IMVT

Ladies and gentlemen, thank you for standing by. Welcome to the Roivant Fourth Quarter 2025 Earnings Call. At this time all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. And to ask a question going into the session, you'll need to press star one one on your telephone. You will then hear an automated message asking if your your hand is raised. We ask that you please limit to one question. And to withdraw your question please press star one one again. Please be advised that today's conference is being recorded. I would like now to turn the conference over to Stephanie Lee. Please go ahead.

Good morning. Thanks for joining today's call to review business updates from Roivant's fourth quarter and fiscal year ended March 31st, 2026. I'm Stephanie Lee with Roivant. Presenting today, we have Matt Gline, CEO of Roivant, and Drew Fromkin, CEO of Pulmovant. For those dialing in via conference call, you can find the slides being presented today, as well as the press release announcing these updates on our IR website at www.investor.roivant.com. We'll also be providing the current slide numbers as we present to help you follow along. I'd like to remind you that we'll be making certain forward-looking statements during today's presentation. We strongly encourage you to review the information that we have filed with the SEC for more information regarding these forward-looking statements and related risks and uncertainties. With that, I'll turn it over to Matt.

Thanks, Stephanie. Thank you everyone for dialing in this morning. I'm glad to be talking. We have an unexpectedly busy agenda with a bunch of topics, so I'm looking forward to going through all of it, including obviously, what we announced this morning, which is the preliminary open-label period data from the 1402 study in D2T RA, as well as a planned spotlight we've been planning to do for a while on mosliciguat getting into that data, which Drew will take us through, and some smaller updates on the brepocitinib program, although exciting. A lot to cover. Before I get into all that, use one small bit of executive privilege and wish my father, Jerry, a happy 75th birthday. Today is his 75th birthday. Happy birthday, Dad. He sometimes listens in on these calls. I don't know if he's listening in now.

If not, he'll catch it on the replay. Into the important topics now. Starting on slide five. This has been a pretty wild 12 months for Roivant. We continue to see just tremendous execution and momentum across our development portfolio. An update that will get drowned in some of the other things for today, but is actually pretty great, is that brepocitinib was awarded breakthrough designation and a rare therapy designation for cutaneous sarcoidosis, which just underscores indication selection and development there in terms of what that could mean for those patients. We announced LPP as an indication for brepo, and that study is already enrolling, and we're excited about how that's going.

A ton of work ongoing in commercial prep for the launch in DM, which assuming FDA goes as we expect it to, will launch by the end of September. Obviously the biggest data update for today in the FcRn franchise is what I mentioned earlier, which is that 1402 showed, we think, clinically meaningful, pretty exciting ACR response rates across ACR20, ACR50, and ACR70 in the D2T RA study in the open label portion. We'll talk more about that's obviously encouraging data that we're looking forward to spending some time on. We're also fully enrolled on CLE with top-line data expected in that study in the second half.

Earlier in this quarter, we announced the failure of the batoclimab studies in TED, but also that the hyperthyroid patients showed normalization, which was supportive of our Graves' studies, which are ongoing and continue to enroll well also. Finally, hard to believe it was this quarter, but earlier this quarter, we also announced our $2.25 billion settlement with Moderna, and we expect to receive the first portion of that payment, the $950 million upfront, in July. Just an incredibly busy quarter of execution for us and an incredibly busy fiscal year for us. It's really hard to believe how much has changed in a year for Roivant. None of that, though, is to say on slide six that we're done. The next 12 months are also incredibly exciting.

Obviously, one of the most important things going on, we will hopefully be launching brepocitinib in dermatomyositis by the end of September. The phase III study in cutaneous sarcoidosis we expect to begin this year as well and we expect the NIU phase III top line data in the back half of this year. A transformative year for brepo as all of that comes around. We'll spend time on this today, but the mosliciguat PH-ILD phase II-B top line data is expected in the second half. That also will potentially underscore that as a really important program and hopefully looking forward to that data and just talking more about it.

Obviously, D2T RA, some of the data is around today, but we're looking forward to providing a pretty significant update later this year with a little bit more data as well as some detailed analysis we're doing at a patient level and hopefully with some feedback from FDA on a go-forward plan given what we've now seen. Obviously we'll get the CLE PoC top line data as well. Next year is a huge year with 1402 data in Graves and MG coming in. A ton to look forward to, and frankly, as much in the windshield as in the rear view mirror. I think I've got the car analogy right there. Great. Okay. I'm going to go in now without spending any more time on the preamble and talk a little bit about this D2T RA data, which I would call surprisingly good.

We were pretty excited to see what we saw here is slowly been a little bit hard to process just how exciting this data is, and so we're still doing a lot of work on it. As a reminder on slide eight of what we're talking about today. This was a unique study design in a few ways. First of all, as I think everyone's aware, this was a study in heavily refractory patients. Every patient in this study, in addition to failing steroids and DMARDs, also had to fail at least two advanced lines of therapy. Most commonly, that's two of, for example, TNFs, JAK, and IL-6s. We'll talk a little bit about that. There's obviously some other things that could be in that bucket as well. The study also had a pretty strict entry criteria on autoantibody positivity.

We had a criteria on ACPA+ above a certain level. That was also specific to the study and the design. The other way in which the study was unique is it was a randomized withdrawal study with two periods. First, an open label active treatment period of 16 weeks at high dose 1402, 600 mg, followed by a period two, 12-week re-randomization where ACR20 responders at week 14 and 16 both are re-randomized into a 12-week randomized withdrawal period, where some of them stay on 600 mg, some go down to 300 mg, and some go down to placebo. What we have to share today is preliminary data. We're still actually cleaning and finalizing it all, but it shouldn't move very much from here. On the top line treatment effect from Period 1.

Period 2 is still ongoing, with more than half of patients still being dosed in the study. We don't have any data or information about Period 2 to share today. Even for Period 1, there's a whole bunch of data like IgG, for example, that we haven't analyzed fully and are not ready to share. Nothing to say about it other than that we're going to be sharing a pretty limited subset of this data today. On slide nine, you can see baseline characteristics for the patients in the study. We wound up with 165 evaluable patients. I'm not going to go through all of this in detail other than say, this is quite a sick patient population. Obviously, by design, it's refractory, and we'll talk more about that in a second.

For example, if you look at the DAS28 CRP score of 6.1, that's quite high for a study like this. There's a bunch of measures on here that suggest a quite sick population, which was the goal, right? This is the population that we set out to enroll, and so we feel good about who's in the study. On prior lines of therapy, specifically on 10. You can see on the right-hand side, we succeeded with our entry criteria. That is basically all of these patients have failed more than two advanced therapy mechanisms. That's very different than either the [NIPPON] study or really any of the later line RA studies that have been run. Actually, one thing that we're highlighting today, which I think is particularly interesting, 65% of these patients roughly have failed, specifically JAK inhibitors.

Notably, and we'll highlight this elsewhere as well, basically every single one of the patients who failed a JAK inhibitor also failed a TNF. This is a TNF and JAK refractory patient population that we're focused on. Look, slide 11 is the headline here. The headline is, with all the appropriate caveats for an open label study, these numbers are high. We saw 73% of patients roughly with ACR20 responses. Not just that, but we saw quite deep responses. We saw over half of patients with an ACR50 and over 1/3 of patients with an ACR70. Notably, once you get onto the deeper end of that with ACR50s and ACR70s, you just don't see a lot of placebo response in that level of responder analysis.

It feels to us like looking at this data, there's something going on that's meaningful and interesting with this drug and something that merits enthusiasm and a lot of further investigation. We're certainly doing all that work now as we get ready to take the program forward. I'll highlight on slide 12 the one other bit of interesting data from the study that we're able to present today, which is we pulled out the subset of patients who are JAK experienced. Remember, those patients, 107 of them are both JAK and TNF experienced, all of them. Some of them have also failed something else as well. One of the things that I think is maybe most exciting about this data is it's basically fully preserved in that subset.

As you think about that opportunity where these patients have really failed all of the most advanced options available to them, we're able to deliver in an open label setting, pretty exciting response rates for those patients, which I think bodes well for the exact biological thesis with which we ran the study to begin with, that autoantibody positivity is an orthogonal mechanism to some of the other anti-inflammatory options, and that for ACPA+ patients, this could be an effective treatment option. Look, I think on slide 13, just to reiterate what we're showing here. Look, these are sick patients, a difficult to treat patient population who have failed a lot or all of the available options and come in with highly active disease.

We showed really great response rates in the data that we're excited to see how they evolve through the rest of this study and on deeper patient-level analysis. Notably, this is the largest patient population dosed with IMVT-1402 to date. It was safe and well-tolerated in the study. Nothing new drug-related from a safety signal perspective identified. A clean data set overall and further underscoring what we think we've got with 1402. Fast-forward from here. Obviously, you look at this data and you feel pretty good about what this could be. Significant potential benefit, a differentiated mechanism, a difficult to treat population with not a lot of options. We're actively working right now to get ready to talk to FDA about this data and plan a path forward. The data is encouraging.

I'll make one comment about it, which is the depth of responses is exactly what's exciting about the data set. It's exactly what makes us believe there is something beyond placebo happening in the data set. As you'll recall, the randomized withdrawal period, the primary endpoint of Period 2 is, do patients taken off drug lose their ACR20 response in 12 weeks? Which was a relatively short period to begin with, and almost certainly would've been fine if we had seen more marginal benefit on ACR20. The truth is, once you're looking at ACR50 and ACR70 responders, I think the bar has actually gotten a fair amount higher for Period 2. Paradoxically I think we still have a good shot of success there, but in some ways, Period 2 was less meaningful than it might otherwise have been.

I think there are plenty of scenarios where we don't see a P value in Period 2 and continue forward with the drug given the overall quality of this data. Conversely, depending on FDA's feedback, potentially situations where we do see a P value in Period 2 and just need to make sure we're comfortable with the plan forward. I think much more interesting than the Period 2 data at this point is more patient-level analysis, as well as the results of those FDA discussions. We expect to share all of that in the second half of this year. We're working on it right now. My hope, given the quality of this data, is that we'll be coming back to you with an enthusiastic update about next steps here that lay the groundwork for just a really big opportunity.

Remember, we presented some data at our investor day suggesting this is at least a 70,000-patient population and some more specific revised commercial analysis that Immunovant has now done that looks like that number could be 85,000 or higher. It's a big patient population in need, and I think underscoring that the speed with which this trial enrolled, the enthusiasm that physicians have for putting patients on study is just further evidence that there's really something interesting here. With that, I actually just want to also just give a shout-out to the Immunovant team who have continued to execute really well. Obviously, the data itself is strong, but also the speed of enrollment, the speed with which we're moving through these studies, the full enrollment on CLE, and I think that spans all of our programs.

I think we're excited about obviously what Priovant's been able to do with brepocitinib from a clinical enrollment perspective. We're excited about the speed of enrollment for mosliciguat. Obviously, the quality of that data we'll find out soon. look, we're really excited about what we've been able to do across the portfolio on clinical execution. So much appreciation for the enormous number of people who are working towards those goals. Cool. I'm going to pivot now to mosliciguat and do a little bit of a data preview there because the next time we get together, that data could potentially be very close in front of us. we wanted to get out ahead of that and give people a chance to just ground themselves in what's coming, as we did last year around this time or a little later for brepo in dermatomyositis.

