Immunovant Inc Aktie

Good day, and welcome to the Brepocitinib Program Expansion and Batoclimab update. [Operator Instructions] Please note, this call is being recorded. I would now like to turn the call over to Stephanie Lee. Please go ahead.

Good morning, and thanks for joining today's call to review Brepocitinib Program Expansion and an Update on Batoclimab. I'm Stephanie Lee with Roivant.

Presenting today, we have Matt Gline, CEO of Roivant, and Ben Zimmer, CEO of Priovant.

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 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.

Good morning, and thank you, everybody. Thank you, Steph, thanks for dialing in on short notice, as always, with these things. We have 2 agenda items today. We had originally intended to schedule a call right around now, to take you through our new indication of Priovant like [indiscernible], and we're going to do that and excited about that. I think that's going to be a really great addition. And then just because it happened to lineup timing-wise that we just got the Phase III data in tandem batoclimab, we put out a press release on that this morning, and we'll cover it for just a few minutes at the end of the call and take questions on both.

So I'm going to kick it off on Slide 4, starting with LPP. So look, I think it will come as no surprise to any of you that we are, at this point, super excited about what brepocitinib could be and frankly, proceeding with urgency around the idea that it's going to be a large opportunity to expand across multiple indications and to build -- I don't love the phrase pipeline and a product generally. I think it's overused, but a pipeline and a product. We -- so far on Slide 4, look, we've set some criteria for ourselves for the things that we really care about in terms of what indications are going to work well. Starting with the sort of orphan immunology space where we're looking at indications that have, call it, mid-tens to very low hundreds of thousands of patients, with a lot of morbidity and sort of severe disease with a lot of unmet need.

We're also looking for indications where the pathobiology aligns with our specific unique mechanism hitting both JAK1 and TYK2 and ideally, where there's some proof-of-concept data highlighting the potential benefit of either JAK1s or TYK2s or both, and we have something specifically useful on that here.

And finally, we're looking at indications with high unmet need where there's really not much approved right now. So I think everyone is familiar with the sort of first three indications in our portfolio there. Obviously, dermatomyositis, first of them with the PDUFA date in the third quarter, NIU with Phase III top line data coming in the back half of this year and cutaneous sarcoidosis with Phase III study starting in the second half of this year. And I'm pleased to announce that there's another one now lichen planopilaris. We'll talk more about the disease in a moment, where we're beginning an effectively direct to registrational combined Phase IIb/III program. In fact, began, I would say, last month. And so that study is now underway and represents a fourth leg to the stool here, that we are really excited about.

So LPP on Slide 5, and then I'm going to hand it over to Ben to talk a little bit more about the indication and sort of why we're excited about it. Look, this is a severe and deeply unpleasant disease. It's a highly morbid inflammatory scalp disorder. There's nothing approved for it now. And it localized -- it's really -- it's an inflammatory scalp where the inflammation localizes to the permanent part of the hair follicle, which first of all, leads to generally irreversible hair loss, but it's also scarring can be permanently disfiguring and in many cases, is intensely painful, has a lot of itch, burning, redness, scaling. This is a really, really tough disease for these patients. When you see the sort of polypharmacy and some of the other things we'll talk about later in the call, these patients require a lot of medical care and have bad comorbidities.

There are no FDA-approved therapies for LPP, and these patients require chronic aggressive multimodal therapy and are largely poorly responsive to first-line therapy like steroids and ISTs, hence the polypharmacy, hence, the pain management. This is not a well-controlled disease at all. And it's a fairly prevalent disease. It's got sort of a large orphan size. It's -- I'd call it DM-like in population size with probably up to 100,000 U.S. patients and the [ leaders ] are indicating the prevalence and diagnosis is increasing over time. So we think this is just right in the center of the bull's eye for us. It's the kind of disease. You'll hear more about our understanding for why our mechanism is good for it, but the kind of disease with high unmet need and a lot of severity that we think brepocitinib is exactly the right kind of drug for.

So with that, I'm going to hand it over to Ben, starting on Slide 6, just to talk through what the experience of these patients is like and a little bit more about why we're excited about it. Ben, take it away.

