilead’s Executive Vice President, Research and Development and Chief Scientific Officer. “Based on promising Phase 2 data, we believe CYT387 could provide important clinical benefit for patients with myelofibrosis, including potential improvements with regard to anemia and decreased dependence on blood transfusions. We look forward to advancing CYT387 into a Phase 3 study as quickly as possible and to exploring its potential in other myeloproliferative diseases with significant unmet medical need.”
Myelofibrosis is a progressive, chronic bone marrow disorder in which the marrow is replaced by fibrous scar tissue, making it difficult for the bone marrow to sufficiently produce blood cells, leading to anemia (low red blood cell count) and thrombocytopenia (low blood platelet count), severe constitutional symptoms and spleen enlargement. JAK inhibitors modulate cytokine-stimulated intracellular signalling and decrease the circulating levels of proinflammatory cytokines associated with the pathogenesis of myelofibrosis.
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