Look, I'll do a little bit of an introduction here, and then you all heard from Drew back at Investor Day in December. He's in the room with me and is going to talk through a little bit more about the program. Look, intense unmet medical need. These patients, in the extreme, a significant proportion of them die. They're very sick. There's currently only one approved mechanism with two therapies, and we think there's probably 200,000 patients across the U.S. and Europe. That one mechanism for prostanoid underscoring multiple really great launches at this point. We're excited to see the commercial enthusiasm and excited to see these patients have access to something that provides real benefit already, and we're hoping to add to that. Mosliciguat has a completely differentiated mechanism of action for the disease. It's an sGC activator. It's an inhaled sGC activator.

It is potentially the first non-prostanoid that could be available for these patients. We expect this to be a polypharmacy combination therapy market as PAH has been, and we think mosliciguat has a chance to be first line, has a chance to be a major part of the treatment paradigm, and we're just looking forward to getting this data and moving forward there. In our phase I data across healthy volunteers and pulmonary hypertension patients, and Drew will remind us of this data specifically, we saw among the best PVR reductions to date. one of the things we're going to remind people of today is that although we saw a 38% PVR reduction in some of those patients, that basically anything that has ever shown 20+% PVR reductions has been able to deliver clinically meaningful benefit.

I think it's true that there has not been any class of drug showing a 20+% PVR reduction that has not gone on to be a commercially successful class of drugs. Finally, as a reminder, unsurprisingly, the top-line data from that study is on track, and we expect to get it in the second half of 2026. It's a 135-patient study. With that, I'm going to hand it over to Drew, who's going to take you through the next handful of slides here on the program, and then I'll come back for a little summary at the end and the rest of the presentation. Drew?

That's great.

Thank you.

Thanks a million, Matt. I can tell you there's a lot of excitement about mosliciguat. Mosliciguat is an inhaled sGC activator that's delivered directly to the lungs to activate sGC and restore impaired sGC function. sGC is a key enzyme in the NO/sGC/cGMP pathway, and in oxidative stress environments like PH-ILD, nitric oxide may be reduced and the sGC binding site can become impaired, leading to sGC dysfunction. Now, typically, sGC is activated when nitric oxide engages sGC in the presence of heme, and cGMP is then produced. Unlike cGMP sGC stimulators that requires nitric oxide and heme to activate the sGC, inhaled mosliciguat binds to the heme pocket independent of the need for NO and heme, producing cGMP, which results in vasodilation of the pulmonary arteries and potential reduction of fibrosis and inflammation of the lung tissue. Next slide.

We know many pulmonary diseases are heterogeneous in nature, and that fact can make patient treatment complex. To start, there's disease of the pulmonary vasculature and disease of the lung parenchyma. The combination of these two disorders is embodied in pulmonary hypertension with interstitial lung disease, which is the first indication we're exploring in our phase II PHocus study. We believe mosliciguat has the potential to address both the pulmonary vascular and the lung parenchymal diseases experienced with patients with PH-ILD. Mosliciguat. Next slide. I want to make sure that-

What I'm going to do is call out the slide numbers. Everyone's got-

Okay. I'll call out. You call out the slide numbers for me.

You can call them out.

Okay.

Thank you.

Thank you very much. I appreciate that. I want to make sure we're advancing. Okay. Mosliciguat preclinical properties led Bayer to take mosliciguat into phase I trials in a total of 170 patients, including healthy volunteers and patients with Group I PAH and Group IV CTEPH. In the phase I study, Bayer studied mosliciguat in 132 healthy volunteers and 38 PH patients. The healthy volunteers underwent studies with single and multiple dose formats, and mosliciguat proved to be well-tolerated, active, and have an extended half-life of approximately 40 hours. In the phase I-B ATMOS study, 38 patients with PH were dosed in a single ascending dose format, and mosliciguat again proved to be very active, producing deep PVR reductions, and was very well tolerated. On to slide 20.

Given mosliciguat's mechanism of action inhaled route of administration, one would expect to see notable reductions in pulmonary vascular resistance associated with hemodynamic changes. With one dose of mosliciguat in PH patients, that's exactly what we saw. A single dose of mosliciguat reduced PVR in these patients early and sustained through the three-hour observation period with a mean PVR reduction of greater than 30% and a mean peak PVR reduction of approximately 38%. This places mosliciguat's PVR reductions amongst the highest reductions seen in single and multi-dose trials in PH treatment space. With one dose of mosliciguat, we also saw cGMP levels rise as measured in plasma with no associated clinically meaningful systemic side effects, including systemic blood pressure and heart rate.

We also observed the desired impact on other hemodynamic measures, including mean reduction in mPAP of up to 20% and mean increase in cardiac output of up to 25%. Slide 21. Mosliciguat was also well-tolerated in phase I patients, in healthy volunteers, and patients with PH, with treatment-emergent adverse events being mild to moderate in intensity across both groups. All doses were well-tolerated, and we did not see significant cough, which is often exacerbated by inhaled treprostinil. We did not see clinically relevant systemic side effects, which we believe in great part was due to the inhaled direct delivery of mosliciguat to the lungs and the limited bioavailability of mosliciguat in circulation. Slide 22. With mosliciguat's phase I tolerability and clinical profile, we look to take mosliciguat into phase II development, an indication where there exists a major unmet medical need.

We felt that PH-ILD was an exciting opportunity for development. Given the primary site of PH-ILD, it's in the lungs, involving the pulmonary vasculature and the lung parenchyma, and the currently approved treprostinil treatments have high treatment burden, as well as tolerability challenges with highly variable efficacy. Mosliciguat lines up really nicely in this moment. Since it was delivered directly to the lungs as a once-daily dosing, that's been very well tolerated and produced limited incremental cough and systemic side effects in phase I, and has the potential to address both the pulmonary vascular and lung parenchymal diseases. Slide 23. To go a little deeper into PH-ILD patient populations and the opportunity, PH-ILD represents a large and underserved market where new drugs are sorely needed for these patients.

There are up to approximately 200,000 patients in the U.S. and Europe, likely underdiagnosed given the lack of treatment options in particular. This is a sick population and severe subgroup of PH, less than a five-year median survival, and the combination of PH-ILD represents an increasingly poor prognosis compared to each alone. I mentioned previously the lack of treatment, as there are currently only two approved FDA treprostinil drugs, leaving room for significant improvement. Slide 24. Now the core field of drugs in development for the treatment of PH-ILD is rather sparse. There are three companies, all with treprostinil treatments in different formulations, and all of these treprostinil treatments continue to have a range of challenges.

Seralutinib, with its different mechanism, has also run into recent challenges as Gossamer's phase III PROSERA trial in PAH did not meet its primary endpoints, coming off challenges in phase II as well. The result of the recent PROSERA trial outcome, Gossamer has paused its planned studies in PH-ILD. Mosliciguat on the other hand, with its first-in-class opportunity as an inhaled sGC activator, has once-daily dosing, positive tolerability, and positive activity in its profile from phase I studies. This really positions mosliciguat to be a leader in the treatment of patients with PH-ILD upon its approval. This is slide 25. I also wanted to share our thoughts about how we see PH-ILD and the market and how it's going to develop. We actually think the PAH market provides a likely roadmap for that development.

In the early days, supportive care was the only option for patients with PAH. This is what we currently see, and that's the reality of PH-ILD patients in most regions outside of the U.S., where there are limited treatment options. Over time, drugs with newer mechanisms were approved, and combination therapy involving multiple mechanisms of action became more common. As the median survival of these PH patients has also steadily increased as time went on from 2.5 years to where they are today at 12-15 years, the treatment guidelines evolved alongside the data, which reinforced the evolution of the treatment paradigm.

Today, revenue in the PAH market has really reached a stellar level at $100 billion in aggregate sales and a robust $7 billion per year, with 15 drugs approved, and there remains a good pricing environment and commercial opportunity for these newer therapies because this is driven by the complex nature of PAH. Finally, key takeaway is that today over 40% of patients with PAH initiate their treatment with dual therapy, and 15% of these patients will add a third therapy by the end of the year. This combo therapy, as Matt said, is really the norm. We are currently deep into our phase II study exploring mosliciguat in our blinded phase II placebo-controlled and randomized study in adults in PH-ILD. The study is a multicenter study across the globe. We're targeting 120 patients. We ended enrollment with 135 patients.

During the screening period, the investigators looked hard to find patients to confirm ILD, elevated baseline PVR indicative of PH, and limits on the level of fibrosis and emphysema as determined by CAT scan. If eligible for the study, the patients then randomized two-to-one, drug to placebo, and then they go through a rapid uptitration, and that moves from 1 mg-2 mg to 4 mg. Matt may have spoken about it, but we've seen really great progress there with the vast majority, over 95% of our patients achieving that 4 mg dose and sustaining well through the week 16 period. That's been very attractive and positive. At week 16, the primary endpoint is change from baseline PVR, and that's determined at 16 weeks alongside the secondary endpoint of change from baseline six-minute walk and change from baseline NT-proBNP.

The patient moved on to week 24, secondary and exploratory endpoints, and then they all go on drug if they weren't on drug into the long-term extension. Slide 27. very importantly, and as we get closer to data in the second half of this year, we've focused very heavily in designing our phase II study and defining our patient population. we carefully designed around the Seventh World Symposium on Pulmonary Hypertension, and these guidelines are crucial for PH-ILD patient selection. We targeted patients with worsening symptoms of PH, mild to moderate impaired lung function based on pulmonary functional testing, elevated PVR and mean pulmonary arterial pressures were crucial, and also we excluded severe emphysema to ensure a cleaner ILD population. The result is that the study population closely mirrors the recommended guidelines in more severe patients.

On slide 28, as you can see, this effort is reflected in our baseline data in PHocus. Our mean PVR came in at 7.1 Wood units, so very elevated. Mean pulmonary arterial pressures of 39.3, consistent with our desired thresholds and confirming we enrolled patients with significant hemodynamic involvement. The lung disease mix also looks well-balanced, and we protected for emphysema both in number of patients and level of severity as determined by the CAT scan. This was very important from all of those learnings. We also explored background therapy, including exploring PDE5i on background, and this is also consistent with real-world practice. This careful patient selection and enrichment gives us confidence we've enrolled the right population to detect meaningful treatment effect, and are very much looking forward to our phase II data in the second half of this year. Matt, back to you.

Awesome. Thank you. Thanks, Drew. Look, a lot to be excited about on the program here. Just a couple quick reminders and a summary on slide 22 and 23 here. On slide 22, so Drew talked about this in detail, but just as a reminder, the primary endpoint of this study is PVR. That is the same as the primary endpoint for the phase II programs across a variety of other PH-ILD studies or mechanisms or drugs. We're doing the same thing, following a well-trodden path there. We will then, in phase III, move to a six-minute walk and other clinically relevant endpoints as the way that the trial is measured. I want to remind everybody, this study is not powered to achieve a P value on six-minute walk.

We may or may not achieve a P value, and what we're really looking for is affirmation of dosing, affirmation of safety, affirmation of PVR in this patient population, and we will obviously look for interesting trends in patient-level data on six-minute walk. I want to make sure we've been clear ahead of time. This is not a study designed to achieve a P value on six-minute walk, and that's not what we're looking for as our own criteria to go from here. That's the point I wanted to highlight. I wanted to highlight it now while having not seen any of that data, so that I can't possibly be telegraphing anything about the study other than how it was designed. On slide 23, just to recap what Drew has said here.

