Hi All, just as a quick update, Incyte has started the phase 1 trial for the CALR anyibody and they also disclosed a new potential treatment for the JAK mutation which may enter clinicial trials in the coming months which they say could also be disease modifying. See some quotes from their 3Q 2023 earnings call transcript below. It's early days in terms of evaluating these treatments but it is promising and exciting. Incyte developed Rux.
"We also dosed the first patient for the Phase I study of our novel anti-mutant CALR targeted monoclonal antibody with the potential to eradicate the malignant clone in certain patients with myeloproliferative neoplasms and significantly modified disease outcomes. CALR mutations are responsible for disease development in approximately 25% to 35% of patients with MF and ET."
We are disclosing today for the first time, a program targeting the JAK2V617F mutation, the most common somatic mutation in myeloproliferative neoplasms. The JAK2V617F mutation is located in the JH2 domain of the JAK2 receptor and is present in 55%, 60% and 95% of patients with MF, ET and PV, respectively."
"Okay. Great. Thank you. So as Pablo said in his remarks, a remarkable effort from our research group to come up with compounds that now target new areas of biology. So in terms of mutant CALR it's about 25% to 30% of myelofibrosis and ET. It's a neoantigen that's expressed and the antibody targets that and could eradicate the clone. So you could be talking about a very new treatment paradigm that's disease-modifying or potentially in “curable” if you eliminate the clone in those settings. Obviously, we're early in the clinic. We need to prove it safe and get there. But there's a lot of excitement and obviously, you've got a plenary at ASH last year because of that with the mutant CALR antibody.
In terms of where it fits in, it won't be an agent that's in the way we think about spleen volume reduction and symptom improvement, it could be, as I said, to be a little bit repetitive, eliminate the clone and sort of get rid of the disease, if you will. The same with V617F, a target that many have pursued for a long time. And again, credit to our research group for coming up with, as Pablo pointed out, a very novel way of targeting the mutation in the JH2 domain.
And then again, the idea would be to eliminate the clone and disease modified, and this is a bigger population. It's about 50% of MF, 60% of ET and 95% plus of polycythemia vera. So for the first time now, we've been able to show you that I mean we've come up with a target in PV where it's an area where we haven't been able yet to give you anything new beyond Rux. So we're very excited about that. Again, it's early. We have to get the IND across the finish line and get into the clinic, but it's a superb science and would be a very different way of thinking about those entities. So thanks for the question."
Effective Management of Polycythemia Vera With Ropeginterferon Alfa-2b Treatment