Great. Thanks, Matt. So as Matt mentioned, an indication with very high patient burden. A lot of that is the direct symptoms and manifestations of the disease, as Matt walked through. Also on Slide 6, you can see LPP is associated with an increased risk of many severe comorbidities, including both skin cancer and other autoimmune diseases. And as Matt mentioned, no FDA-approved therapies given the severity, a lot of different drugs are attempted off-label, but generally with limited efficacy and high rates of discontinuation based on tolerability and efficacy issues. So really an area of very high unmet need, very high sense of urgency to treat quickly and with efficacious therapies, and we think there's really a significant opportunity for a new efficacious drug.

And turning to Slide 7, we're optimistic that brepocitinib can be that drug. Like cutaneous sarcoidosis, LPP is a disease-driven primarily by Th1-polarized T-cell aberrant behavior. And this is a category of indication where the biology really aligns with TYK2/JAK1 inhibition, interferon gamma and IL-12 are two of the critical cytokine -- signaling cytokines within the Th1 pathway and a JAK1/TYK2 inhibitor is distinctively able to suppress signaling of both of those cytokines. And then I bring up cutaneous sarcoidosis because through that study and other Phase II studies, we've really seen that play-out in the clinic with excellent data from brepocitinib in indications with similar biology. And so mechanistically, we really feel this fits into the sweet spot of where brepo can be a potentially highly efficacious treatment.

In addition to brepo specifically, there's a large number of case reports and investigator-initiated trials of both JAK1 and TYK2 inhibitors that generally establish clinical validation for this mechanism and gives us the excitement around moving quickly and rapidly into a potentially pivotal program.

And turning to Slide 8. One of these is actually in brepocitinib itself. This was a small investigator-initiated trial conducted at Mount Sinai. Unlike many of the other investigator-initiated trials, this one was placebo-controlled. There was only 3 patients in the placebo arm. It was also using the LPPAI, which is a generally noisy instrument that is actually not that preferred by clinicians. And so in our program, we're using different endpoints. So small study really not to be overread into in terms of the specific data. But big picture, you see the brepo treatment arm clearly getting better over time and really overall amidst the totality of other data furthers our confidence around the POC for this drug and moving quickly into a potentially pivotal program.

And before Matt walks through the design of our trial, I would also just note on Slide 9 that although the clinical data with a small study in the LPP AI is, I think, around a somewhat noisy endpoint, they're still persuasive. Actually, what I think is probably most powerful about this study result is the biomarker data, which is on Slide 9, where you see a very clear and convincing effect of brepocitinib on multiple markers of Th1-driven disease activity, including both interferon-gamma and IL-12 themselves as well as other important chemokines that are markers of Th1-driven inflammation like CCL5. So I think all of this together sets the foundation for what we view as a high probability of success study in an indication with very high unmet need, and we're really excited to be moving very quickly into a potentially pivotal program that should hopefully deliver some excellent data.

So with that, I'll hand it back to Matt.

Thanks, Ben. Appreciate it. So on Slide 10, you can see the trial design that we're -- that we've initiated for brepo and LPP. And this is really designed to function like a single straight to registrational trial, except -- and this is sort of the -- there are many benefits to pioneering new clinical development areas. One, cost to pioneering new clinical development areas is there's some work you generally have to do from a regulatory perspective. And so this set up effectively as a sort of combined Phase IIb/III, where we have a 72-patient Phase IIb portion of the study. And then immediately at the end of that, we will just go straight into enrolling patients in effectively the same study into a Phase III pivotal Part 2, where we expect the end to be approximately 270, although we'll do a sample size re-estimation after the Phase IIb. And that will allow us to go through sort of proper endpoint validation and to get the data we need once we ultimately do read out the Phase IIb portion to finalize the regulatory work and read out the Phase III. So this should be -- we're not ready to guide today on enrollment. Obviously, we've gotten a lot of enthusiasm from the investigator and patient communities as we've gotten the program up and running. Ben and the team have been engaging super actively with this population of physicians. We're not ready to guide today on time line, but the plan here is for this to function like straight to registrational program, and we're excited for what that means for time lines and what that means for our opportunity to get a new option to patients quickly. So we're looking forward to playing that through.

