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Image of Janus-associated kinases (JAK) – showing the pathophysiology of polycythemia vera
Image of Janus-associated kinases (JAK) – showing the pathophysiology of polycythemia vera Image of Janus-associated kinases (JAK) – showing the pathophysiology of polycythemia vera

Overactive JAK pathway signaling is a key driver of PV2,3

Two Janus-associated kinases (JAK) play a role in signaling2,3:

Image that shows two Janus-associated kinases (JAK) playing a role in signaling - JAK1: Plays major role in signaling of key proinflammatory cytokines and JAK2: Mediates signals for hematopoietic growth factors Image that shows two Janus-associated kinases (JAK) playing a role in signaling - JAK1: Plays major role in signaling of key proinflammatory cytokines and JAK2: Mediates signals for hematopoietic growth factors

JAK=Janus-associated kinase; PV=polycythemia vera; STAT=signal transducer and activator of transcription.

Image that shows three people and says – Identify Appropriate Patients for Jakafi

IDENTIFY PATIENTS WHO MAY BE APPROPRIATE FOR JAKAFI

Jakafi targets the primary driver of PV1

Jakafi targets and inhibits JAK2 regardless of mutation status.

  • It is active against both mutant and wild-type JAK2 5*
Image that shows Jakafi binds in the JAK2 kinase domain, not at the site of the JAK2V617F mutation

JAK=Janus-associated kinase; STAT=signal transducer and activator of transcription.

*Jakafi binds in the JAK2 kinase domain, not at the site of the JAK2V617F mutation.

Image that says What is the mechanism of action of Jakafi? – Watch an MPN Specialist Explain Targeted JAK Inhibition

What is the mechanism of action of Jakafi?

WATCH AN MPN SPECIALIST EXPLAIN TARGETED JAK INHIBITION

  Video

Mechanism of Action of Jakafi® (ruxolitinib)

Hematology specialist Dr Harry Erba reviews the mechanism of action of Jakafi® (ruxolitinib), a JAK1 and JAK2 inhibitor, highlighting how Jakafi works to inhibit overactive JAK pathway signaling. Dr Erba also discusses safety data from the RESPONSE† trial, which compared Jakafi to best available therapy for patients with polycythemia vera who were either intolerant of or had an inadequate response to hydroxyurea.

WATCH NOW

†RESPONSE=Randomized study of Efficacy and Safety in POlycythemia vera with JAK iNhibitor ruxolitinib verSus bEst available care

Image of Dr. Harry Erba
Image that says What is the mechanism of action of Jakafi? – Watch an MPN Specialist Explain Targeted JAK Inhibition

What is the mechanism of action of Jakafi?

WATCH AN MPN SPECIALIST EXPLAIN TARGETED JAK INHIBITION

Image of 3 people – Identify Appropriate Patients for Jakafi

IDENTIFY PATIENTS WHO MAY BE APPROPRIATE FOR JAKAFI

References

  1. Jakafi Prescribing Information. Wilmington, DE: Incyte Corporation.
  2. Rampal R, Al-Shahrour F, Abdel-Wahab O, et al. Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis. Blood. 2014;123(22):e123-e133.
  3. Keohane C, Radia DH, Harrison CN. Treatment and management of myelofibrosis in the era of JAK inhibitors. Biologics. 2013;7:189-198.
  4. Quintas-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(15):3109-3117.
  5. Mascarenhas J, Mughal TI, Verstovsek S. Biology and clinical management of myeloproliferative neoplasms and development of the JAK inhibitor ruxolitinib. Curr Med Chem. 2012;19(26):4399-4413.

Indications and Usage

Jakafi is indicated for treatment of patients with polycythemia vera who have had an inadequate response to or are intolerant of hydroxyurea.

Jakafi is indicated for treatment of patients with intermediate or high‐risk myelofibrosis (MF), including primary MF, post–polycythemia vera MF and post–essential thrombocythemia MF.

Important Safety Information

  • Treatment with Jakafi® (ruxolitinib) can cause thrombocytopenia, anemia and neutropenia, which are each dose‐related effects. Perform a pre-treatment complete blood count (CBC) and monitor CBCs every 2 to 4 weeks until doses are stabilized, and then as clinically indicated
  • Manage thrombocytopenia by reducing the dose or temporarily interrupting Jakafi. Platelet transfusions may be necessary
  • Patients developing anemia may require blood transfusions and/or dose modifications of Jakafi
  • Severe neutropenia (ANC <0.5 × 109/L) was generally reversible by withholding Jakafi until recovery
  • Serious bacterial, mycobacterial, fungal and viral infections have occurred. Delay starting Jakafi until active serious infections have resolved. Observe patients receiving Jakafi for signs and symptoms of infection and manage promptly
  • Tuberculosis (TB) infection has been reported. Observe patients taking Jakafi for signs and symptoms of active TB and manage promptly. Prior to initiating Jakafi, evaluate patients for TB risk factors and test those at higher risk for latent infection. Consult a physician with expertise in the treatment of TB before starting Jakafi in patients with evidence of active or latent TB. Continuation of Jakafi during treatment of active TB should be based on the overall risk‐benefit determination
  • Progressive multifocal leukoencephalopathy (PML) has occurred with Jakafi treatment. If PML is suspected, stop Jakafi and evaluate
  • Advise patients about early signs and symptoms of herpes zoster and to seek early treatment
  • Increases in hepatitis B viral load with or without associated elevations in alanine aminotransferase and aspartate aminotransferase have been reported in patients with chronic hepatitis B virus (HBV) infections. Monitor and treat patients with chronic HBV infection according to clinical guidelines
  • When discontinuing Jakafi, myeloproliferative neoplasm-related symptoms may return within one week. After discontinuation, some patients with myelofibrosis have experienced fever, respiratory distress, hypotension, DIC, or multi‐organ failure. If any of these occur after discontinuation or while tapering Jakafi, evaluate and treat any intercurrent illness and consider restarting or increasing the dose of Jakafi. Instruct patients not to interrupt or discontinue Jakafi without consulting their physician. When discontinuing or interrupting Jakafi for reasons other than thrombocytopenia or neutropenia, consider gradual tapering rather than abrupt discontinuation
  • Non-melanoma skin cancers including basal cell, squamous cell, and Merkel cell carcinoma have occurred. Perform periodic skin examinations
  • Treatment with Jakafi has been associated with increases in total cholesterol, low-density lipoprotein cholesterol, and triglycerides. Assess lipid parameters 8-12 weeks after initiating Jakafi. Monitor and treat according to clinical guidelines for the management of hyperlipidemia
  • The three most frequent non‐hematologic adverse reactions (incidence >10%) were bruising, dizziness and headache
  • A dose modification is recommended when administering Jakafi with strong CYP3A4 inhibitors or fluconazole or in patients with renal or hepatic impairment. Patients should be closely monitored and the dose titrated based on safety and efficacy
  • Use of Jakafi during pregnancy is not recommended and should only be used if the potential benefit justifies the potential risk to the fetus. Women taking Jakafi should not breastfeed during treatment and for two weeks after the final dose

Please see Full Prescribing Information for Jakafi.

Jakafi and the Jakafi logo are registered trademarks of Incyte.
All other trademarks are the property of their respective owners.
© 2014-2018, Incyte Corporation. All rights reserved.
MAT-JAK-00067  11/18

Jakafi and the Jakafi logo are registered trademarks of Incyte.
All other trademarks are the property of their respective owners.
© 2014-2018, Incyte Corporation. All rights reserved.
MAT-JAK-00067  11/18