Incyte Corporation (INCY) Earnings Call Transcript & Summary

All right. Well, I think we'll get started with our afternoon session here at the Wells Fargo Healthcare Conference. My name is Derek Archila. I'm one of the senior biotech analysts here at Wells. Our next fireside discussion is with Incyte. And from the company, we have CEO, Herve Hoppenot; and as well as the Head of R&D, Pablo Cagnoni. I tried.

No, no, it was very good.

So Herve, maybe to start, just kind of level set us in terms of like kind of state of the business, and then we can kind of dig deep into some of these questions.

Okay. No, thank you for inviting us. So basically, when we look at today's Incyte, what you have is the commercial portfolio first and both on Jakafi and Opzelura are doing very well, in fact, in multiple indications. So we can speak about the details, but that's one component. I mean the growth of revenue continues to be very strong. And the fact that Opzelura is growing obviously faster than the rest of the portfolio is really important because over time, that's what we want to see happening. On the pipeline, obviously, you have different components. The first one is the IAI dermatology, immunology pipeline, where some of the new Opzelura indication continue to be developed. And again, we can speak about that in HS and prurigo nodularis. We have Povo, our selective JAK1 that is in 3 indications in pivotal studies and is also making a lot of progress. We can speak about when the data will be available, but we think it's a very important component. And then we had the acquisition of Escient and now a new series of products in a fairly unique mechanism and very advanced science with X2 and X4. So that part is really developing. It's becoming a new part of Incyte. It's not just about cancer, hematology. Now it's also about all of these other indications where we have a very promising and interesting product. On the Onco side, the way I think of it is basically in 2 different categories. There is a current portfolio, which is the one that we know that has been in development for a while where we got very good news over the past few weeks. One was the approval of Axa in GVHD. So FDA approval for axatilimab in chronic GVHD. We had positive data for Tafa in follicular lymphoma, Phase III. And we have positive Phase III studies with retifanlimab in squamous cell anal carcinoma. So all of that is going to contribute to revenue very soon. '25, it's going to start building from there. And obviously, we have the -- know the franchise management with Jakafi with BET, ALK2 and Axa, all of that making progress. And then is there is what I think of as the new onco pipeline of Incyte. And there are 5 drugs that are being developed. It's CDK2. It's V617F. It's CALR, It's KRAS 12D and TGF-beta PD-1. So they are all totally unique profiles in Phase I. So all of them are in the clinic. And frankly, I'm speaking to them because that's what's driving a lot of our resource allocation exercise that also took place over the past few months where we see a lot of excitement. You will see at ESMO next week. In fact, some of the FERC data with CDK2 in ovarian cancer and some other indications. And we have obviously a lot of optimism for the other fiber product there for the other 4 products on top of CDK2. And that's what's leading to the other big event of the past few weeks, which is the resource allocation that took place. The first part of the resource allocation for Incyte is obviously R&D and how much we are investing in our R&D -- in our portfolio through our R&D. And what we did first is the reprioritization of the portfolio. So number of projects were killed, in fact, technically, either because of data or because of competitive situation. So that was important. And then obviously, we acquired Escient. So that was around $750 million investment to add this new mechanism to the portfolio. And we got a gift which was Tafa, second half of Tafa that ended up being basically integrated to -- fully to our portfolio. And at that point is when because of this very promising pipeline when we decided to do share buybacks through a Dutch auction that was successful. In fact, the fulfillment rate was 97%. So it was relatively well calibrated and that was also executed over the past few weeks and is now behind us. So that was basically retiring 33 million shares from the share count. So that's sort of the exciting few months we have. I think there is a lot of positive coming out of this evolution of the pipeline, which has been something we have been obviously working on for a long time. And there is also a lot of positive on the commercial side with the growth that we are seeing from the current portfolio.

Great. You've been busy.

It will be busy time and very exciting. I must tell the level of internal excitement about what's going on is that is very high in many ways. And part of it is a science and the fact that the pipeline is evolving in the right direction.