First of all, again, with appreciation to the Pulmovant team, this study enrolled very quickly with all the patients enrolled within 12 months of the first patient being dosed. Early discontinuation rates compare favorably to what we've seen in previous PH-ILD studies. Look, with this and 20 bucks, you can buy two pizzas at Domino's, but our investigators are enthusiastic about the program. They're excited. The feedback's good. I think we're feeling great about how the study is being run. This is a great thing for safety. It's a great thing for the opportunity. As Drew said, 95% of the participants reached the maximum dose during their titration, and all of the blinded safety reviews and the ongoing assessments by the DMC have continued to affirm the safety of the program and allowed people to run the study.

Obviously, there's lots of things that don't get revealed until the data's unblinded, but it certainly gives us comfort that the patients are achieving high dose and that things are moving as they should be. Again, thank you to Drew. Happy to provide this update now ahead of that data. I'm really looking forward to seeing the outcome from this program in just a few short months at this point. Looking forward to it. Lastly, in terms of the pipeline updates today, I'm just going to give a brief recap of where we are on brepo. Brepo has been the focus of so much of our conversation for the past 10 months. It's less of a focus today as we're in execution mode there. Just as a reminder on slide 25 here. Sorry, I'm looking at the wrong slide numbers.

As a reminder on the next slide, on the first slide of the brepo section, it's slide 32, sorry. Look, this is a huge opportunity for us. There's possibly close to 300,000 patients addressable by the existing indications and just a ton of data coming over the next 12-24 months between the potential approval, obviously, in dermatomyositis, but also the NIU data, the potential for the NIU launch, the ongoing program that we'll start enrolling soon in cutaneous sarcoid, the currently enrolling study at LPP, and potentially more indications to come. Just a lot of great stuff coming for brepo and a really exciting moment from here. On slide 33, we've put this up a few times, just to remind people. First of all, these are sick patients, and there are really very few options for them in dermatomyositis.

As a reminder, 75% of these patients are on principally steroids, and in many cases on very high doses of steroids, over 10 mg a day for a good portion of the year. Beyond that, it's a combination of IVIG, which, as a reminder, the sort of established treatment paradigm for IVIG in dermatomyositis is somewhere between four and five days a month consecutive in an infusion center. A really arduous path. Other than that, it's off-label stuff, much of which has not been successful in studies, but is used because there's no other option. We feel really great looking forward here to our ability to bring a new option to these patients. On slide 34, further underscoring, and again, this is not new, we've presented this before, further underscoring the need here.

These patients are treated, as with PH, for that matter, with polypharmacy on multiple lines of therapy. They're bouncing around. They have accumulated organ damage with high systemic steroid exposures. It's just a tough experience for these patients, and we think a new option is going to go far. We're not saying a lot on slide 35 about our commercial progress. First of all, it is a, and will become, a more competitive field, and second of all, we're mostly just head down in execution mode. I'll just say, suffice to say, we're doing all the things that you would expect us to be doing at this stage. We're in the thick of payer engagement. We're working with the physician community. We're partnering with specialty pharmacies to make sure distribution is effective for these patients.

We've built a strong commercial team that we're really excited about, and we continue to do unbranded patient engagement. We talked about dermatomyositis.com when we got together in December. I'm super pleased with the work that team is doing. I think they are executing on the commercial side with the same vigor that they executed on the clinical side. I'm excited to see what we're able to do there later this year and beyond. We've also been moving along on the scientific and medical side. If you look at slide 36, this is a small subset of the presentations that have been made of this data, but the data's been presented all over at this point and continues to be presented all over, both at the major medical meetings as well as at a whole host of regional myositis meetings and rheumatology meetings.

Notably, in March, the phase III data was published in NEJM, which is a testament to how exciting the data is, a testament to the importance of the study, the quality of the study, and we couldn't be more excited for that publication as well. Finally, just a super quick recap on LPP, which we announced just about a month and a half ago. A fourth indication for brepocitinib. It's a highly morbid disorder with no FDA-approved therapies. These patients are miserable. They are in a ton of pain. It's a really tough disease that, in addition to pain, causes itch, burning, redness, scaling, generally irreversible hair loss. There's probably 100,000 or so such patients in the U.S. It's been growing in prevalence over time, and there's nothing approved, so we have an opportunity to do something really interesting for these patients.

Our trial design on slide 38, we talked about when we first unveiled the program, is a sort of continuous enrolling phase II/III pivotal that's designed to give us endpoint validation and is going to get us into, hopefully, registration there. We're really looking forward to that. There's just a ton of reasons to be excited about the program on slide 39. The high unmet need in LPP. The mechanistic rationale for brepo is strong. It's a Th1-dominant disease where dual JAK1/JAK2 inhibition should work specifically well. We think we've got the right trial design, and there's obviously some overlapping prescriber base and KOL community with our existing indications. It all sort of fits together, and we're excited to see how that program continues from here. Great. Okay. I'm going to wrap up quickly with the financial update, and then we'll get to Q&A.

I'm not going to spend a ton of time on this. Financial quarter was relatively straightforward. We continue to be in a strong position from a cash perspective. $4.3 billion in cash equivalents as of 3/31 before the Moderna settlement. No debt. We continue to retire shares. We purchased a fair amount in this quarter. We continue to have an active program. Spend continues to be sort of as it has been. Over time, R&D has grown a bit as the scope of the programs have increased, but that's all for the good, and looking forward to the future.

There is a couple of slides in here that I'm not going to talk to now, but we've gotten a few questions on accounting treatment as the launch gets closer, and so there's some good reference material in here on slides 44 and 45 if you're trying to build models or understand our financial statements in the future. Look, I've talked about this a fair amount already, but on slide 46 and 47, we just have a great run ahead of us here. We got a lot to do. Obviously, we've been fortunate and have had high-quality execution so far with the quality of our data. It sets a high bar for the stuff coming next. Which I couldn't be more excited for.

A lot of really great data coming in our existing programs and new programs, and looking forward to sharing all of it in the period to come, as well as obviously getting back on the commercial arena and watching all of that play through. With that, I'm going to say thank you again. I'm going to say thank you to, obviously, all of you for listening. Thank you to all of our teams, Pulmovant, Priovant and Immunovant for continuing to run high-quality studies, executing well, generating quality data. Couldn't ask more of these drugs, couldn't ask more of these teams. Obviously, a great thank you to the investigators and the patients who work with us and make this happen. Thank you to everybody who makes this work. I'm going to pass it over to the operator for Q&A so that we can get to it.

As a reminder to ask a question, please press star one one on your telephone and wait for your name to be announced and to withdraw your question, please press star one one again. We do ask that you please limit to one question. Our first question is going to come from Corinne Johnson with Goldman Sachs. Your line is open.

Good morning, and happy birthday to Papa Gline as well. Maybe you could just contextualize the ACR responses you saw here at 16 weeks first. I think more kind of typical in later-stage studies, there's a 24-week reporting timeline. How would you expect those responses to trend with more time on therapy with kind of implications then towards the randomized withdrawal phase? Thank you.

Yeah, perfect. Appreciate it. Look, I think the first answer to that question is, we don't know. This is the first time patients have been treated with this drug and first time this patient population has been studied this way in detail. Sicker people tend to need more time to get better in general, and that's why I made the comments I made about the phase II sort of randomized withdrawal period. In terms of week 16 versus week 24, I don't know. I'll say I don't think there was anything specific about the data leading into week 16 that suggested we were done. I think there's certainly a possibility for continued improvement with therapy over time. We'll find out as we look at that part of the patient population. Thanks, Corinne. Appreciate the question.

Thanks.

Thank you. The next question is going to come from Yasmeen Rahimi with Piper Sandler. Your line's open.

Congrats team and congrats to Papa Gline for also achieving a major milestone of 75 years. Happy birthday to him as well. Quick question on mostly congrats. We're very much looking forward to the data. You've been very granular on sort of the baseline as well as what you're seeing of up titration and safety. Have you been able to look at whether your assumptions for standard deviation in PVR and six-minute are sort of tracking in alignment with what you're seeing? I'll jump back in the queue.

Yeah, thanks. I appreciate it. Look, I think the short answer to that question is we are largely blinded to all of that data and don't have a lot of information about it, so it's hard to say. I think given the patient population we enrolled, we feel pretty good about where the study's headed, and we think we've got an efficacious drug. We don't have a lot of information about sort of ongoing distributions because the way the study has been blinded. Thank you.

Thank you. The next question will come from Andy Chen with Wolfe Research. Your line's open.

Hey, thank you for taking the question. Matt, I'm aware that you said with Immunovant you haven't analyzed IgG reduction, but that's still my biggest question. Other FcRn drugs, they don't seem to be able to achieve this level of efficacy in RA, and people blame it on Fab glycosylation. Do you somehow have ACPA antibody reduction data, or will we see that data before you unblind the Period 2 data? Do you expect ACPA reduction to be less than IgG reduction? Thank you.

Look, I don't have that data now, as I said, so I can't answer the question. We know from our phase I studies that IMVT-1402 suppresses IgG quite deeply relative to other drugs. Given the quality of the clinical data we've seen on ACR, I think it's certainly a thing to speculate on that the overall profile of 1402 is part of what's contributing to our ability to deliver this data. Obviously, it's also a different patient population that has been studied, and it could also be partially patient selection, and I think that could certainly be playing a role here. I think those are both important. Look, I think we will continue to analyze this data.

I don't know at this stage exactly when we're going to present what data, so I don't have a good answer to what you're going to see before or after the Period 2 is unblind. I think we will provide more information about what we've seen, about what our analysis looks like, when we're sort of prepared to talk about the full future of the program. I'll say I think mostly this has been a blessing, but also it's a curse. We've been a leader wonder if this data is going to also establish a leadership role for us along the lines of which others may follow. I do think we're going to be a little bit conservative on what exactly we say from a competitive perspective.

Overall, I think the data are starting to speak for themselves here in terms of the quality of what we're able to do, and I hope we are continued able to see that as the data mature. Thanks, Andy.

Thank you. Our next question will come from David Risinger with Leerink Partners. Your line is open.

Yes, thanks very much. Congrats on the phenomenal data this morning. My question is on mosliciguat. If the phase II PHocus study surprisingly shows a statistically significant benefit on six-minute walk. Could it represent a pivotal study? What would the requirements be in that scenario for a future NDA filing? Then just one other on mosliciguat. Is the company considering development of mosliciguat in any additional indications? Thanks so much.

Thanks, Dave. On [stat sig] at six-minute walk, I think it's impossible to say exactly what we would do until we saw the data. If the data looked good enough to support a productive conversation with FDA, I think we would have a conversation with FDA. The FDA has been aggressive lately on conversations about single pivotal designs. Never say never is the answer. I want to be clear, it's not the base case expectation, and the study is not powered to show a benefit on six-minute walk, so we'll see what we see. Look, I think given where we're at, we'll certainly take that as we go. On other indications, I'll say every sign around mosliciguat is pointing to an effective, exciting agent with a lot of things we could do with it.

