JAK dysregulation

Learn about the many abnormalities that can contribute to JAK dysregulation4

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Clinical evidence

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

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JAKAVI MOA

See how JAKAVI works to improve splenomegaly and myelofibrosis symptoms3

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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.

References
  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, et.al. 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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