Understood. Well, I'd love to start a discussion around the upcoming data that you're going to present for CDK2 at ESMO. So maybe you can just kind of tee that up, what we should be expecting in terms of patients. And ultimately, we hear about a lot of CDK2s that are out there. So I guess, how do you think ultimately, this data will either set years apart or kind of support your development strategy with your CDK2?

So our CDK2 inhibitor, which we are predominantly developing in ovarian cancer, that's been an area of focus for us, and I'll talk about why in a minute. We think in ovarian cancer, we have the potential to be first. We know who our competitors are. There's 2 other programs that have been in the clinic for some time, one from Pfizer, one from Blueprint. They have presented small amounts of data in ovarian cancer with minimal modest single-agent activity. So we decided this was the right time to present the data, and I'll tell you a little bit more about that in a second. And at the same time, give you an idea of where we're going to go in terms of further development. We think we have in our hands a developable drug that the efficacy, the safety in ovarian cancer warrant for the development, and that's what we're going to talk about next week. It's a pretty substantial number of patients. We've been doing dose escalation. We just had a range of doses. We tested a couple of different schedules and we're going to present data across that. We're obviously going to present the safety. We have seen what we believe is a very manageable level of hemologic toxicity. You would expect hemotoxin CDK2 inhibitor, we think is manageable. We have [indiscernible] toxicity, which is something that we have been asked because one of our competitors have had a clinical hold based on that. We have not seen it. We've seen responses, and we're going to talk about that. The procedure is going to be focused on ovarian cancer. We have a second tumor type. We're going to talk about it a little bit. We haven't disclosed what that is. It's not breast cancer where we have seen efficacy as well. We've seen, obviously, as you would expect, with CK2 inhibitor, stable disease is an important component here. These medicines are not necessarily cytotoxic, but we have seen single agent responses. So another question is what do we do next, and that's going to be part of the conversation next week. We think of ovarian cancer and the competitive landscape there. Obviously, mirvetuximab approved not too long ago, and now as part of AbbVie. We believe based on data that we have internally, if we use CCNE1 overexpression, which is what we're going to use for eligibility for the studies, we need to define the overexpression cut off with FDA. But we've been using an internal cal, which I think is very reasonable. I would say about half the patients that are CCNE1 positive, let's call them that, or full receptor alpha negative. So the overlap there is this 50-50. And we believe that about 40% to 50% of patients that are ovarian cancer are CCNE1 positive. So it's a sizable patient population. And the areas where we think this drug can be and should be developed our platinum-resistant later line that patients that currently -- if they're not eligible for mirvetuximab, they're treated with chemotherapy. It's a long list of different chemotherapy agents, none of which work very well. They have responses in the 10% to 15%, with PFSs in the 4, 4.5 month range. So that's one bucket. The second bucket, if we move to earlier lines is after second-line chemotherapy platinum-sensitive patients, those patients get right chemotherapy and then maintenance with bevacizumab. Some patients do get PARP inhibitors there. We are going to start a combination with Bev. We think that maintenance with Bev is another important pocket for us. And then the third one is after first-line chemotherapy maintenance therapy, that's the biggest bucket really because those patients get very long duration of therapy, their PFS is very good. And we think that's another area. And we think that there, because the toxicity that we've seen so far is manageable and there's no -- doesn't seem to be any chronic lasting side effects. It's basically hemotox, we think we can have an advantage even over emerging bispecifics in that particular bucket of patients. So that's what you're going to hear about next week. So just to say one thing because people -- sometimes the data cutoff for this data releases are confusing. There's an abstract that has a very early data cutoff. There will be a presentation at the meeting, and meaning oral presentation on Saturday has a different data cutoff later. And then the investor event that we're doing Saturday night has a later data cutoff. So that's the data you want to focus on. It's the most recent, most mature, most detailed data disclosure. That's the one people should focus on.