As we watch the field around us, others are showing us good ideas all the time in terms of how these mechanisms might work. We have some of our own that others haven't shown us yet. I think there are absolutely opportunities for indication expansion. Although, I remember we got this question about 40 times when we first unveiled mosliciguat, and our comment then, which is still our comment now, is PH-ILD is an area with a lot of unmet need. Even if it were the only thing we ever did with mosliciguat, it's a big opportunity with a lot of value to deliver to patients. I think there's a lot of different ways to go there.

Thank you.

Thank you. Our next question will come from Yaron Werber with TD Cowen. Your line's open.

Great. Thanks so much, and also congrats on that difficult-to-treat RA study. Question actually about that. Is there any chance you can amend that protocol and essentially run Period 1 and then sort of get new patients completely into Period 2, so you're not going to have that step-down issue? Secondly, based on our analysis, we think that about 75% of patients are ACPA+. Is that still kind of what you think the data shows? Thank you.

Thanks, Yaron. Look, I think on your first question, there's a lot of things you could imagine doing. I think the truth is between this data and detailed patient-level analysis of this data plus the Period 2 data, we're going to have a pretty good sense for what we've got and a pretty good sense for what we need to do going forward. I don't know that we would gain that much from dragging this study out given the quality of the data we're seeing here. I think we're going to do that analysis in detail. I think we're going to have the conversation with FDA, and I think we're going to plot a course forward. I think we'll have a pretty clear sense. Then, look, we've done some commercial analysis of the market in various settings.

There's an updated version of analysis actually in Immunovant's 10-K that was filed today. I think your number is within the range of what we have seen in the literature for ACPA+ patients generally.

Thank you.

Thanks, Yaron.

Our next question comes from Brian Cheng with JPMorgan. Your line's open.

Hey, guys. Thanks for taking our question. In this RA Explore trial, since there's no washout period between Period 1 and 2, I'm curious if you have some thought around the tail of the efficacy from those going from drug to placebo. You said that Period 2 might be less meaningful. Are you saying that 12 weeks may not be enough to fully drive the separation? Thank you.

Yeah, thanks. I appreciate the question, Brian. Just to reiterate, I think, first of all, it's hard to know exactly what the tail will be at the end of dosing at the end of week 16. That's one piece of this. Obviously, Period 2 is blinded, so we don't know now anything about what's in there. That's all sort of a part of that. Look, I'll say the other thing is, and just to reiterate what I said earlier, I think given that the Period 2 primary endpoint is losing an ACR20 response, if you imagine a patient who has achieved an ACR50 or an ACR70 response, even if they start worsening on the first day of Period 2, it just takes some time to give up that level of response.

That's where I'd say the quality of the data in Period 1 is in some ways counting against Period 2, irrespective of the pharmacokinetic effects of withdrawal of the drug. I think remember, every ACR70 responder is an ACR50 responder, is an ACR20 responder. It just takes time to come off that hill. We have people who've achieved a lot of benefit. That's that. Thank you.

Thank you. Our next question will come from Dennis Ding with Jefferies. Your line's open.

Hi. Good morning. Thanks for taking our questions. For PH-ILD, I'm curious what are your thoughts around the phase I-B data and the interpretability of that data in the small number of patients. Specifically, why did the 4 mg cohort outperform so much relative to the 2 mg dose on cGMP, and also cardiac output? I wonder if you should expect a big increase in cardiac output since mosliciguat is locally delivered to the lungs and it's not really a systemic. Thanks so much.

Thanks, Dennis. I appreciate the question. I think the first answer is 4 mg is twice 2 mg, so there's just a lot more drug being delivered. The second point I'll make is, remember, there are 170 patients across the Healthy Volunteers program. While the specific study that you're referring to may have had a smaller patient, we have a large body of evidence at this point across mosliciguat being administered in a lot of different settings. I'd say the dose-dependent improvements in cGMP were broadly consistent across all of that data. The dose-dependent improvements in PVR were broadly consistent across all that data. I think we generally think we know what we've got.

I think with a single dose-

You saw real robust growth and immediately right away in cGMP. I think the thing that was exciting for us is it demonstrated that the inhaled approach was really buffering us from a systemic result, and that was really important for us. I think we'll see that as we go forward. This inhaled approach is so important because you can get the drug to the well-ventilated parts of the lung without worrying about those systemic effects. I think that's the biggest takeaway was we saw cardiac output, we saw mPAP reductions. These are the things you want to see, but these were single-dose studies, so now we'll see them much more robust fashion in our phase II.

Thanks, Drew. Yeah, the other thing I'll say, it just occurred to me as Drew was answering that question is, look, I think one of the things that makes PH-ILD exciting as a commercial opportunity is it really requires inhaled therapy precisely because of this effect.

Yeah.

The competitive landscape will be thinner and the ability to develop drugs for this market will be more challenging because you need to sort of thread the needle on systemic vasodilation. We feel that gives us an advantage as well and frankly increases the level of need for the patients. Look, I think it is all setting up in that way. Thanks, Dennis. Appreciate the question.

Perfect. Thank you.

Thank you. As a reminder, please limit to one question. Our next question comes from Derek Archila with Wells Fargo. Your line's open.

Good morning. This is Jacob on for Derek. Thanks for taking our question and congrats on the 1402 data. Real quick on safety, just want to clarify, confirm there were no LDL changes or other events of interest observed, right? Secondly, given the strong activity in period one, how is this informing your trial design strategy in the future? I know you mentioned that this is likely one of a couple registrational trials, do you think this data changes that?

Thanks, Derek. Great questions both. I'll remind politely for the other analysts we're trying to keep to one given the number in the queue. I appreciate both questions and I'll take both of them. On safety. What I can say here is not just in this study, but across now hundreds of patients dosed across 1402 studies the DMC has been watching that issue and we have seen no impact on albumin or LDL across the hundreds of patients dosed with 1402. While I don't have the very specific data to share for this study numerically, I think the answer is we've seen literally nothing on albumin or LDL from 1402. Look, given the level of activity in Period 1 on trial design, I think the answer is we're going to have to take this data when we get it.

We're going to have to look closely at it and we're going to have to have a conversation with FDA about where we stand and what we need to do. Obviously, the stronger the data from the first study or from this study overall the more compelling that conversation is. That's why I think we're excited about this data. Our belief is that we should be able to run a lean program from here, given the patient population we're focused on, given the level of need in this patient population. That's a conversation we're going to have to have together with FDA in the months to come. Thanks for the question.

Awesome. Thank you.

Cool. Thanks.

Thank you. Our next question comes from Samantha Semenkow with Citi. Your line's open.

Hi, good morning. Thanks for taking the question and congratulations on the data this morning and all the progress. Now that you have this first data in RA for 1402, I'm wondering also how we should be thinking about the CLE data coming up in the second half. Will that readout include the entire 52-week study or will that just be the 12-week randomized portion? What magnitude of treatment effect do you think would be meaningful here? Thanks very much.

On first question. Thank you. Appreciate the questions. On the data, that will just be the 12-week period. That's what we'll have by then. That's what we'll be able to share. In terms of what treatment effect will be meaningful, look, I'll say two things. One is we will have an opportunity to continue to talk about what we expect to see from that study over time, and we'll probably do a little preview of that data before it comes. Secondly, CLE is a little bit different than some of these other indications in that it is commercially more competitive and there's other mechanisms coming. I think the bar for us is not just sort of per se clinical meaningful. I think the bar is do we think our data is good enough to support a program in the face of where the landscape is headed?

We're going to look closely at that data. We're going to look at what we see, and we're going to make a decision based on the totality of the data. I think the bar there is pretty high, and I think we knew that going in. Thanks for the question.

Thank you. Our next question is going to come from Thomas Smith with Leerink Partners. Your line's open.

Hey, guys. Good morning. Congrats on the really stellar RA data here for 1402. Just wanted to ask one if I could, on the pivotal Graves' program. Any updates you can share with respect to patient enrollment? I think you were initially kind of gating some of the scale-up activities and trying to get a sense for how the early enrollment trends were going. Just wondering if there's anything that you could share there in terms of pace, cadence and maybe patients being enrolled, anything differing from initial expectations. Thanks so much.

Thank you. Yeah, it's a great question. Look, I think the short answer is we had a pretty high bar for ourselves when we started the study, and we didn't exactly know because there hadn't been a lot of development in Graves' disease. I think we can now say enrollment's going great. We're on track. We'll have the data in 2027 as we previously discussed and a lot of enthusiasm and a growing amount of enthusiasm as we continue to add sites, as docs continue to get comfortable with the study. I think overall really happy with how that program is evolving. I'll again take the opportunity to say I think all of our main teams at this point are executing at a really high level from a clinical enrollment perspective, and I think that's been a real driver of value for us. Thank you.

Thank you. Our next question is going to come from Alex Thompson with Stifel. Your line's open.

Hi, guys. Congrats on the data. This is Patrick Culliton on for Alex. I guess just building on the path forward here in RA. Looking at Period 2, I guess if your 300 mg performs just as well as 600 mg, how are you guys thinking about your dosing strategy going forward in phase III?

It's fun to sit here and think about what happens if in the phase II study we see as good. First of all, it's a randomized withdrawal study, so I was trying to figure out exactly what it would look like for the 300 mg and 600 mg to perform equivalently. Look, I think overall it's just too early to say. We've got to look at the data. This is a patient population with extremely significant unmet need, and to say without a lot in development is an understatement. I think basically we are plowing a new course with this patient population, so I think we've really got to look at that data and get an outcome from it. I think the inclusion of 300 mg and 600 mg the study was important because FDA, especially in new indications, especially an indication like RA, is likely to want some dose-ranging information.

I think we're going to have some flexibility, and we're going to get to see. Historically, there has been separation in IgG reduction, obviously between 300 mg and 600 mg. We'll see how that translates in this population. I think we got a lot of options here. Thanks for the question. I appreciate it.

Thanks.

Thank you. The next question comes from Prakhar Agrawal with Cantor Fitzgerald. Your line's open.

Hi. Thanks for taking my questions, and congrats on these impressive data. Maybe on the RA front, given the sample size is quite large, but ultimately this trial was open-label and some of the ACR responses can be susceptible to open-label nature of the trial. Maybe just if you can expand if you have any data on some of the secondary endpoints which might be less susceptible to open-label design of the trial, and how much efficacy degradation would you assume as you move from an open label to more of a placebo-controlled trial in a registration trial? Thank you.

Yeah, thanks. Look, it's a great question. It's obviously what was on our mind from the day we first saw the data. I think it is certainly helpful that we're talking about ACR50 and ACR70 responses and just ACR20 responses. I think once you get to that level, sort of spontaneous placebo-style remissions of those kinds are less frequent. We don't have any of the secondaries or additional markers to share. We've been looking at that data hard, and we feel excited about the data based on what we've seen in terms of everything hanging together. That's about all we're able to say at this point because that's about all we know at this point. One other thing is the way the study is designed, the people doing the joint assessments are blinded.

They are doing the assessments without knowing anything about the study, what patients are on, where in the study they are, or whether they're on drug or placebo. That's obviously only one component of the total here, but it is one way for us to get a little bit of objectivity into a study that is otherwise, at this stage, open label, and that is helpful and pretty objective. Thank you.

Thank you. Our next question comes from William Pickering with Bernstein. Your line's open.

Hi. Congrats on the updates, thanks for the question. On mosliciguat, you also have a phase II open label with patients on background treprostinil. What are you hoping to see in that study? How are you thinking about broader evidence generation strategy to support reimbursement of mosliciguat in combination with treprostinil? Thanks.

