BESREMI ACHIEVES PATIENT-SPECIFIC TREATMENT GOAL... - MPN Voice

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BESREMI ACHIEVES PATIENT-SPECIFIC TREATMENT GOALS IN POLYCYTHEMIA VERA: FINAL RESULTS FROM THE PROUD-PV/CONTINUATION-PV STUDIES

Manouche profile image
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« No phlebotomies were required to maintain hematocrit <45% in the 6th year of treatment in 81.4% of patients receiving Besremi compared with 60.0% of patients in the control arm (p=0.005).

Depletion of the JAK2V617F alle burden, which may lower the risk of progression to myelofibrosis, was observed in Besremi treated patients; JAK2V617F allele burden <1% at 6 years was achieved in 19/92 (20.7%) patients in the Besremi arm with baseline allele burden >10%. One patient met this threshold in the control arm (1/70 [1.4%]; p=0.0001).

Event-free survival (risk events: disease progression, death and thromboembolic events) over ≥6 years of treatment was significantly higher among Besremi treated patients than the control group.

Conclusion

Long-term Besremi therapy fulfils treatment goals important to patients with PV: a good quality of life as indicated by a low symptom burden and phlebotomy requirement, the potential to influence myelofibrosis risk, and better event-free survival versus Best Available Treatment (BAT). »

library.ehaweb.org/eha/2022...

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Manouche
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Elizka profile image
Elizka

Thank you for letting us know about this important update.

Meatloaf9 profile image
Meatloaf9

Thank you for posting, sounds like good news.

jmctrek profile image
jmctrek

20% treated with RoPeg achieving allele burden <1% is lower than I had hoped for, considering the risks vs benefits of Besremi for someone with allele burden slightly over 10%. Would be interested to know if the allele burden was still reduced in the 80% treated with RoPeg, but just not to the <1% range. It does seem to reinforce RoPeg being a superior treatment to HU for allele burden reduction, low symptom burden, and phlebotomy requirement. Thanks for sharing!

Manouche profile image
Manouche in reply to jmctrek

IMO, 20% achieving an AB <1% is a huge achievement. It means that 20% have potentially achieved a stage of « functional cure ».

MPNBlog profile image
MPNBlog in reply to Manouche

Hi Manouche. Thanks for this posting. I agree that for 20% of people it's a great achievement to have a change in the disease itself (as opposed to symptoms). I celebrate for you. That's why I went onto pegylated interferon. However that means there's another 80% (of which I am one), for whom that isn't the case. There hasn't been a lot of information posted on this site about that - maybe it's time to start that thread. I do appreciate the posting. Best wishes.

Manouche profile image
Manouche in reply to MPNBlog

Hi MPNblog,I’m on the boat of those with 80% with an AB very much above 1%. Nothing to worry about. Changes take times both ways! « The growth of the JAK2V617F allele burden from 0.01% to 1% was found to span almost a decade, while further growth to 33% required approximately 7 year ».

onlinelibrary.wiley.com/doi...

monarch5000 profile image
monarch5000

I think it's misleading news because the pegylated interferon alfa formulations (Pegasys & Pegintron) that have been available since the mid-2000's could achieve the same results as could the short acting interferon alfa formulations used in the 1990's:

pubmed.ncbi.nlm.nih.gov/220...

"It is argued that in 2011, the bulk of evidence for the efficacy and safety of pegylated interferons in treating patients with these neoplasms favors the upfront use of pegylated interferons, the goal being to influence the development of the disease at the molecular level and revert patients to a stage of minimal residual disease/operational cure? instead of progressive clonal evolution, genomic instability and leukemic or myelofibrotic transformation during long-term treatment with hydroxyurea."

Manouche profile image
Manouche

Hi Monarch5000,It’s unlikely that all IFN medications can achieve the same results because of the toxicities of the early formulations. In others words, all IFN formulations can potentially lead to an operational cure, but at different rates, because of their various level of toxicities and side effects.

EPguy profile image
EPguy

Thanks for the great find. I've been awaiting 6 year data on ContiPV. This image in the abstract shows the numbers nicely and goes to 7 years+ for some.

We're still with "potential to influence myelofibrosis risk". Some Drs still want to see more proof on that, but I'm all in on "potential".

They refer to " defined symptoms". My big one, malaise, is not on many of these lists. But the diff from HU was not that large in any case.

I agree on the INF formulations, early INF is not as relevant for the recent studies. Currently I think Pegasys is the only comparable INF, with a long record as monarch5000 notes. Some here are also tolerating PEG better than Bes.

But I have posted before a plot showing PEG with increasing allele after 5 years, hence my eagerness to see this report that suggests Bes avoids this.

As expected we'll need to await the Euro conference to see more details, ie how the allele responses are sliced, will we see the general trend continuing down for most patients as jmctrek notes or is there a group where the reductions stop/reverse as the PEG report seemed to show?

ContiPV 6 year EFS
Manouche profile image
Manouche

Hi EPguy, As far as I know, there’s no evidence of an AB increase over time on patients having the same dose of IFN on weekly or bi-monthly injections.

Lemonverbena profile image
Lemonverbena

hi m, very interested in results. could you send link to study?my consultant has said to my local health authority to not fund bes as study too small/ results inconclusive. she favours the peg interferon which i cant have, so stuck on hu.

glad to gather different views.

Manouche profile image
Manouche in reply to Lemonverbena

Here it is: library.ehaweb.org/eha/2022...

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