I guess how should we interpret the data as -- I mean, obviously, we did wish we now and I just want to mostly focus on. But in terms of like the activity that we'll see and just can you maybe relay like how advanced are these patients that you're looking at. Because I mean relative to what you're talking about as your development plans, would we think that these are more advanced or in the same ballpark in terms of...

No. These are very -- this was a Phase I study. and we expand the different dose cohorts to get more efficacy and to get a better understanding of the safety at different dose levels and the pharmacology, but they're very heavily protruded patients. I mean, many, many patients have had 2, 3 for prior lines of therapy, and that's what you will see. Like with any medicine in cancer as you move to pivotal trials, you refine the population and you try to keep the populations, how much genius is possible, and that's what we will do. So the efficacy has to be taken in that context, which I think -- I'm glad you bring it up because I think it's important.

Got it. Okay. I mean anything else that you're going to focus on beyond just those 2 tumor types or any areas that you kind of highlight where you could potentially go beyond those 2?

Well, the question that we are being asked is breast cancer, obviously. And Pfizer has had a big push there. They have a big franchise with the CDK4/6 with palbociclib. We are not -- we haven't given up on breast cancer. We have had -- we've treated patients with breast cancer. We're not going to talk about them next week. I think we have more time to make a decision. Because I think the question there is the combination strategy. We don't have a CDK4/6 inhibitor. As you know, CDK2 is a mechanism of resistance to CDK4/6 inhibition. That's why this has been such a big area of focus for Pfizer. And it's a triple combination because you need to combine with hormonal therapy as well to a little more complex development plan a bit more competitive. We still have not made a decision, to be honest with you. We are not ruling it out, but the focus for now is to try to be first and move fast in ovarian cancer. We think it's a big opportunity. . Ovarian cancer is the fifth largest cause of cancer death in this country. Mirvetuximab aside, there's been nothing happening in that space is bevacizumab, which is quite some time ago and the options for patients that advance these are very limited. So we think we need to move quickly there and be as expansive as we can.

Just last question on CDK2. But -- so if you were to pursue breast would you do it alone? Or would you look to partner like to get access to CDK4/6 or how would that look, just given that's a large...

Yes, CDK4/6 inhibitors are commercially available. Obviously, there's 3 of them approved and the other 2 companies to our knowledge don't have a CDK2 inhibitors. So honestly, we could do a collaboration. We're talking about true partnership to co-develop. We haven't done that, Derek. And we have all the resources that we need to develop these medicines properly and commercialize them eventually. So it's not something we are contemplating right now.

Okay. Understood.

With clinical collaboration it's possible but not a codevelopment.

Got it. Yes, that makes sense. Maybe shifting gears to myelofibrosis. Obviously, I want to tackle both the commercial and the pipeline, but maybe with the pipeline first. So Herve, you said, again, obviously, around CALR, BET, ALK. I mean can you just walk us through how you see these contributing over the next 5 to 8 years in terms of making up for the IP cliff with Jakafi. And I guess, how does it all -- how do all these puzzle pieces fit together?

I think -- first, I mean, the IP cliff for Jakafi the way to address it is not just by working in myelofibrosis. I mean so everything else. The entire portfolio is designed to be contributing revenue at the time when there will be life cycle for some of the older brands. So we don't see it like one-to-one kind of replace. That being said, we have a leadership position in the field. You saw the work we did with Axa and GVHD. So there are 3 components to Jakafi. GVHD, PV and the MF. For GVHD, Axa is now FDA approved. We know it has the potential in third line. If you base it on the performance of some other product that is approved [indiscernible] is also approved in third line. It's around now $100 million a quarter, more or less in that setting. And we are also developing it for first line. So we anticipate that by 2027, '08, '09, we will be more than replacing what is today's Jakafi in GVHD, with Axa. In PV and MF, as you know, in MF, we have a number of projects that are combining Jakafi. Of course, we have Axa, so the once a day formulation. And then we have the combination with Jakafi. And there, I must say, we are still in the process of fully understanding the profile of ALK2. So it's not yet fully solved. And we are looking -- we know we have an active drug with a BET inhibitor, and we are looking at what is the best setting for development, together with the FDA with all of the things that are happening around that. So that's sort of what I mean. When you look at CALR and 617F, it's a completely different game because now it's not just about trying to improve on the safety like ALK2 or the efficacy of Jakafi, it's really changing the goal of treatment. And both of them could have what we call a curative effect on some of the disease, including PV with 617F, including and MF and ET with CALR. And that could be -- each of them separately would be more than compensating for what Jakafi could be losing at the end of the decade. But as I said, when we look at the whole inside portfolio, sort of MF, strategy is a big part of it. So XR, CALR, 617F. But also, you have to look at what the rest of the portfolio will be doing by that time. And that's why we feel fairly confident we are in a very good shape.