Yes. I think in the combo study, we have patients on background treprostinil. Obviously, in the main phase II-B, we don't have patients on background treprostinil. The reason we set this up this way is because we know that polypharmacy is going to be a part of the landscape. In the subsequent study that we run, we're likely to have some proportion of patients on background treprostinil as well, and it felt like going into that state study with no experience treating patients on both drugs was, for a variety of pretty obvious reasons, a liability. I think the combo study is in part really a safety study. It's just designed to make sure these things can be administered safely together.

We will learn from it the information that will help us design the stratification rules, help us understand better who's going to be on what in the subsequent study. I think beyond that, it's hard to say at this point, and the combo study's still in pretty early days, so we don't have much to say about it. Drew, anything to add to that?

I think that's exactly the case. We decided not to go on top of inhaled treprostinil in the first PHocus study. We were initially looking at our drug in single agent activity in PH-ILD, and we wanted to have some time to understand that population, understand mosliciguat. Also, as you know, treprostinils do have a sticky issue with cough, and we wanted to make sure that our drug would have a clear path to be able to demonstrate its tolerability profile, which I think has been relatively impressive. With that, in the later days, we decided with the team to go a little deeper and look at mosliciguat on top of inhaled treprostinil, given the confidence we had in mosliciguat after seeing it in our PHocus study, of course, in an aggregated setting.

With that as a backdrop, as Matt said, we're early in the days, but we actually don't expect there to be much of an issue there. We definitely want to understand that from a dosing and safety perspective.

Thanks, Drew.

Thank you. The next question is going to come from Douglas Tsao with H.C. Wainwright. Your line's open.

Hi. Good morning. Thanks for taking the questions and congrats on the data progress. Matt, I'm just curious, in terms of the RA data, if you've had a chance to sort of talk with some of the KOLs, clinicians on the data. I'm just curious what their sort of feedback is on, and if they were more focused on the depth of response than you saw, or the breadth of response. Obviously you've kind of had both, so you don't necessarily have to choose. If there's anything that was striking to them from the initial data set? Thank you.

Thanks, Doug. Look, we have obviously a bunch of KOLs involved with the study. We have those conversations continuously and with some of the important ones for the field who have been on multiple of these studies as well. I think in general, the answer is they're super impressed. I think one KOL told our team roughly as a quote, "You can't fake ACR70s like this." That's the opinion of one physician. I think it's true at some level. Ultimately we'll have to see what the rest of the studies show. Look, I think docs are excited. They're excited about the depth of responses. They're excited about what this could mean. Look, I think the most important thing is these are physicians who, they're treating these patients. They have no options. Many of these patients are very uncomfortable and in a lot of pain.

I think they see a new option for this population, and they were hoping for something that worked even a little. Obviously this is beating that bar handily. I think there's a lot of enthusiasm. Thanks, Doug.

Great. Thank you.

Thank you. Our next question will come from Dina Ramadane with Bank of America Securities. Your line is open.

Good morning. Congrats on the data this morning, and thanks for taking our question. Just a quick one from us. On the non-responders, could you provide maybe some more color on these non-responders in Period 1? Was there anything you can maybe point to, such as prior lines of failed therapy or baseline characteristics such as maybe antibody levels, that were the reason for not responding to 1402? Thank you.

Yeah. We're looking at that in detail now just to try and get some further comfort and understanding about what's going on. I don't have anything to say about it now. That's exactly the kind of analysis that we're running. You said non-responders. Just a reminder, 72% or 73% were ACR20 responders. We're also looking at some of whom got to ACR20 but not ACR50 and just trying to get a better sense of what happened there. Thank you.

Thank you. Our next question will come from Iris Gao with Guggenheim. Your line is open.

Good morning. This is Iris on for Yatin. Thank you for taking my question. Congratulations on the data and happy birthday to Matt's father. My question is also on 1402. Are there any more colors on what proportion of patients were refractory to rituximab and maybe anti-IL-6 in these MOAs are relevant in seropositive patients? Would like your feedback with you. Thank you.

Yeah, thanks. I don't have that in front of me. It's a good question. We have cleaned some of that data. We had a bunch of IL-6 refractory patients. Rituximab, I don't know. Look, overall, we don't have that to share right now, but I think the answer is that the population is consistent with a heavily pretreated population. They've been on multiple lines of therapy. Many of them have failed things in addition to JAK and TNF. All of those different mechanisms are in. We may eventually share more data on sort of what those different subsets look like. I think we're particularly enthusiastic about the JAK and TNF combined failures. Remember that over 10% of these patients had failed more than three lines of these advanced therapies. Thank you.

Thanks, Matt.

Thank you. Our next question will come from Sam Slutsky with LifeSci Capital. Your line's open.

Hi. Good morning. This is Kate on for Sam. I appreciate you taking the question. I know the strength of Period 1 data has made Period 2 all the more challenging, particularly on ACR20. Looking to Period 2, is there a delta versus placebo potentially on other endpoints that would excite you commercially?

I don't think phase II is really about commercial value at this point. I think phase II is about better understanding the characteristics of the patients, seeing erosion of efficacy, starting to understand, to separate out drug effects from other things. I think it's not so much that we're looking for some commercial bar in phase II. I think the quality of this headline data is such that even if it degrades, we're happy with it. I think even in subsequent studies, I don't know that we're shooting for this bar per se. This is just a great foundation from which to build something pretty exciting in RA.

Makes sense. Thank you.

Thank you. That will conclude today's Q&A session. I will now turn the call back over to Matthew Gline for closing remarks.

Great. Look, thank you everybody again. Appreciate it. There were a lot of questions there, I appreciate everyone's forbearance in helping us get through it all and in limiting the number of questions, which is a great favor to the people lower in the queue who need to come up with questions if theirs has already been asked. Thank you again to everybody for playing along with that. An exciting day for us and exciting data to be able to put out. Thank you again to everybody who made that happen, from the Vant and Roivant teams to the patients and investigators. It takes a village, and it's a great outcome and something that we can really build from here. Once again, happy birthday to my dad. Thank you everyone for listening, and we'll talk again soon. Have a great day.

This concludes the conference call. Thank you for participating, and you may now disconnect.

Good day, and thank you for standing by. Welcome to the Roivant Third Quarter 2025 Earnings Conference Call. [Operator Instructions] Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Stephanie Lee. Please go ahead.

Good morning, and thanks for joining today's call to review positive Phase II results for brepocitinib in cutaneous sarcoidosis and Roivant's financial results for the third quarter ended December 31, 2025. I'm Stephanie Lee with Roivant. Presenting today we have Matt Gline, CEO of Roivant; and Ben Zimmer, CEO of Roivant. For those dialing in via conference call, you can find the slides being presented today as well as the press release announcing these updates on our IR website at www.investor.roivant.com. We'll also be providing the current slide numbers as we present to help you follow along. I would like to remind you that we will be making certain forward-looking statements during today's presentation. We strongly encourage you to review the information that we filed with the SEC for more information regarding these forward-looking statements and related risks and uncertainties. And with that, I'll turn it over to Matt.

Thanks, Steph, and thanks, everyone, for dialing in and listening this morning. I'm going to start our presentation on Slide 5. I was sitting and talking to the team it was about a week ago today, looking at a draft of this morning's presentation and thinking that it was going to be a pretty boring 10-Q. We've gotten together in December for the Investor Day. We had -- we've spoken at the JPMorgan conference, and it turned out to have been a really busy week. So we have some great updates, obviously, most notably the Phase II data in brepo in CS, which Ben is going to present on momentarily. But truth is terrific execution and progress across the board for us this quarter. Obviously, that data is a highlight, but we also can announce today that the NDA for brepo in dermatomyositis that the Phase IIb study for 1402 in D2T RA has fully enrolled, that the Phase II study for mosliciguat in PH-ILD has fully enrolled. And obviously, all of the updates that we're known for, including Immunovant offering earlier that gets us now financed to greatest launch, all behind us. So just a terrific quarter and a terrific set of updates even since early January when we last got together. On Slide 6, 2026 is, again, a very busy year for us ahead. Obviously, some major events later in the year, the brepo NIU Phase III, the pivotal readout in the second half. We're now going to be starting this year a Phase III study in brepo in cutaneous sarcoidosis. Ben will talk a little bit more about that. It's early days and getting that going, but that will be this year. The Phase IIb data for mosli is expected firmly in the second half of this year. We now know that because the study is fully enrolled, obviously. Same thing with the D2T RA data where all of that -- both the open-label period and the randomized withdrawal period will be done by the second half of this year. We are also getting proof-of-concept data in 1402 in CLE. And finally, we are still on track for the jury trial against Moderna starting on March 9, so just a few weeks away now. So a really, really busy year ahead for Roivant. And really, if you look at Slide 7, before we get again to the data for CS, just a pipeline we're really proud of that continues to deliver across multiple dimensions with obviously brepo with now 3 indications in pivotal registrational programs, multiple registrational programs for FcRn franchise, many of which we've talked about and mosli with top line data coming in the second half. So really excited about where we are as a business, really excited about the pipeline. I couldn't be more excited for the beginning of 2026 here. Certainly, off to a good start. And with that, what I'm going to do is turn to the Phase II data for brepo in sarcoidosis. So I'm just really briefly on Slide 9 of the presentation, I'm just going to walk through a couple of highlights, but mostly, I'm going to hand it over to Ben to take you through the data in detail. And the short answer, and we keep saying this, it's a tremendous fortunate, I think, to be able to say, that this drug has done everything we could have asked for us -- for it in this -- in this study. We had a significant -- statistically significant. Remember, we had said before the bar for clinical success here, we thought was sort of 5 points of CSAMI was clinically meaningful. We got a placebo-adjusted almost 22 points, 21.6 point delta with a P-value. And again, the study was not powered for efficacy in this endpoint. 100% of patients on berepo 45 on placebo had a 10-point improvement. Again, clinically meaningful was 5 points. 100% of patients on our high dose had at least a 10-point improvement. So just a tremendous outcome across the board. There's some great supportive data on some of the other endpoints as well. And with safety and tolerability completely consistent with what we've seen for the compound in the past. So a really terrific outcome. And in a disease that needs -- where there's never been a positive placebo-controlled study in an industry-sponsored study to our knowledge. So really a terrific day for those patients. So with that, I'm going to hand it over to Ben to walk you through a little bit about cutaneous sarcoidosis as a reminder and then on to the study data as well. Ben, take away.

