Operator: Thank you. Next question today is coming from Matt Phipps from William Blair. Your line is now live.
Matthew Phipps: Thanks for taking the questions. I wondered on the povorcitinib Phase III plant in vitiligo, how you can structure that trial to complement the current Opzelura utilization opportunity? Is it really just around baseline VASI scores. And then as you think further out about additional opportunities for povorcitinib, what are you keeping in mind considering that it looks based on the profile so far as to work in a pretty wide range of more classical autoimmune indications, but clearly there you might have more competition.
Steven Stein: Matt. Hi, it’s Steven. Thanks for the question. So in terms of vitiligo, as we showed you the data in more extensive nonsegmental vitiligo, we saw a really good effect in terms of facial VASI, facial VASI 75 and above. And then total VASI as well, body repigmentation of 50% or above. We will disclose when we go on to clintrials.gov what the endpoints are and what doses we’ll be using such premature to point you towards that, other than just broadly tell you that the population we target in is people with more extensive body surface area involvement when you compare it to the cream, which is indicated for people who are 10% or below. This would open up the vitiligo community with people with much more extensive body surface area involvement where it becomes a little pragmatically hard to apply cream across the body and an oral JAK can be used in that setting with the right therapeutic ratio.
And as we guided to, we want to get this study going by the end of this calendar year. Povorcitinib is relatively JAK1-specific. You saw the program in HS, both STOP-HS1, HS2 enrolling really, really well based on the – what we think is excellent Phase II data, including that HiSCR100 response. But as you alluded to, we have now data in prurigo nodularis, that’s excellent, and we want to progress that into Phase III. And then ongoing efforts beyond dermatology in asthma and chronic spontaneous urticaria, where the biology points to this kind of JAK1 agent potentially showing substantial benefit in patients with more severe asthma who on inhaled corticosteroids, long-acting bronchodilators and still having early exacerbations. That’s a Phase II proof-of-concept study and then standard endpoints in chronic spontaneous early carrier.
So this drug has demonstrated thus far remarkable activity in those areas where we study in Phase III now, and we’ll see what happens in asthma and CSU. So thanks for the question.
Operator: Thank you. Next question today is coming from Michael Schmidt from Guggenheim Securities. Your line is now live.
Paul Jeng: Hey. Good morning. This is Paul on for Michael. Thanks for taking our question. I just wanted to build on the prior question. Can you talk about how you plan to position povorcitinib [indiscernible] in the planned Phase III relative to sort of how you design the ongoing Phase III studies for Opzelura. Is there a meaningful difference in the target patient populations? And how should we think about the specific addressable opportunities within the end for the two programs? Thank you.
Steven Stein: Yes. Thank you for the question. Just in terms of Herve said this upfront in his remarks, there’s a prevalence upwards of 200,000-plus patients, but there are about 80,000 to 100,000 that currently get treated in the setting. And their main manifestation of their disease is itch and very severe itch. And that’s what the Phase II showed that activity in that setting across the dose ranges. I think it’s premature beyond that to talk about the endpoint and the dose we’ll be using because we’ve just got the Phase II data in. But it will be, again, because it’s an oral agent targeting the more severe spectrum of PN. That’s what I can tell you now. Thanks.
Operator: Thank you. Next question is coming from Mara Goldstein from Mizuho Securities. Your line is now live.
Mara Goldstein: Great. Thanks so much for taking the question. I just was hoping actually to get a little bit more color on the Medicaid penetration with respect to Opzelura? Because last quarter, it was identified as a jump in the payer mix that had an effect, right on Opzelura and the gross-to-net? And then secondarily, I’m just hoping maybe you could talk a little bit about PV for Jakafi. I mean it looks like the percentage just eyeballing it, right, of Jakafi sales from PV has remained relatively stable. And I’m curious as to with this new data and potentially earlier patient starts where you think the growth could be?
Barry Flannelly: Sure. So in part as Medicaid patients for Opzelura goes, it’s about 14% of paid patients. As we said in the past, we had such good coverage for Medicaid throughout all 50 states that it was sort of grew faster than perhaps the commercial patients. So I think that answers part of your question. For Jakafi in PV, I guess if you’re looking at the slide that we had there, PV, it continued in terms of the patient share is about 35% or so. At any given time, for example, this year, year-to-date, there’s more than 8,000 patients on PV. But PV patients stay on the drug for a long time. So we’re talking about what we think now the average is about 41 months that patients are staying on Jakafi for PV. So that’s important.
So every new PV patient becomes that more important. And we think that there’s lots of patients who are currently on other therapies, including hydroxyurea, that would benefit from moving to Jakafi earlier. And now that we have a study where there was no crossover so that you can actually evaluate the long-term thrombosis free survival and in fact, progression-free survival for patients that, that’s really an indicator that you really should start earlier with an effective therapy like Jakafi. And we think that’s really where the upside is here is that each and every PV patient is viable and we can provide them with really effective therapy to manage their disease long-term. So that’s what our growth expectations are. Thanks.
Operator: Thank you. Next question today is coming from Andrew Berens from SVB Securities. Your line is now live.
Andrew Berens: Hi. Thanks. Can you remind us how you see 33989 fitting into the treatment paradigm for MF relative to the JAK agents? And then do you see the regulatory pathway leveraging surrogate endpoints for approval? Or would you want to show a decrease in malignant transformation in this subgroup?
Steven Stein: Andy, were you are asking about, Steven, just to clarify your question about mutant CALR in V617F in the future, we couldn’t hear clearly your first part of question?
Andrew Berens: Yes. Just I’m trying to understand how you see that fitting into the treatment paradigm relative to the JAK agents?
Steven Stein: 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.