Got it. So maybe just -- I want to dissect a couple of those. So with XR, so Jakafi XR, I think you're going to give us an update at some point in terms of, I guess, some of the data -- I don't know if you generated the data, but I guess with the FDA and ultimately, what you're going to do to get that approved. I think that was coming maybe next year. So just to clarify that. And then the other thing is, is that just going to be a pure switch strategy? And is that some -- is that risky with payers today? I'm just kind of curious like what kind of differentiation beyond the just extended release can you push to payers so that, again, it's not just like an old school spec pharma switch strategy?

Okay. Let me talk about first and probably want to talk about the switch strategy. So what we've said at the end of last year is that we first had to run a bioavailability study with new tablets. So we had to make new tablets for this based on the feedback we got with the FDA in 2022, at the end of 2022, beginning of 2023. So that was done. We did a bioavailability study. That's done. Now, the next step is to do a true [ biocoalency ] study. That will be run. The results will be available next year. We haven't given any more precise time line, quite honestly, because these tablets have to be put on stability, and we need to figure that part out. But that's all really a box-ticking exercise mostly. There's a little bit of finesse in there. So once we have the data, we'll submit. We should have -- if everything goes well, XR should get approved no later than the first part of 2026. So -- and that gives us 2.5 or so years before the patent expiry.

So in terms of ambition for XR, you have the first level, which is once a day, it has a pattern that goes to the 2030s. And if we have a number of patients on the once a day, specifically new patients are in treatment. By the time the twice a day patent is expiring, you can imagine that the curve, the erosion curve is slower -- going down slower than it would without. So by itself, it has value, limited value. It has some value doing that. The second piece, which is way more interesting is once a day combined with once a day. And the question is, what kind of new product will be -- once a day product will be available for treatment of any of the disease by then. And obviously, you zoom on myelofibrosis and you find that the BET inhibitor, our BET or other BETs are once a day. And obviously, the ALK2 is once a day. And there, you have basically 2 ways to look at it. One is to do a fixed dose combination like a tablet that contains both that takes time and it's feasible, and we will plan to do it. But even before you do that, you can do a co-packaging like [indiscernible] same concept where you basically have the 2 tablets in the same box, and then you have all the advantage of what to -- the fixed dose combination would do in terms of commercial impact. And so that's what -- that would be like the load take, if you want, first approach that would be feasible by them. If we have the data that we hope for BET for ALK2, where we would be able to do that co-commercial -- I mean co-commercialization in the same container.

Remember that the median duration of treatment Jakafi and MF is close to 2 years. And in PV, it's probably about 40 months. So patients that get started on once a day in '27, '28, are likely to stay on XR, not all perhaps, but a significant number of them are likely to stay on XR after the patent cliff. And that could potentially smoothen the...

And then I wanted to talk about CALR because I mean that's something that, at least from [indiscernible] checks, people are very excited about this mechanism. So maybe just talk about -- I think we're supposed to get to maybe potentially early data next year, but how important is this to your myelofibrosis franchise? And obviously, you kind of talked a little bit about or alluded to maybe curative effects here, something like that. So that would be really interesting if could you just highlight that a little bit more.