Great. Thanks so much. Great to be here with everyone. Starting on Slide 10, I just wanted to bring back to what this disease is, walk through this at the Investor Day in December, but cutaneous sarcoidosis is a really debilitating skin disease and among skin diseases stands out for its rapid progression towards permanent scarring and destruction of tissue as well as its disfiguring nature given the particular prevalence on the face and scalp of the disease. Turning to Slide 11. I would note that there is no approved therapies, not only for cutaneous sarcoidosis, but for any form of sarcoidosis. And so as we think about our development program in CS, really a great opportunity for brepo to meet this overall unmet need and become the therapy of choice if we're going to be successful in Phase III as we hope and expect we would be on the basis of this data to really be a promising option for all patients with skin involvement in their sarcoidosis that would include patients both with only skin involvement as well as those with other organ involvement as well. Turning to Slide 12, really just briefly here on the alignment between the pathobiology of the disease and the mechanism. And I think this is important because, as Matt alluded to, and I'll walk through in a bit more detail, we really have great data here that we're very excited about. And I think in a small study, the data is very, very compelling. It's hard to argue on its own, but it also really aligns with what you would expect to see given the mechanism of this drug. Sarcoidosis -- all of the forms of sarcoidosis, including cutaneous disease are driven by the polarization and recruitment of effector T cells and particularly Th1 polarized cells. And brepo really distinctively inhibits Th1-related pathways by hitting both IL-12 through TYK2 and interferon gamma through JAK1. So really an opportunity here mechanistically to see the benefits of JAK1, TYK2 inhibition specifically. And I think that's really part of what's flowing through to our clinical data that I'll walk through now. Slide 13, study design, very straightforward, 31 patients in the United States, randomized 3 to 2 to 2 to brepo 45 milligrams, 15 milligrams and placebo, 16-week study evaluated several different efficacy endpoints that I will walk through. On the baseline demographics and disease activity, Slide 14, I do want to highlight a few things. First, if you look at the duration of disease and background damage of patients, brepo 45 milligrams and placebo, very well balanced between those 2 arms, but 15 milligrams actually quite a bit lighter on duration of disease and damage, which would mean really a higher bar for both brepo 45 and placebo. And then I would also call attention to the plaque predominant morphology, cutaneous sarcoidosis can present through both plaques and papules. In general, the plaques are viewed as more treatment resistant. And you see this plaque predominant morphology, most pronounced and most common in the brepo 45 milligrams arm, followed by 15 milligrams followed by placebo. So sort of punchline of this is there were some imbalances. Those imbalances actually made it harder for brepo 45 milligrams to demonstrate efficacy, both as compared to placebo and as compared to brepo15 milligrams. And in spite of that, as I walk through, we really see exceptional data from the brepo 45-milligram dose arm. So turning to Slide 15 to get into the efficacy results. On the left hand of the slide, you see the mean to CSAMI activity score change from baseline, both doses, statistically significant separation from placebo as early as week 4, the first time point evaluated and then sustained at every visit out to week 16 at the end of the trial. And then on the right here, we see the achievement of investigator global assessment 01 and a 2-point reduction. So as a reminder, this is -- the IGAs are a standard FDA supported endpoint for cutaneous disease. This is similar to the IGAs used in other skin indications with scores from 0 to 4, clear, almost clear, mild, moderate and severe. So to achieve both a 2-point reduction and at 0 or 1 is a very high bar. And notably, it's a high enough bar that 0 placebo patients cleared it. So you may be confused where the placebo line, the placebo line and the x-axis line are the same thing on this chart. And you see here, again, some early progress for both dose arms at week 4, really significant or substantial improvement at week 8 and then static improvement at week 12 and 16. And then here on this higher bar endpoint, you do start to see brepo 15 milligrams begin to -- sorry, brepo 45 milligrams begin to separate some from the 15-milligram dose arm. Slide 16 has the CSAMI responder data. Again, really compelling data. I think this chart on the left, quite remarkable. As Matt alluded to, we were hoping to see a mean improvement of 5 points. And what we saw was not only a mean far in excess of that, but we saw 100% of patients in the brepo 45-milligram arm achieved twice that, twice the minimum clinically important difference. So really every brepo 45-milligram patient a responder in this trial. And as I'll walk through momentarily, that's really corroborated by an independent patient-reported outcome as well. And then you see on the right-hand side of this chart, achievement of a CSAMI less than 5. Notably, this is not an improvement by less than 5. This means that the absolute score by the end of the trial is 5 or less, which is a standard for functional remission. And you see 62% of brepo 45-milligram patients achieving that compared to no placebo patients. So again, this data quite in line with the IGA 2-point improvement to 0, 1 that I walked through before. So again, seeing pretty consistent data here across multiple endpoints. Turning now to the patient-reported outcomes. Slide 17 has the Skindex-16. This is, again, a pretty established standard metric in inflammatory skin disease trials. We see excellent data here with the placebo group worsening, brepo 45 milligrams and 15 milligrams, both improving substantially, well above the minimum clinically important difference. Again, here with brepo 45 milligrams outperforming 15 modestly and both doses really far better than placebo. Slide 18, we have the KSQ skin domain. So this is the King's sarcoidosis questionnaire. It's a PRO for sarcoidosis overall, not just limited to skin disease. What we focused on in our initial TLR was the skin-specific domains. And you see here very in line with the Skindex in terms of the data. So just yet another data point of very compelling evidence of benefit. And finally, on the efficacy side, I alluded to this before, but on Slide 19, we would call it the patient's global impression of change. So this is a single question where patients are asked since they started taking the study medication, how would they describe the overall change in their sarcoidosis symptoms, and they can answer no change or some degree of improvement or some degree of worsening. I think this is a powerful endpoint for simplicity. And notably, 100% of brepo 45-milligram patients reported that they have improved, again, consistent with the CSAMI data where we saw a 100% response rate. So very compelling here. Brepo 15 milligrams also very considerable improvement for most patients, although 2 patients in the brepo 15-milligram group did not -- not only did not report improvement, but actually reported worsening. And then in the placebo group, very little improvement and most patients reported either worsening or no change. Turning to Slide 20, safety data. I think very well, brepo was very well tolerated during the study. We had no SAEs in the study and all adverse events were graded mild or moderate in severity. So against the backdrop of this efficacy data, in particular, certainly, the safety data we see would tee up a potentially very favorable benefit risk profile for brepocitinib for these patients. Obviously, we have over 1,500 patients of data in brepocitinib. And so the overall safety database is characterized by much more than just these results. But certainly here, nothing that would really add anything to what's already known about the drug from that perspective. And I think, again, starting to dose it now in this particular patient population, I think we see the early signs of a very indication-specific compelling benefit risk profile. So just to wrap up very quickly before handing it back to Matt, really compelling evidence of benefit. The effect sizes we see here are extremely large. We see them very consistently across multiple different endpoints, including independent patient-reported and physician-reported assessments, very high response rates, including the 100% response rate for the brepo 45 milligrams arm and a rapid onset of action sustained over time. So really exciting results. We're really excited to move this ahead to Phase III and potentially have the first approved therapy for sarcoidosis. So I look forward to discussing any questions later, and I'll hand it back to Matt.

Thanks, Ben. Yes, look, we're just terrifically excited about this data and about what it means for us and what it means for these patients. On Slide 22, just sort of as a reminder of what the picture for brepocitinib now looks like, people toss around the phrase pipeline and a product for a lot of different products. I feel at this point, looking across the indication set for brepo, even with what we've talked about already with CS, DM and NIU, where we get to a very large addressable patient population, these are patients who in every one of these indications lacks efficacious therapies and is in need of options, and we continue to add legs of the stool or opportunities that grow into these sort of first-in-class orphan inflammatory diseases that are high unmet need in important areas. And I think we've got more to come there. So stay tuned. But just starting to feel like brevcitinib is a really important medicine for us and hopefully for patients. So looking forward to continuing that journey. I'm going to brief through a couple of other highlights or updates across the portfolio, little quick financial updates, and then we'll do Q&A at the end. Super quickly on Slide 24, as a reminder, IMVT-1402 remains a huge focus for us at Immunovant. We think we've got an FcRn with potential best-in-class efficacy with a safety profile that looks favorable even within the class, obviously, convenient administration with a subcu auto-injector and we use the phrase again here, pipeline and product potential, again, with Graves' among our lead indications where we're expecting pivotal data in 2027. We're now, as I mentioned earlier, expecting the D2T RA data later this year, and that study is fully enrolled. We actually enrolled 170 patients in that study, up from the anticipated 120 originally, and that was in part just due to speed of enrollment and the level of enthusiasm from the patient in that community. Moving over to mosli on 25, and we'll definitely spend some time later this year talking more about PH-ILD and mosli and setting the stage for what we expect there. But that study is fully enrolled with thanks to those patients investigators and the Pulmovant team. PH-ILD remains an exciting opportunity for us where targeted delivery gets at a disease where lung is the primary site of disease activity. We think we have a convenient once-daily dosing regimen in a disease where existing therapies mostly have multiple daily inhalations. And there aren't very many existing therapies bluntly. We expect or hope for tolerability benefits. And then as I think you know, we showed really the best ever PVR reductions in the PAH population. And if that translates, we may be able to get some best-in-class efficacy as well. So really excited about what we could do there later this year. I think it will be a really important part of our story in the coming months. And then finally, and as before, I'm not going to spend a ton of time talking about this today because we're so close in here, but the jury trial in the Moderna case is scheduled for March 9. We continue to make progress there and the sort of major update there in the recent weeks is that we got the -- earlier this week, we got the first of the summary judgment decisions, which covered a few things and had some puts and takes generally. But one thing we were quite happy with is the favorable decision on Section 1498, which sets us up for the case that we were sort of "hoping for" in this trial where almost all of the doses that we have asserted are going to be covered in this jury trial. So looking forward to that and obviously, more to come there. Finally, just a really brief financial update on Slide 28. R&D expense of $165 million, adjusted non-GAAP of $147 million for the quarter, G&A of $175 million, adjusted non-GAAP of $71 million for a total non-GAAP net loss of $167 million. Cash remains very strong, $4.5 billion of consolidated cash in the business. So plenty of capital to get us to profitability with dry powder to do other things as well. As a reminder, we still have share buyback authorization and are happy to have that sort of capability. On Slide 30, as discussed, just a really catalyst-rich period ahead of us. A couple of these things checked off now. Obviously, the beginnings of the summary judgment also make progress and just feeling good across the board with a lot more updates to come this year. It should be a big year for us. And a big few years on Slide 31 before I go to Q&A, multiple commercial launches potential in the coming years. Obviously, brepo and DM would be first with that NDA now in, multiple NDA and BLA filings. We continue to have even sort of more future POC study readouts even among the ones we've already announced and now 9 or more pivotal study readouts, including cutaneous sarcoidosis coming over this time line, which is just a really exciting slate for us to build on. So with that, thank you again for listening. I'm going to stop talking and open up the line for Q&A.

[Operator Instructions] Thank you, operator. Our first question comes from the line of Corinne Johnson with Goldman Sachs.

I think you've mentioned today and previously that you'd consider further development expansion opportunities for brepocitinib. And I'm curious how these data kind of inform the direction you'd like to go. Maybe you could also help us kind of size the opportunity set, particularly with respect to like what percentage of the patient population you think are great candidates for this relative to NIU and dermatomyositis.

Yes. Perfect, Corinne. Thanks. It's a great question. Look, I think the first thing is we are absolutely enthusiastic about further development of brepo. We have other indications that Ben and the team are hard at work at. I don't -- I think the -- what I would say the main thing about this data is just that it continues to underscore how strong an agent brepo can be in these patient populations that need it and sort of drives enthusiasm, but I don't know that it reveals anything specific or new other than we're continuing to think about other forms of sarcoidosis, et cetera. CS is another indication where we will be the first and only drug approved if we're successful from here. And then on patient population, look, I think this is right in the sweet spot of what we've been trying to do, not just bluntly for brepo, but across the different drugs we're developing, where we're in this kind of large orphan market. And again, we might do things outside of this category, but it's been a really good space for us and for others with tens of thousands of patients, a big opportunity, high unmet need. And we think it will be the kind of thing that we can attractively launch and that we can make a successful franchise around. So it feels great from an ability to benefit these patients' perspective and from a commercial perspective as well. Ben, anything you'd add there?

