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JAK dysregulation

Learn about the many abnormalities that can contribute to JAK dysregulation4


Clinical evidence

Read about the most comprehensive myelofibrosis trials completed to date2,3



See how JAKAVI works to improve splenomegaly and myelofibrosis symptoms3


For your patients with myelofibrosis, you can reduce the burden like never before3

JAKAVI is now approved for the treatment of disease-related splenomegaly or symptoms in adult patients with primary myelofibrosis (also known as chronic idiopathic myelofibrosis), post-polycythaemia vera myelofibrosis, or post-essential thrombocythaemia myelofibrosis.1

Reduce disease burden and raise treatment expectations with JAKAVI.2,3

  • JAKAVI is the first approved JAK1/JAK2 inhibitor
  • Regardless of patients’ JAK2V617F mutation status, JAKAVI improves splenomegaly, symptoms, and quality of life2
  • Studied in the most comprehensive clinical trial program in myelofibrosis to date: the pivotal COMFORT-I and COMFORT-II Phase III Trials2,3
  • JAKAVI directly targets the universal MF attribute of JAK-dysregulation, the underlying mechanism of the disease2
  • SIGNIFICANT improvements vs. control regimens in reducing splenomegaly and symptoms (Ρ<0.0001)2,3
  • RAPID reductions in splenomegaly by Week 4 — and improvement in symptoms by Week 1*2,3
  • DURABLE response that was sustained through the entire study duration (up to 48 weeks)2,3
  • Well-characterised and manageable safety profile1

*As measured by palpable spleen length.

  1. JAKAVI® (ruxolitinib) tablets: EU Summary of Product Characteristics. Novartis; October 2014.
  2. Harrison C, Kiladjian J-J, Al-Ali HK, et al. JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis. N Engl J Med. 2012;366(9):787-798.
  3. Verstovsek S, Mesa RA, Gotlib J, et al. A double-blind, placebo-controlled trial of ruxolitinib for myelofibrosis. N Engl J Med. 2012;366(9):799-807.
  4. Thoennissen NH, Krug UO, Lee DHT, Prevalence and prognostic impact of allelic imbalances associated with leukemic transformation of Philadelphia chromosome–negative myeloproliferative neoplasms. Blood. 2010;115(14):2882-2890.

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