Yes, we think the mutant CALR antibody program is, first of all, I think as Herve described, I think it's very exciting for patients. I mean this is if we are right with this hypothesis, you really are starting to talk about potentially a functional cure for patients with MF and ET in the case of the mutant CALR antibody. With P617F, you bring PV into the story as well. We have been in the clinic for about 9 months now. The program is going well between patients with MF and with ET. And we will present data next year. We haven't said specifically the timing. That will depend on a few moving parts. Phase I study sometimes you can predict the time lines quite very accurately. And you expect to see over time, obviously, resolution of some manifestation of the disease, but the key endpoint that is a little bit different for mutant CALR and 617F that would be for Jakafi is the reduction [indiscernible] maybe to try to see over time, we can reduce the number of cells with the malignant clone and then over time, the normal clone without complete demolition clone, that will lead to replacement of malignant hematopoiesis with normal hematopoiesis that would lead to what we believe one can define potential as a functional cure. It's not a perfect analogy, but one way to look at it is obviously Gleevec, and all the BCR able transcript that go down over time. And over time, obviously, normal hematopoiesis corrects that. It's a very different way to treat CML with Gleevec that it was [indiscernible] which is you killed everything, the patients got a little bit better because you try to suppress hematopoiesis. So that's the story with a mutant CALR antibody. So yes, it's a key program for us. About 25% to 35% of patients are mutant CALR antibody positive, maybe to CALR positive. With ET and with MF, it's a big percentage of patients. If you bring 617F into the story, basically almost 100% of patients with MF, ET, PV are positive for one of those 2, CALR or V617 amputation. So not only we think it's a different way to treat this disease, it's important for patients, but we basically can transform the entire MPN space in a totally addressable population.

Perfect. And then just on the commercial side of MF. So I guess Jakafi has been last quarter -- or second quarter this recent quarter, you saw some volume growth and continue to see volume growth like in the first half. So I guess, what's kind of driving that given that there's income and competition. Even we had surveys kind of suggesting that there might be more not a lot in use, but it doesn't seem like that's really coming to fruition. So like I guess what's driving the resilience? And also, is it just kind of category growth also? Or is it more just you guys growing and the other ones growing a lot slower?

In MF specifically. I mean if you look at the Jakafi growth today, I mean, it's driven by GVHD and PV. And PV is a key driver of the overall growth of the brand. In MF, we are very flat. We can see it's like 1%, 2%. I mean, it's very low growth in volume and very low on price, in fact. And I think what's driven is that Jakafi is the standard of care. The tolerability is well better than momelotinib. And because when you look at the safety profile of both products, there are some important differences. And people are starting their treatment with Jakafi. And when Jakafi doesn't work anymore, which is most of the patient at some point, they will look at different alternatives. And what we find from market research is that momelotinib is used after Jakafi in most of the cases where it is used. So it's sort of expanding the market. So I guess if you add the 2 of them the overall market of MF is growing because momelotinib is doing very well, in fact, some second-line kind of setting, but it's not really changing the position in the first line of Jakafi as a standard of care.

I mean do you think in MF that just kind of flat to modestly up volume is sustainable for the next couple of years? Or do you think you'll start to see...

For Jakafi?

For Jakafi, yes.

I think yes, we see that the existing -- an existing book. As I said, the growth we are anticipating between today and the 2030 or 2029, is basically coming from GVHD NP.

Yes. This is to understand the stability of MF, but you think it's going to be pretty stable.

We anticipate it to be very stable.

Got it. Okay. Then maybe just shifting gears to Opzelura. So obviously, a lot of excitement and obviously, Vitiligo and atopic derm and then some of the expansion opportunities. So maybe just give us a sense of like how that's growing right now in the on-label indications and what you think are the most interesting indication expansion opportunities for Opzelura?

