Pathophysiology of polycythemia vera (PV)
Two Janus-associated kinases (JAK) play a role in signaling2,3:
JAK, Janus-associated kinase; PV, polycythemia vera; STAT, signal transducer and activator of transcription.
IDENTIFY PATIENTS WHO MAY BE APPROPRIATE FOR JAKAFI
Jakafi targets and inhibits JAK2 regardless of mutation status.
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.
What is the mechanism of action of Jakafi?
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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.
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†RESPONSE, Randomized study of Efficacy and Safety in POlycythemia vera with JAK iNhibitor ruxolitinib verSus bEst available care
References
Indications and Usage
Jakafi is indicated for treatment of polycythemia vera (PV) in adults who have had an inadequate response to or are intolerant of hydroxyurea.
Jakafi is indicated for treatment of intermediate or high‐risk myelofibrosis (MF), including primary MF, post–polycythemia vera MF and post–essential thrombocythemia MF in adults.
Jakafi is indicated for treatment of steroid‐refractory acute graft‐versus‐host disease (GVHD) in adult and pediatric patients 12 years and older.
Important Safety Information
Please see Full Prescribing Information for Jakafi.
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