Look, on Slide 11, just to summarize, and I think we hit these points all pretty clearly here. First of all, this is a disease with tremendous high unmet need. I'm confident as the investor community does work on it, talks to physicians, talk to patients, you'll see a disease with a high burden and a lot of unmet need. These patients are very uncomfortable. We have a drug that is distinctly suited mechanistically to LPP. LPP has a Th1-dominant immunophenotype. It's really exactly down the fairway of where we've succeeded elsewhere. We think we've got a creative, aggressive development strategy that will get us to market hopefully quite quickly. And we think we've got good synergy from a commercial perspective in the sense, not just in the sort of literal cost perspective, meaning, but we know these docs, we know these centers, we know this community. Priovant has done a phenomenal job and the team of building relationships at tertiary medical derm centers in some of these other indications, and we think we're really going to be able to leverage those relationships. In fact, they were some of the very same relationships that help us sort of key in on LPP as a desired indication to begin with. So really looking forward to that, super appreciative of all the work the Priovant team has done and excited to announce that trial is now up and running. And so I look forward to sharing more updates and answering questions about it today and in the future.

Before we go to Q&A, I just want to turn quickly to the next topic, which is the Phase III study results in TED. So as I'm sure many of you saw Immunovant announced this morning, turn to Slide 13 that our Phase III TED study had failed to meet the primary endpoint for batoclimab. As a reminder, I think everyone is clear on this, batoclimab is the first-generation anti-FcRn antibody at Immunovant. The subject of the vast majority of our future -- all of our future development at this point is IMVT-1402. So this was effectively the last study to read out from the first-generation program. And it was not a focus area for us, for that reason, as we've said in other context. Obviously, disappointing to see the study failed to meet the primary endpoint. Batoclimab had succeeded, as you may remember, in an earlier Phase II study in TED. Ultimately, in the long-mark of our future, I suspect the meaning of TED for us is largely going to be that it was what guided us to Graves' disease and got that program up and running, and we'll talk more about some of the data we generated there. But first, just really quickly on what we saw in the study. So as a reminder, this study was actually designed pretty similarly to our Phase II study in Graves. It had a 12-week period of high-dose batoclimab designed to get IgG as low as any FcRn can take it, followed by a 12-week period of lower dose batoclimab, which suppresses IgG in general, more like what we see in some of the other FcRns currently on the market, and we actually have that number later in the deck in terms of what we saw in that period, at least in a subset of patients. The primary endpoint of the study was 2 millimeter -- greater than 2-millimeter proptosis responder rate, and that's the endpoint that we failed to meet. We measured some secondaries as well. What we said in the press release, and I just want to reiterate here, again, not trying to dress up a failed study. This is not a study that supports sort of further progress in TED. But in terms of things that we were looking for, there were probably two key things we were looking for in this study other than success. One was continued evidence that our deeper IgG suppression matters. And I think there's like a few ways to read that in this study. But I'll say, first of all, consistently across everything we looked at in the study, patients did better in the first 12-week period broadly than in the second 12-week period. Again, it was a relatively noisy study in terms of some of the endpoints, but there's a lot of different data points pointing in that direction. We take a lot of signal from that, including, frankly, the fact that at least one other FcRn inhibitor failed on futility in TED, and we would not have failed on futility. We saw separation in a positive direction, in multiple endpoints, and we'll talk more about that in a second. And then the other thing we were looking for is evidence of read-through to Graves' disease and trying to understand as this -- although it was not a study focused hyperthyroidism, in fact, very hyperthyroid patients were not allowed into the study, there were nonetheless a relatively small proportion, but large in the context of studying hyperthyroid patients with FcRns of hyperthyroid patients. So we wanted to continue to confirm our hypothesis there. And I think we've had some good outcomes there, too.

On Slide 14, there are a lot of different data points we could have shown in terms of like the benefit in the study. And I think anyone who's familiar with TED will look at these numbers and agree. Numerically in the context of treating TED patients, these are not like super exciting proptosis improvements. But we did see meaningful numerical separation from placebo on, for example, change in proptosis at week-12. In fact, when you pull the two studies together, that was sort of nominally significant in a post-hoc statistical analysis. Again, with that $20, you can buy a sandwich. But I think it is evidence that the drug was, in our view, doing something and that we were seeing a benefit for these patients. Probably most importantly, these numbers all got worse, and I don't have that slide in here, but these numbers all got worse as you went from week 12 to week 24. So as you step down FcRn dose and saw lower IgG, the level -- the amount of proptosis improvement degraded, which I think is an important point. And I think also, as we think about this patient population, this was an active TED patient population that has sort of later stage, more advanced TED, the kind of populations that have been studied in other TED programs, by the way, many of which have, I'd say, underperformed recently as I think the disease landscape of TED has changed a little bit. But there is plenty of evidence in this data set, including the slide you're looking at on Slide 14, that suggests that we will improved proptosis and potentially delay proptosis development in Graves patients. And I think that is important to us as we continue to measure all of those things in the ongoing Graves disease program for 1402. And I think the study does broadly support that we should be able to deliver a benefit of that kind in our Graves program.