So I will do the -- I mean, the 2 indications, AD and Vitiligo are growing very well. In fact, they are growing at the same speed. So the ratios are not changing very much. Maybe they are, but we don't see it. I mean, from all the data we have, it's still around the same. . It's 2 completely different drivers. So it's interesting because it's 2 disease with 2 different pattern of growth. In atopic dermatitis, the profile of Jakafi is excellent in terms of speed of action, in terms of safety, obviously, as a topical. And the question is, simplicity of prescription because there are millions of patients who could benefit from Opzelura who are not because it requires prioritization. And there are a number of hurdles that have been built and created to prevent this prescription to go through, which by the way, it's sort of weird because if you can look at it as a product that is economically very valuable for the payers and for the insurer. But anyway, so we are working with the PBMs, and we are working with the insurance company to make that process easier. We had already some of our contracts, including the use in first line and the use with less steps required before you can go to Opzelura. And we have seen a positive impact on the volumes. And, in fact, a relatively good impact on the simplicity for physicians. So that's the goal over the next 5 years. If you think of it long term is make the prescription of Opzelura easy for the prescribers because dermatologists don't want to spend their time on the phone, justifying their atopic dermatitis eczema prescription. Now they will do that for vitiligo. And in fact, in vitiligo, it's because of the competitive situation, the hurdles to prescribe Opzelura are different from what they are in atopic derm. What we have in Vitiligo is a very good uptake of new prescriptions when you look at the data and where we are still short of our ultimate ambition is on the number of refills to the compliance of patients with twice a day treatment over a period of multiple months because it takes months to see the effect of Opzelura in Vitiligo. It takes minutes in eczema, Vitili 5 minutes. So that's what we are working on. We see the roles continuing but we also see that there is a lot of potential that we can improve on simplicity of access in atopic derm and refills and compliance in vitiligo.

What do you think you need to do to address that? Is it more just kind of like patient education or physician education to do it?

There is a physician -- physicians need to speak to their patients more. And it has to go quickly. So there is a time investment from dermatologists with vitiligo patients to explain it will take 3 months before or 2 months before you start seeing meaningful repigmentation. So that patients don't go through the first 2 and then decide to give up because it doesn't work. We know from the data. So there is still an education of the patient, by the physician and obviously, by every other channel that we know we can use reach the patients...

And where are you in terms of like -- because I think you initially had said you'd hope to see 10 tubes per year...

We are not there. We have room to grow, and that's something we are working on very actively. I see there is a potential -- I see it as a good news in some way, I see it as there is a lot of potential to do better. And as we know, I mean, we are -- in our career, we all have worked on these issues with compliance and how patients will basically follow what was the protocol in the clinical studies, and we know it's difficult, but we also know there are tools that can make it happen.

Got it. And then just in terms of those expansion opportunities, like which ones do you think are very attractive for Opzelura.

So we presented data early this year and in patients with mild-to-moderate hidradenitis suppurativa. Obviously, HS is a very important indication for povorcitinib. It's been developed -- it's in pivotal trials for moderate-to-severe HS. That pivotal trial is going to read out in the first quarter of 2025. So it's really quite a milestone for us, a first pivotal data on povo, which is a big part of the pipeline strategy. But based on the really, really impressive antiinflammatory effect that Opzelura has as Herve described, is very quick patients in AD feel better very, very rapidly. We decided to test a mild-to-moderate HS. And that data, which we presented clearly shows there's a benefit to the right topical agent in patients with early stages of HS. The challenge is because patients with mild HS particularly don't have draining tunnels that you can't quite use the same endpoints you used for approval that we use for systemic therapy like povo in the same setting. So we are having conversations with FDA to try to define the endpoints in the right way, and they will make a final decision whether we run a pivotal trial, it would simply be part of a publication strategy for HS. And the other one is, of course, prurigo nodularis, that it's ongoing. Again, PN is an indication where rapid relief is critical. These patients have 20, 50 in some cases 100 intensely pruritic nodules in the skin that just don't let them sleep and scratching leads to scarring and it's a really debilitating disease. We believe that there's potential for atopic antiinflammatory effect for patients with more limited disease. Again, the data we presented with povo and PN shows very rapid improvement in itch much faster than you see with Dupi if you put the data side by side. So we think povo has a little potential there. But once again, for earlier-stage patients, potentially Opzelura can have an impact...