I would just add that I think -- and this is something we've felt already, but this data really enforces that of the alignment of TYK2/JAK1 inhibition to T cell polarization, both as we see here, predominantly Th1 driven, but also Th17 driven. And the mechanism of TYK2/JAK1 inhibition really does align to that through IL-12 and interferon gamma for Th1, IL-6, now IL-23 for Th17. And I think that's really one of the mechanistic hypotheses around the distinctive benefits of TYK2, JAK1 inhibition. Others are obviously the type 1 interferon suppression that's very important in dermatomyositis in addition to the T cell polarization. But I would kind of highlight that this data really enforces that NIU has some overlapping mechanism as well, where obviously, we had really strong Phase II data, excited to see that Phase III result. But I think just as we think about not just kind of the unmet need of indications as Matt articulated, but also diseases where TYK2/JAK1 inhibition is going to really be, in our view, potentially better than any other form of immunosuppression. I think this data kind of reinforces some of our hypotheses there.

Our next question comes from the line of Dave Risinger with Leerink Partners.

Let me add my congrats as well, Matt and team. So obviously, the data was phenomenal. I had a couple of questions. First, with respect to the headline CSAMI numbers, they were similar between the 2 arms. The press release obviously mentioned different baseline characteristics. Could you just add a little more color on that? Second, with respect to the FDA time line, obviously, OCTAGAM is approved for dermatomyositis. But is there a chance for the FDA to elect to grant priority review? Could you talk about that a little bit? In DM I'm talking about.

Thanks, Dave. Those are both great questions. On the CSAMI point, I think Ben hit on this well in his presentation as well. Look, I think if you look at the table, I can pull up the slides in a second. But if you look at the table in the presentation on baseline characteristics, I'd say there are some relatively small -- this is a small proof-of-concept study. It's a relatively small in each arm. And so you can see some relatively significant differences on some aspects, including duration of disease as well as morphology of disease with more plaque predominant patients, which are those more recalcitrant patients on our 45 arm than on our 15 arm. And I think that's probably in part what's responsible for the sort of headline numbers looking similar. And you can see that they separate more, again, as Ben hit pretty well in the presentation on the more stringent endpoints like the proportion of patients hitting a 10 or more point CSAMI benefit. So we feel pretty good about that translating into Phase III. And then on the FDA time line, look, I think the answer to that question is DM is a severe disease with not a lot of options. And so there's certainly a chance, but that ultimately is up to FDA.

Our next question comes from the line of Yaron Werber with TD Cowen.

Congrats. Really nice to see this data. I got a couple of questions. One is price. The IVIg is around 180, but the concomitant sort of price for VYVGART for these indications around $870 gross. So maybe help us understand how you're thinking about pricing of brepo. And then secondly, as you -- and I know this might be a little premature, but from Pfizer owns 25% of the JV, you'll obviously consolidate all sales of brepo. How do we handle their 25% ownership? Because you're not going to be paying a dividend, but I imagine you'll have to sort of give them their 25% of the profits. What is that going to hit the P&L?

Yes. Thanks, Yaron. Those are both good questions. Look, I think on price, it's -- we obviously have not decided on a price yet. It's too early to have an answer to that question. What we've said before is taking bookends that are not so different from the ones you quoted there. I think our view is IVIG is probably a little bit more expensive than that in practice those bookends are a reasonable place to think about in terms of the pricing envelope for these indications is what we said before, and I think that continues to stand. I think it gives us a lot of room. So I think stay tuned, but this will be an orphan price drug. And then on the -- what I think is really sort of an accounting math question. So we'll fully consolidate all of the results, losses, sales, everything. And then there'll be a below-the-line minority interest that attributes the portion of Pfizer's earnings. But again, it will be below the net income line. And then in terms of how cash comes out, obviously, if we distribute cash out, Pfizer will get their portion of that cash and we'll get our portion of that cash. The only other comment I'll make there is, and we said this elsewhere, the early portion of the relationship with Pfizer had dilution protection for their ownership stake. That's been exhausted now. And so for any further capital into Priovant, Pfizer will either need to match their portion of our spend or will be diluted and we'll wind up owning more.

Our next question comes from the line of Brian Cheng with JPMorgan.

Congrats on the data here. Two questions from us. As we think about the Phase III, what's your latest thinking about the size and the dose that you have picked? And just curious if you have any thoughts about how we should think about the stability of efficacy going from a Phase II to Phase III for this indication. It seems that you have a pretty large gap going from 22 to the 5-point delta that seems clinically meaningful. How should we think about deterioration? And I have one quick follow-up as a housekeeping question.

Yes. Thanks, Brian. Look, I'm mostly going to hand over to Ben for these questions, but I'll just say it feels like we've got a fair amount of cushion in the quality of this data. And also, a, this was a relatively small study. There aren't a lot of other studies to go on in CS. So we kind of got to take our guidance from here. But it was nice to see a low placebo response. Ben, do you want to talk a little bit about that and about whatever we can share at this point on Phase III design?

Yes, sure. I mean, first, just on erosion, obviously, it would be hard to do any better than this. But I think that the minimum clinically important difference, as we've discussed, is 5 points. Here, we have over 20 points, we could have significant erosion and still have a very compelling data set and a very compelling product profile for patients and physicians. That said, I would also note this is -- it was a U.S.-only study, but 15 sites for the 31 patients. So this was a multicenter, multi-dose placebo-controlled trial, very rigorous for a smaller proof-of-concept study. So while I think that there's always some risk of erosion, in particular, while the very low placebo rate is consistent with natural disease course, you can never be sure of the behavior of placebo in these inflammatory disease trials, particularly when you move to larger global trials. But broadly speaking, I think this data gives us an incredible cushion to still have an effect size in Phase III that maybe is as large or maybe is not quite as large, but still would be extremely compelling. As far as the design of the Phase III in terms of size, I think we would probably be looking at sort of similar size per arms to the DM trial roughly, but we need to kind of take this data into consideration and think more about the powering and have final discussions with FDA on it, including as related to the indication safety set that they would want to see to support approval. So we'll have more to share on that after we engage with FDA. And the same is true on dose. I would say that I think our incoming hypothesis to this trial is that 45 milligrams is based on the totality of the 1,500 patient data, we have a very compelling potential option for these patients balancing benefit and risk. And certainly, I would say, in totality, this data reinforces that. You see really excellent efficacy results from the 45-milligram arm, including on some of these higher bar, more stringent endpoints starting to see real separation with 15 milligrams. And then certainly, in terms of the safety data, nothing that would suggest the overall safety profile of 45 milligrams that we've seen across all of the different indications in which it's been studied, that nothing in this data to suggest there's anything specific to cutaneous sarcoidosis separate from those. So I think broadly speaking, I would say we're very excited about 45 milligrams coming into the study. We're even more excited about it coming out of the study. 50 milligrams also performed very well, and that's great to see. It really just speaks to the overall efficacy potential of the product. And so we'll kind of have a final update on that after we engage with the agency.

Got it. And maybe just one quick one on the housekeeping side. So -- looking at the 10-Q from Immunovant, can you give us a little bit more color on the return for certain rights around batoclimab, [indiscernible] HanAll? Is there any read-through to how we should think about the setup for the TED data readout later this year?

No is the short answer to that question, meaning there's no read-through anything. It's just as we get closer to that data, depending on what we decide to do with batoclimab, we decide to further develop, we'll have to make a decision around how to work together with HanAll on next steps there. So that's really nothing to say.

Our next question comes from the line of Dennis Ding with Jefferies.

This is Anthea on for Dennis. Congratulations on the data. I wanted to ask 2 questions on upcoming catalysts. First on Daubert, can you explain how important Dr. Mitchell's testimony is to the case improving direct infringement and whether or not there's any risk to that being taken out, so to speak, ahead of trial? And then on PH-ILD, thoughts on the competitive landscape and if sotatercept could work in the disease as well?

Thanks. Both good questions. Look, on Genevant, as we said, we really can't talk too much about an ongoing litigation. There are a variety of Daubert motions in front of the court, what they are visible, and the judge will make a decision on all of them and anything within the range as possible. Obviously, we're hoping for favorable best outcomes in each case. On the PH-ILD question, look, I think the answer is, in theory, any drug that improves PVR could work in PH-ILD. Systemic vasodilation has not in and of itself been a great approach in PH-ILD, but sotatercept certainly could work in PH-ILD. Right now, we are slated, I believe, to be the first non-prostacyclin non-treprostinil in PH-ILD. I suspect given the amount of unmet patient need, there will be others behind us, but I think we have a really favorable profile as we enter that space.

Our next question comes from the line of Yasmeen Rahimi with Piper Sandler.

As an Immunovant covering analysts would love to spend time on 1402 and get some color around your near-term RA readout. Obviously, the study is upsized. Help us understand as the study is coming to an end reading out, what you hope to see and how you're sort of preparing for filing and how soon you could actually get ready for that first Phase III registrational study to be shared? And then I'll jump back in the queue.

Thanks. I appreciate the question. Look, I think -- in terms of expectations for RA, I think the short answer to that question is, on the one hand, these are patients with high unmet need. And so in some sense, the bar for efficacy is relatively low compared to what we may be used to seeing in RA. On the other hand, there's just very little precedent data for drugs in late-stage RA with sort of this level of pretreatment. And so it's hard to know. I think we're doing some work on that very question now, and we will share some guidance on what would cause us to run the second study before we put out that data. So I'd say stay tuned for that. Remember, these are burned out patients with pretty tough disease at this point. So obviously, if we're excited about the data, there's a potential for it to be a big product. Obviously, we will engage with the agency once we've got the data and think about what a plan looks like. I think the base case expectation should be that this is one of a couple of studies that we'll have to run just because this is a relatively smaller randomized withdrawal trial. But we'll see the data, and then we'll better answer that question.

Our next question comes from the line of Prakhar Agrawal with Cantor.

Congrats on these amazing results. So maybe on brepo in CS. Just wanted to better understand the market opportunity here. You've talked about 40,000 eligible patients. Would all of these be eligible for brepo therapy and meet the inclusion/exclusion criteria for the trial? And if that's the case, do you think this is a similar size opportunity as dermatomyositis, and maybe just one follow-up on the Phase III design. Would the time point of the endpoint be 16-week similar to your Phase II, given your -- you already have the safety database? Or would you have to test longer? Just trying to figure out if there is any ways to accelerate development here.

Yes. Thanks, Prakhar. Great questions. Look, I think the short answer on market opportunity is this is a patient population that's sick with high unmet need. And assuming our Phase III data looks similar to our Phase II data, I think a lot of these patients are going to be enthusiastic about a better treatment option. It's probably a modestly smaller indication than dermatomyositis just in terms of total end. I mean, obviously, DM is 40,000 patients in treatment, but 70-plus thousand total patients. So I probably think of this as an exciting opportunity, but a little bit smaller than the DM opportunity, although, again, it depends on the Phase III data. And then I think the short answer on Phase III design is let's just wait until we've had the conversation with the FDA before we sort of talk about final outcomes, but we're going to be looking to leverage as much as we can of what we've learned from the Phase II study. And obviously, to the extent that we can match parameters on which we're confident, we'll do that.

Our next question comes from the line of Samantha Semenkow with Citi.

