Updated on 11 December 2012
Hope for myelofibrosis patients - Phase III studies of Jakavi (INC424, ruxolitinib) by Novartis shows promise
Singapore: Phase III studies by Novartis has demonstrated that Jakavi (INC424, ruxolitinib) treatment resulted in sustained reductions in spleen size, a hallmark of myelofibrosis, while also improving quality of life and extending overall survival as compared to placebo or the best available therapy (BAT).
Jakavi (INC424, ruxolitinib) is an oral inhibitor of the JAK 1 and JAK 2 tyrosine kinases and was approved by the European Commission in August 2012 for the treatment of disease-related splenomegaly or symptoms in adult patients with primary myelofibrosis.
"As these phase III studies continue over the long term, it is encouraging to see how treatment with Jakavi consistently alleviates the myelofibrosis disease burden and may improve overall survival," said Dr Francisco Cervantes, hematology department, hospital clínic, IDIBAPS, University of Barcelona. "Just one year ago, we didn't have a truly effective treatment to offer our patients with myelofibrosis. Now, it appears we can significantly improve a patient's quality of life while also potentially extending their life."
"The COMFORT program, which supported the European Commission approval for Jakavi, is the most extensive clinical trial program in myelofibrosis to date and continues to demonstrate significant results for Jakavi-treated patients," said Hervé Hoppenot, president, Novartis Oncology. "We are encouraged by these findings and look forward to evaluating how Jakavi may help patients with other myeloproliferative neoplasms associated with a similar mechanism of disease."
Myelofibrosis develops when uncontrolled signaling in the JAK pathway, which regulates blood cell production, causes bone marrow scarring and faulty blood cell production, resulting in severe complications. Jakavi directly targets an underlying mechanism of myelofibrosis, significantly reducing splenomegaly and improving debilitating symptoms regardless of JAK mutational status, disease subtype or any prior treatment, including hydroxyurea.