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Home > Efficacy

JAKAVI provides a robust response in patients who are resistant/intolerant to hydroxyurea (HU)[1]

Primary response at Week 32[1]

Javkavi primary response at week 32 chart

All JAKAVI-treated patients in the RESPONSE trial were resistant/intolerant to HU[6]

In the same study, JAKAVI reduced spleen volume in the majority of patients (38% of JAKAVI-treated patients achieved a ≥35% reduction in volume at Week 32 vs 1% in the BAT arm)[1]

BAT, best available therapy.

For many patients, hydroxyurea fails to deliver sufficient symptom control[2]

Symptoms in HU-treated and non-HU-treated patients (MPN-10)[2]

HU-treated versus Not HU-treated by symptom control chart

70% of HU-treated patients report clinically deficient QoL and 94% of pruritus cases are unresolved[3],[4]*

Overall prevalence of symptoms in PV (n=145)

  • Prevalence of symptoms in the overall PV population (n=145): fatigue (91.7%), itching (65%), early satiety (62.1%), concentration problems (61.2%), inactivity (57.9%), night sweats (57.4%), abdominal discomfort (49.3%), bone pain (47.5%), weight loss (36.2%), and fever (17.9%)[5]
  • About half of MPN patients who experience fatigue describe it as very severe[5]

Only JAKAVI provides PV patients with the symptom relief they need[1]

Change in symptom scores (MPN-SAF) from baseline to Week 32

Jakavi versus BAT change in symptom score (MPN-SAF) from baseline to Week 32 chart
  • Nearly all JAKAVI-treated patients demonstrated improvement in key symptoms by Week 32[1]
  • Symptom burden is a serious concern for all PV patients, including those treated with HU—make sure you’re monitoring regularly for symptom progression
MPN, myeloproliferative neoplasm; MPN-SAF, Myeloproliferative Neoplasm Symptom Assessment Form.
*PV treatments included hydroxyurea, acetylsalicylic acid, clopidogrel, anagrelide, coumadine, or interferon-alpha.
BAT includes HU, interferon or pegylated interferon, pipobroman, anagrelide, lenalidomide, thalidomide, or no medication.

Understand the risks associated with elevated haematocrit (HCT)

Time to cardiovascular death or TE by HCT level[6]

Time to cardiovascular death or TE by HCT level
  • HCT ≥45% is associated with a 4-fold increase in risk of TEs or CV death[6]

Only JAKAVI provides sustained reductions in HCT over time[7]

Jakavi provides sustained reductions in HCT over time chart
  • In the RESPONSE trial, only 1 patient who received JAKAVI experienced a TE vs 6 patients who received BAT[1]

Is long-term HU treatment leaving some of your patients at risk? Switching to JAKAVI significantly reduces the risk of TEs

In a real-life analysis, switching from HU treatment to JAKAVI resulted in a 15% reduction in the risk of TEs

Switching from HU treatment to Jakavi resulted in a 15% reduction in the risk of TEs chart

Results from a study evaluating the incidence of TEs in HU-treated patients with PV (median treatment duration, 27 months). The study used records from the US OPTUM database between 2007 and 2017. Machine learning was then used to build a precise and scientifically robust model to predict the occurrence of TEs in PV patients with/without a history of TEs and HU failure (defined by either ELN haematologic criteria or TEs).

  • After ~3.5 years (41 months) of HU treatment, half of patients experienced one TE per year
  • In an analysis of the RESPONSE trial, JAKAVI effectively and consistently lowered allele burden throughout the duration of treatment, with a 40% mean reduction by Week 208[1]
  • In one study, molecular response (reduction in allele burden) was more frequent in patients treated with JAKAVI vs BAT, including IFN (29.4% vs 17.9%), and was shown to be correlated with a reduction in TEs[10]*
*Results from a phase 2, randomised 1:1, open-label study of BAT vs JAKAVI in 306 high-risk PV or ET patients who were resistant to or intolerant of HU.  A complete molecular response was defined as reduction of any specific molecular abnormality to undetectable levels.  A partial response was defined as a reduction of ≥50% from baseline value in patients with <50% mutant allele burden at baseline or a reduction of ≥25% from baseline value in patients with >50% mutant allele burden at baseline.[10]


  1. Vannucchi AM, Kiladjian JJ, Griesshammer M, et al. Ruxolitinib versus standard therapy for the treatment of polycythemia vera. N Engl J Med. 2015;372(5):426-435.

  2. Geyer H, Scherber R, Kosiorek H, et al. Symptomatic profiles of patients with polycythemia vera: implications of inadequately controlled disease. J Clin Oncol. 2016;34(2):151-159.

  3. Harrison CN, Koschmieder S, Foltz L, et al. The impact of myeloproliferative neoplasms (MPNs) on patient quality of life and productivity: results from the international MPN Landmark survey. Ann Hematol. 2017;96(10):1653-1665.

  4. Siegel FP, Tauscher J, Petrides PE. Aquagenic pruritus in polycythemia vera: characteristics and influence on quality of life in 441 patients. Am J Hematol. 2013;88(8):665-669.

  5. Scherber R, Dueck AC, Johansson P, et al. The Myeloproliferative Neoplasm Symptom Assessment Form (MPN-SAF): International Prospective Validation and Reliability Trial in 402 patients. Blood. 2011;118(2):401-408.

  6. MarchioIi R, Finazzi G, Specchia G, et al; for CYTO-PV Collaborative Group. Cardiovascular events and intensity of treatment in polycythemia vera. N Engl J Med. 2013;368(1):22-33.

  7. Verstovsek S, Vannucchi AM, Griesshammer M, et al. Ruxolitinib versus best available therapy in patients with polycythemia vera: 80-week follow-up from the RESPONSE trial. Haematologica. 2016;101(7):821-829.

  8. Verstovsek S, De Stefano MD, Heidel FH, et al. US Optum database study in polycythemia vera patients: thromboembolic events (TEs) with hydroxyurea (HU) vs ruxolitinib switch therapy and machine-learning model to predict incidence of TEs and HU failure. Presented at: 61st American Society of Hematology Annual Meeting. December 7-10, 2019; Orlando, FL.

  9. Vannucchi AM, Kiladjian JJ, Griesshammer M, et al. Ruxolitinib versus standard therapy for the treatment of polycythemia vera. N Engl J Med. 2015;372(5):426-435.

  10. Curlo-Garcia N, Baxter J, Harris E, et al. Molecular analysis in MAJIC PV correlation with clinical endpoints. Presented at: 24th congress of the European Hematology Association (EHA). June 13-16, 2019; Amsterdam, the Netherlands.