Congrats on this very good safe data. I'm wondering what percentage of patients in the BEACON study had organ involvement, if you have that? And were you able to collect any data that would allow you to assess whether brepocitinib impacted organ-specific manifestations? And then just as a follow-up there, do you see a path to expand into other forms of sarcoidosis with brepocitinib?

Yes, thanks. Look, I'll take the second of those questions, which is certainly it's something we will evaluate in terms of further places to study brepo. And as I said before, we have ideas inside and outside sarcoidosis that are exciting. So stay tuned, and we'll be back with it. On the first question in terms of patients' organ involvement and what we can learn from it. Ben, anything you'd share about that?

Yes. Around 60% of the patients had some pulmonary involvement and around 30%, inclusive of that 60% had some other organ involvement, mostly ocular involvement. We did take some exploratory endpoints related to those in the trial. We haven't analyzed that yet. Ultimately, the study was not designed or set up to evaluate benefit in those other organ systems. So I don't expect us to learn anything too meaningful from that, but it's certainly something we will take a look at. And I think the important point to note is this is a real-world cutaneous sarcoidosis population, given these -- many of these patients do have multiple organs involved.

Our next question comes from the line of Yatin Suneja with Guggenheim.

A quick one for me on brepo on the data that you provided. Like if you look at the curves, they continue to deepen over 16 weeks. So I'm just curious to understand from you, how should we think about further -- do you expect further deepening, further separation? Just talk about if somebody gets treated for a year, how should we think about it? And then if you can just talk about the scope and the size, I don't know if you touched on that already of the Phase III study. Should it be similar to what you did in DM?

Yes. Thanks. I mean just to reiterate on Phase III, and I think Ben shared a thought about that. But I think in general, until we talk to FDA, it's like -- it's hard to commit to a specific study design. So I think like let us get through that, and then we'll be back with a full accounting of the study design. But I think we're prepared to run and enroll a nice sizable study if that's what we need to do. I think we feel good about what we need there. And then in terms of -- look, in terms of continued deepening we're just looking at this data for the first time this week. So I think we're continuing to explore all the various features. I think it's one of the KOLs who was also involved with the study, gave a quote to some journalists. When I think his comment was if the data had been half as good and there have been twice as many side effects, it still would have been a great outcome. Look, obviously, long story short, there are certainly potential ways for this data to be even better with longer therapy with other parameters, but I think the answer is if we can come close to replicating this in a Phase III program, it would be a huge win. So I think we should be offset there.

Our next question comes from the line of Douglas Tsao with H.C. Wainwright.

I guess, Matt, I'm just curious with brepo, how broad are you now thinking about the opportunity, right? I mean I think we've seen great results, obviously, in CS today on DM as well as NIU. There is obviously a lot of data with JAK inhibitors in various indications, but not necessarily full randomized trials or proof of concept. I mean is that the breadth of universe? Or is there other white space that you're also thinking about where JAKs haven't been explored at all, but perhaps it's worth exploration just given the magnitude of effects that you're starting to see?

Sorry, could you just -- yes, how broad we think about the brepo opportunity? Thanks, Doug. Great question. Look, I think the short answer is, I think you can see from our indication selection already that we've been creative and thoughtful in going after indications with high unmet need, including lots of places where JAKs have not been explored. And I think there's a lot of opportunity here. I'll just reiterate something Ben said, and Ben, if you want to do it again as well. I think it's a really good point to hit. Look, I think anywhere that TYK and JAK are both important is a particular area of focus for it because it gets with the uniqueness of our mechanism. And I think we've done a really nice job, again, thanks to Ben and Priovant as well, the Priovant team on exploring that biology. I think we have more ideas in that category. Ben, anything you can sort of add there mechanistically or otherwise?

No. I mean, I think I covered it earlier. I would say that the answer is both. I think there are some indications where there's maybe some IITs or clinical reports from off-label use of other JAK inhibitors where we think TYK2, JAK1 inhibition is really optimally suited for it. And I think those are indications we're evaluating that would obviously be highly derisked. I also think as we -- to your point, as we continue to see more and more excellent data here, I think we're definitely looking into some obviously higher risk, but also exciting potential opportunities where there's less proof of concept, and we would see what we end up with there.

And Matt, if I can, one follow-up. Just obviously, business development has always been such a big part of the Roivant story. But just given the sort of expanding horizons for both brepo as well as IMVT-1402. How are you thinking about capital allocation in terms of external versus sort of just internal R&D investment?

Dollars go to the best opportunity wherever they are is the short answer to that question. Look, we're funded through profitability on our existing portfolio. Obviously, things like running the Phase III program in cutaneous sarcoidosis are no-brainers at this point, and we're definitely going to do it and adding additional indications for brepo or 1402 or for mosli are attractive options because those mechanisms are strong and will work in other places. That said, and I'm sitting across the table from Mayukh right now, the world is full of attractive opportunities, and we look at all of them. So I think we've absolutely got opportunities to deploy sort of externally as well, and it continues to be a core part of what we believe we are good at.

Our next question comes from the line of Derek Archila with Wells Fargo.

Congrats on the data. So just quickly on Immunovant in terms of -- we saw positive data for nipocalimab in systemic lupus. So curious about how you think about the read-through to cutaneous. And then second question, just in terms of commercial synergy between brepo and 1402. Obviously, we're Immunovant covering analyst. So just curious how you think about fielding a sales force in the most cost-effective manner to leverage both brepo and 1402 between the 2 companies.

Yes, thanks. Look, these are both really good questions and important areas for us. On SLE, first of all, I was on record long before the brepo study in SLE saying that anybody who wasn't afraid of a lupus study is, I think the word I used idiot. And so I'll say congrats to J&J on the positive data in SLE. It's always impressive when people are able to deliver those kind of results. It certainly supports the use of FcRns in diseases with a lot of complicated immune activity going on at the same time. There's probably some read-through to CLE in the sense that there's some pathophysiological overlap there. But every lupus study of any kind is its own special flower, and we'll have to be successful in CLE on our own. We like cutaneous lupus in part because we know that derms are pretty good at reading those kinds of endpoints. And so we feel good about that. Again, CLE is a different competitive landscape than SLE, and we're watching that bar as well. On the sort of commercial question, look, the first thing I'll say is even bluntly within a big pharma company these days, the truth is that for de novo launches, mostly you deploy a field apparatus that is specific to the program because you want to engage with those very specific physicians because you want sort of full voice share of your field force on the product. And so I'm not sure I think of like "sales force" as the most important commercial synergy, but we are definitely thinking about things like contracting expansively to make sure that we can get maximal benefit from commercial scale across the portfolio. And there definitely are areas where that is top of mind for us that I think will translate to benefit both for the commercial performance brepo and for the commercial performance of 1402 as those launches progress.

Our next question comes from the line of Ash Verma with UBS.

So for bato, just upcoming the TED results, the data that you're expecting. Just curious how you're thinking about that in the light of recent Vyvgart setback in TED. In your case, how confident are you that a positive Graves' disease readout would translate to success in thyroid eye disease?

Thanks. Look, I appreciate the question. Obviously, TED is out there, and that data is coming when we have both studies in the first half of this year. I don't think there's like a ton of -- a ton to say about that at this point. Those studies are going to happen, and we'll put the data out. Obviously, we know from our own Phase II study in TED as well as from our own Phase II work in Graves' that the drug is active in patients with hyperthyroidism. And I think that should translate in both indications to some degree of efficacy. And we don't think there's a lot of read-through from TED either in argenx' case and argenx obviously also doesn't as well or in our own situation in -- to Graves' disease in the sense that we have -- look, obviously, both -- we have all of our Phase II data in Graves' and the diseases are pretty different. Like the TED study enrolled mostly euthyroid patients. So they're pretty different fundamentally in terms of who was in the studies. So I feel like we are confident in the efficacy or potential efficacy of FcRns in Graves' disease and not particularly focused on what information there is from TED. Obviously, once we get the TED data and can talk about it, there will be information there from patients who happen to be hyperthyroid at various points in that study and how those patients look, and we'll take full advantage of that data in optimizing our Graves program. But beyond that, I'd say not much read-through between the programs and looking forward to getting all that TED data together once we've got it.

Our next question comes from the line of Thomas Smith with Leerink Partners.

Great to see the rapid enrollment and the over enrollment for 1402 in D2T RA, and I appreciate the update on the data timing. I just want to clarify, should we expect that you'll report both the open-label and randomized data from this study together? Or is there potential we could see some of that open-label period 1 data first? And then as a follow-up, we noticed on Slide 31, the expectation for Graves' launch by the end of '28, but not MG, although you're expecting Phase III data for both indications in '27. Just wanted to ask if that's purely a function of data timing there or if there are some other strategic considerations with respect to pricing or competitive landscape?

Thanks. I appreciate both questions. Look, I think -- on the data release timing for the RA study, I don't think we've made a final decision on how exactly we'll put that data out and when. But I think it's reasonably likely now that we know both are coming this year that we'll wait for the randomized withdrawal period before we talk about it. Obviously, that first period is open label, and so we'll get some information from it as we go on. And then I don't think there's much to read into the exclusion from MG in 2028. In fact, there's probably some possibility it actually does, in fact, also launch in 2028. And so I think stay tuned once we get that data, once those studies are -- once we know the exact time line of those studies, we'll be able to provide more guidance on specific launch time lines.

Our next question comes from the line of Alex Thompson with Stifel.

Maybe one on sort of the competitive landscape in Graves. I guess with argenx entering the area and maybe trying to follow their strategy of chasing fast follower indications here, like how confident are you that you can maintain your lead in Graves' if argenx were to run maybe 26-week studies or even 1 instead of 2 studies?

Obviously, the extent of our lead in Graves' -- thank you for the question. The extent of our lead time in Graves' will depend a little bit on argenx' study design and what they decide to do. And until we know what that design is, it's going to be hard to say. Certainly, shorter studies will be faster than longer studies mechanically. I think we have a lead in Graves' that will be significant roughly no matter what design argenx runs. We have great relationships with those KOLs and the doc community. We've been out there. One of our studies is also 26 weeks. As a reminder, the 2503 study is 26 weeks. So look, I think the answer is we will have a significant lead in Graves' disease. How significant that lead is may depend a little bit on what the competition does. But this is also one of those -- whatever going out run the bear situations or whatever. I think mostly our focus is just getting those studies done and out as quickly as we can and getting out into that population, and it's such a large and exciting population that it just doesn't -- it doesn't really matter. The other thing I'll say is, as a reminder, we feel like we showed pretty conclusively in our Phase II data that the deeper IgG suppression that we expect to deliver will matter in this population. And I think especially on remission. And I think that will also be a significant factor in Graves' disease. So looking forward to getting all that data together.

And this concludes the question-and-answer session. I'd now like to turn the call back over to Matthew Gline for closing remarks.

Great. Thank you, operator. Thank you, everybody, for the good questions. Thank you all for listening this morning. I want to once again thank everybody involved in all of this, including particularly with the cutaneous sarcoidosis data, the patients and investigators involved in that program as well as the Priovant team for their execution there, but also everybody at Roivant and all of the investigators on all of our studies. And look, we've got a lot more to come this year. So I'm sure we'll be back together soon, and I'm looking forward to continuing the discussion. Thank you, everybody, and have a great day.

This concludes today's conference. Thank you for your participation. You may now disconnect.