Masarova Discusses Ruxolitinib for Polycythemia Vera After Hydroxyurea

Video

Lucia Masarova, MD, PhD, discusses therapeutic options for patients with polycythemia vera who are refractory to hydroxyurea.

Lucia Masarova, MD, PhD, assistant professor, Department of Leukemia, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, discusses some of the therapeutic options available for patients with polycythemia vera (PV) who are refractory to hydroxyurea.

Masarova first highlights the phase 3 RESPONSE (NCT01243944) and phase 3b RESPONSE-2 (NCT02038036) trials which each evaluated ruxolitinib (Jakafi) in this patient population. In these studies, ruxolitinib demonstrated superiority vs best available therapy (BAT). In the RESPONSE-2 trial, this was in terms of hematocrit control, normalizing blood cell counts, and improving PV symptoms at week 28. Findings from both the RESPONSE and RESPONSE-2 trials provide long-term, clinical trial data supporting the use of ruxolitinib in patients with PV.

Then, she discusses results from the MAJIC-PV (ISRCTN61925716) study which compared ruxolitinib to BAT among patients with PV. In this trial, patients with PV who are intolerant or resistant to hydroxycarbamide chemotherapy had superior responses when treated with ruxolitinib.

Transcription:

0:10 | For patients with PV refractory to [hydroxyurea], we have approved ruxolitinib, which is the JAK inhibitor that has solid data in the field after [being refractory to] hydroxyurea, based on results from the RESPONSE and RESPONSE-2 trials. It will be 10 years since we had refractory patients treated with ruxolitinib. It is an excellent drug for controlling the symptoms and spleen count.


0:37 | Last year, we had a very exciting study called MAGIC-PV, which was reported by our European colleagues that showed the advantage of ruxolitinib for decreasing the rate of thrombosis hemorrhage. It also improved event-free survival, death, and adverse events in terms of progression to myelofibrosis. So, it was exciting. If we consider disease modification as what is going to prevent the disease from going into myelofibrosis, I think that it will be exciting to see how far we can get in that field.

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