About Jakafi Treatment
Jakafi: First and only FDA-approved agent for myelofibrosis
Jakafi is indicated for treatment of patients with intermediate or high-risk myelofibrosis, including primary myelofibrosis, post–polycythemia vera myelofibrosis and post–essential thrombocythemia myelofibrosis—collectively known as myelofibrosis diseases.1
Identifying intermediate or high-risk myelofibrosis2-4
In order for a patient to be classified as having intermediate or high-risk myelofibrosis, he or she must have 1 or more of the following characteristics:
- Age >65 years
- Presence of constitutional symptoms
- Hemoglobin <10 g/dL
- White blood cell count >25 × 109/L
- Blood blasts ≥1%
- Platelet counts <100 × 109/L
- Unfavorable karyotype*
- Red cell transfusion dependence
Jakafi significantly reduces spleen volume and improves symptoms of myelofibrosis
In both phase III studies, a significantly higher proportion of patients receiving Jakafi achieved a ≥35% reduction in spleen volume vs those receiving placebo or best available therapy.1 Learn more about splenomegaly efficacy.
- Superior reductions in spleen volume vs placebo1,5
- 41.9% of patients receiving Jakafi achieved a ≥35% reduction in spleen volume at Week 24 vs 0.7% of patients receiving placebo (P < 0.0001)1,5
- Superior reductions in spleen volume vs best available therapy1,6
- 28.5% of patients receiving Jakafi achieved a ≥35% reduction in spleen volume at 48 weeks vs 0% of patients receiving best available therapy (P < 0.0001)1,6
Significantly more patients receiving Jakafi achieved a ≥50% improvement in symptoms vs those receiving placebo.1,5 Learn more about symptoms efficacy.
- Superior improvements in symptoms vs placebo1,5
- 45.9% of patients receiving Jakafi achieved a ≥50% improvement in Total Symptom Score (TSS)† vs 5.3% of patients receiving placebo (P < 0.0001) at Week 241,5
Responses were seen in patients regardless of JAK2V617F mutational status.5
- Reductions in spleen volume and improvements in TSS were seen with Jakafi in both JAK2V617F-positive and JAK2V617F-negative patients, relative to placebo5
- Patients with myelofibrosis have dysregulated Janus kinase (JAK) signaling, regardless of the presence or absence of the JAK2V617F mutation7
Treatment with Jakafi can cause thrombocytopenia, anemia and neutropenia, which are each dose-related effects, with the most frequent being thrombocytopenia and anemia. Serious bacterial, mycobacterial, fungal and viral infections may occur. The three most frequent non-hematologic adverse reactions were bruising, dizziness and headache.
Similar and low discontinuation rates were observed in both the Jakafi and placebo arms (11% and 10.6%, respectively).1
Starting dose for Jakafi is based on platelet counts. Dosing should be modified based on
- Patient response
- The presence of thrombocytopenia
- Organ impairment
- Concomitant administration of CYP3A4 inhibitors
- Anemia and neutropenia
*Unfavorable karyotype: complex karyotype or sole or two abnormalities that include +8, –7/7q-, i(17q), –5/5q-, 12p-, inv(3), or 11q23 rearrangement.
†At baseline, mean TSS was 18.0 in the Jakafi group and 16.5 in the placebo group.1
- Jakafi Prescribing Information. Incyte Corporation.
- Passamonti F, Cervantes F, Vannucchi AM, et al. A dynamic prognostic model to predict survival in primary myelofibrosis: a study by the IWG-MRT (International Working Group for Myeloproliferative Neoplasms Research and Treatment). Blood. 2010;115:1703-1708.
- Cervantes F, Dupriez B, Pereira A, et al. New prognostic scoring system for primary myelofibrosis based on a study of the International Working Group for Myelofibrosis Research and Treatment. Blood. 2009;113:2895-2901.
- Gangat N, Caramazza D, Vaidya R, et al. DIPSS Plus: A refined dynamic international prognostic scoring system for primary myelofibrosis that incorporates prognostic information from karyotype, platelet count, and transfusion status. J Clin Oncol. 2010;29:392-397.
- Verstovsek S, Mesa RA, Gotlib J, et al. A double-blind, placebo-controlled trial of ruxolitinib for myelofibrosis. N Engl J Med. 2012;366:799-807.
- Harrison C, Kiladjian JJ, Al-Ali HK, et al. JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis. N Engl J Med. 2012;366:787-798.
- Anand S, Stedham F, Gudgin E, et al. Increased basal intracellular signaling patterns do not correlate with JAK2 genotype in human myeloproliferative neoplasms. Blood. 2011;118:1610-1621.