The VERIFY trial demonstrated that 77% of patients on rusfertide achieved the primary endpoint of phlebotomy independence, compared to only 33% in the placebo group. How clinically meaningful is this reduction in phlebotomy need for PV patients, and what impact could it have on disease management?

Rusfertide-treated patients required a mean of 0.5 phlebotomies during the study period, compared to 1.8 in the placebo group. Given that frequent phlebotomies can contribute to iron deficiency and fatigue, how important is this reduction in terms of improving patient quality of life?

Current PV treatments include phlebotomy and cytoreductive agents like hydroxyurea or interferon. How does rusfertide compare to these approaches in terms of efficacy, tolerability, and long-term disease management?

The study met key secondary endpoints related to patient-reported outcomes, including significant improvement in fatigue scores. Could rusfertide have a broader impact on symptom burden beyond hematocrit control, and how might this influence treatment decisions?

Rusfertide was well tolerated, with no new safety concerns or increased cancer risk observed in the trial. Given the long-term nature of PV treatment, what additional safety data would you like to see before this drug is widely adopted?

Do you see rusfertide being used primarily as an add-on for patients struggling with hematocrit control on standard therapies, or could it eventually be used earlier in the disease course to prevent progression and thrombotic events?

Given that the VERIFY study met both the U.S. primary endpoint and the EU-mandated endpoint, what are the next steps for regulatory approval? How do you anticipate the approval process differing between the FDA and EMA?

If approved, rusfertide would be the first erythrocytosis-specific agent for PV. How could this shift the treatment paradigm, and do you see this drug expanding to other myeloproliferative neoplasms in the future?