|Jakafi||Superior reductions in spleen volume and improvements in Total Symptom Score (TSS) vs placebo.1,2 Learn more at www.jakafi.com.|
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Jakafi®—the first and only FDA-approved agent for intermediate or high-risk myelofibrosis1,3
Dear Dr Kankonde,
Consider Jakafi for your patients with intermediate or high-risk myelofibrosis. Jakafi reduces splenomegaly and improves the symptoms of myelofibrosis, as measured by TSS.* Symptoms measured by TSS were abdominal discomfort, early satiety, pain under left ribs, pruritus, night sweats and bone/muscle pain. In a clinical study, most patients receiving placebo experienced increased splenomegaly and worsening of symptoms.1,2
Jakafi regulates JAK1 and JAK2 signaling1,2
View the Jakafi Mechanism of Action (MOA) video >
MPL=myeloproliferative leukemia virus oncogene; SOCS=suppressor of cytokine signaling.
Jakafi demonstrated superior reductions in spleen volume and significant improvements in symptom scores1,14,15
Reductions in spleen volume and improvements in TSS were seen with Jakafi in both JAK2V617F-positive and JAK2V617F-negative patients, relative to placebo.2
Learn more about how Jakafi can help your patients >
IncyteCARES (Connecting to Access, Reimbursement, Education and Support)
IncyteCARES offers free educational support for your patients taking Jakafi.
Order the IncyteCARES Patient Starter Packet >
Indications and Usage
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.
Important Safety Information
Please see Full Prescribing Information.
References: 1. Jakafi Prescribing Information. Incyte Corporation. November 2011. 2. Data on file. Incyte Corporation. 3. Quintás-Cardama A, Vaddi K, Liu P, et al. Preclinical characterization of the selective JAK1/2 inhibitor INCB018424: therapeutic implications for the treatment of myeloproliferative neoplasms. Blood. 2010;115:3109-3117. 4. 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. 5. Verstovsek S, Kantarjian H, Mesa RA, et al. Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis. N Engl J Med. 2010;363:1117-1127. 6. Kralovics R, Passamonti F, Buser AS, et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med. 2005;352:1779-1790. 7. Levine RL, Pardanani A, Tefferi A, Gilliland DG. Role of JAK2 in the pathogenesis and therapy of myeloproliferative disorders. Nat Rev Cancer. 2007;7:673-683. 8. Scott LM, Tong W, Levine RL, et al. JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis. N Engl J Med. 2007;356:459-468. 9. Pikman Y, Lee BH, Mercher T, et al. MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. PLoS Med. 2006;3:1140-1151. 10. Kralovics R. Genetic complexity of myeloproliferative neoplasms. Leukemia. 2008;22:1841-1848. 11. Tefferi A, Vaidya R, Caramazza D, Finke C, Lasho T, Pardanani A. Circulating interleukin (IL)-8, IL-2R, IL-12, and IL-15 levels are independently prognostic in primary myelofibrosis: a comprehensive cytokine profiling study. J Clin Oncol. 2011;29:1356-1363. 12. Verstovsek S. Therapeutic potential of JAK2 inhibitors. Hematology Am Soc Hematol Educ Program. 2009:636-642. 13. Fourouclas N, Li J, Gilby DC, et al. Methylation of the suppressor of cytokine signaling 3 gene (SOCS3) in myeloproliferative disorders. Haematologica. 2008;93:1635-1644. 14. 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. 15. 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;366:787-798.