So those would be more like kind of 80 in terms of more instant itch really versus vitiligo that's going to take longer. So again, maybe the compliance or the adherence and the number of tubes per year would be higher on the outside.

Yes.

Okay. Helpful. A couple of minutes left, so I want to just hit a few things. So one, povorcitinib also a very interesting asset, and you had some data in HS and also could look like a pipeline of product. I guess, where do you kind of think that in terms of this like overall kind of peak sales, I guess, like HS is a big market, some of these other indications, again, a JAK with some JAK liabilities. So like I know a lot of the orals in I&I are trying to move away from those more kind of black box warnings and liabilities. But I guess, where do you think that will fit, particularly in some of the indications that you're pursuing with that asset?

I'll let Herve comment on the peak sales question. What I can tell you is povo is right now been developing 3 pivotal indications, HS, PN and vitiligo. The data would be HS early '25, vitiligo and PN come in '26, maybe '27, depending on accrual. And also in the second half of next year, we'll have randomized Phase II data in asthma and CSU. So 5 indications in the next couple of years, povo III pivotal to randomized Phase II data. So obviously, a lot of opportunities here. And...

I think we can speak for the first indication in HS. I mean you know the range of forecast depending on who you have, you get the very big numbers. But we know because we have been now one of the precursor, one of the first companies developing a product for HS. We know it's very much under diagnosed in the U.S. and even more outside of the U.S. We know there is a clear benefit from this treatment. And so we will have with povo, we need to see the final Phase III result before we can give some guidance or some number, absolute number, but what we see that will be the first oral treatment with a biologic-like efficacy and a very good safety profile. And I think it would be one of the key players in the field of HS. And if you think of all of the different new drugs that will be available, it will certainly be one of the leaders.

Got it. And then just quickly, last one. Mast cell diseases, as you did the deal for Escient in that in terms of the MRG mechanism. I guess you got a couple of readouts coming out next year for that asset. What are kind of expectations for that mechanism? And I guess, particularly relative to like what we see maybe with some of the kits...

Yes. So with the acquisition of Escient, we took in 2 programs, MRGPRX2, which is a mast cell focused target is expressed in mast cells, but not just mast cells, mast cells and connected tissue and the skin. We were very interested in the target, and we wanted to make sure we were first in class, and we are certainly in that spot right now. We're going to have 3 readouts for MRGPRX2 next year. Early next year, we have a study ongoing in chronic inducible urticaria, both cold-induced and dermographism. We have a randomized double-line study in chronic spontaneous urticaria and a randomized double-blind study in atopic derm. And the second program, and I'll come back to a question about kit. The second program is an MRGPRX4 inhibitor X4 is a receptor that is affected by bile acids and biosalts. So we have a study ongoing in cholestatic pruritus in patients with both primary biliary cirrhosis and primary sclerosing cholangitis that study also will have data over next year. So 4 readouts from the Escient acquisition. Look, when it comes to CKD inhibitors, there's no question that if you give a CKD antibody that basically kills mast cells, you're going to have a very strong efficacy in mast cell diseases. The way we see it is this is going to be a balance between safety and efficacy. Patients with chronic urticaria, chronic by definition, they need long-term therapy. They start with antihistamines. The dose of antihistamines has increased. Some -- about half the patients don't respond. Those patients need something else. The question is what's going to be the first line after antihistamines. When we saw the X2 safety data from the ongoing studies is an extraordinary clean safety profile, which we think combined with good efficacy, will make for this the preferred agent after antihistamines. Is oral, well-tolerated key for chronic therapy? Maybe the efficacy will be comparable to a kit antibody. We don't know. It's not certainly what we expect. But we think that the overall profile will be very important in patients with these diseases.

Okay. All right. Well, I think we'll leave it there. Gentlemen, thank you so much.

Thank you.

Thank you.