Fedratinib is a JAK inhibitor, oral JAK2/JAK1, has impact on FLT3. We had the large JAKARTA randomized Phase III trial versus placebo and in the JAKARTA-2 study, a second-line study led by Professor Harrison and I. At this year’s EHA meeting, Professor Harrison demonstrated a analysis on both progression-free survival and overall survival with JAKARTA-1 and JAKARTA-2.
In JAKARTA, that was a trial that the length of follow-up is somewhat limited because of the cessation of that trial at that point in time due to the concerns of Wernicke’s encephalopathy...
Fedratinib is a JAK inhibitor, oral JAK2/JAK1, has impact on FLT3. We had the large JAKARTA randomized Phase III trial versus placebo and in the JAKARTA-2 study, a second-line study led by Professor Harrison and I. At this year’s EHA meeting, Professor Harrison demonstrated a analysis on both progression-free survival and overall survival with JAKARTA-1 and JAKARTA-2.
In JAKARTA, that was a trial that the length of follow-up is somewhat limited because of the cessation of that trial at that point in time due to the concerns of Wernicke’s encephalopathy. All of that said, with the data we are able to analyze it and see that there is strong evidence of an impact of fedratinib on improvements in progression-free survival with, in JAKARTA, as well as a suggestion of overall survival improvement as well, even accounting for the limitations of length of follow-up on the medication. With JAKARTA-2, we similarly see data suggesting, compared to recently published data regarding second-line therapies in myelofibrosis, likely improvement in both progression-free and overall survival.
So, I think that this is important data and I think it’s also consistent data. That, increasingly, we’re seeing that benefit with JAK inhibition have clearly been demonstrated to improve survival with ruxolitinib. As I presented at this meeting, I think clearly, we’re having benefit in terms of survival with momelotinib, particularly in patients who receive, who have transfusion independence. And it stands to logic, that we see improvements in survival with fedratinib as well.
I think JAK inhibition remains an incredibly important part of therapy for patients with myelofibrosis. I would anticipate as data matures, we likely will see a similar benefit in survival with pacritinib, and that as we look at the future of myelofibrosis single and combination therapies, I think JAK inhibition will remain an important cornerstone of, at a minimal, doublet-type therapies when appropriate because of their impact on survival.