And then the last thing, which is probably the single most important thing to come out of this data set in terms of readthrough Immunovant prospects here is on Slide 15, which this is -- on the left-hand side, the pooled results across the 2 studies, and they're pooled simply because the ends are small overall of the hyperthyroid patients in the program. Again, the study didn't allow very hyperthyroid patients. But within the boundaries of what we permitted, there were about 20 hyperthyroid patients between the two active treatment arms of the studies. And what you see here is in those two studies as pooled, there was a 75% mean IgG reduction. So batoclimab did consistently what it has done in all of these studies from an IgG supression perspective. And actually, what we saw was an 80% responder rate using the same responder definition, normal T3 or T4, at least T3, T4 below the upper limit of normal with no increase in ATD doses. And again, the same definition we used in the Phase II. And we said 80% responder rate, which was just bang on the same at the end of week 12, as the responder rate we saw in the more severe Graves population in the Phase II study for batoclimab. And one thing that's comforting is this was a very different patient population, a very different study design. Remember, a very different study sort of structure. The Phase II was a single-site study with no placebo, whereas this was a placebo-controlled study with many patients across many different centers and a different hyperthyroid population. So you see that consistent effect, especially at the high dose is helpful. I also think it's notable, as with the Phase II study, we saw a lower responder rate after the 24-week, after the second 12-week period as we reduced IgG suppression. And in fact, nicely, although I can't claim given the end that it's like a perfect correlation, the IgG suppression wound up a little bit lower in that population and the responder rate wound up a little bit correspondingly lower in that population. And I think that just further underscores that in a disease like Graves' disease, the deeper you can get IgG lowered, the better you're going to do with these patients. So I think that is also, again, a helpful outcome from an otherwise disappointing study. So look, again, there was a lot of debate here about how much to say about this given the outcome, which is disappointing for these patients. I want to say, as I'll say again at the end of this, thank you to the investigators, to the patients to the Immunovant team. These studies are hard to run whether they work or not and everyone trusts us with their care. And I'll say, I think the useful scientific evidence that came out of this, on supporting our thesis around treating proptosis via Graves and on deeper IgG suppression mattering and being able to Graves patients will certainly help inform our plans. Notably, we're only sharing a relatively small amount of this data now. I think that we've said consistently is that we think there is important and useful information in this study, that informs how we are managing the Graves study super actively. And so I expect we will share more of this over time. But for now, we're being relatively quiet in terms of the breadth of what we're sharing. Happy to take questions broadly, though.

Look to wrap up for the day before we open it up to Q&A on Slide 16. Our pipeline to me looks better and more mature every time we get on the phone. I'm really excited about the addition of LPP here. Brepo is really shaping up to be a broad franchise opportunity across multiple indications. And I think there are potentially many more lines to add to this graph as we think about where we're working right now and the Priovant team has done an awesome job of executing thus far on clinical programs and excited to see the outcomes from this study and more. I'm really happy with where the FcRn franchise looks. Obviously, IMVT-1402, firmly the drug to beat there and excited about the data coming later this year, both in D2T RA and in CLE and excited for 2027, which is one of the, if not the most important years, at least in Immunovant's history and potentially Roivant between the breath of launch and the Graves' disease data that's coming.

Not to mention, which won't be subject to this call, mostly signal-out with the Phase IIb data in PH-ILD coming in the second half of this year. So a rich catalyst calendar on Slide 17, a bunch of stuff upcoming that we're excited to talk about, just a huge year for us and disappointed about the outcome on TED, but otherwise, just really excited about what we're doing here. So I'm going to stop there. I'm going to open it up for Q&A. Excited to take questions on LPP. Obviously, also happy to take some questions on the TED study as well as I'm sure people have them.

And so with that, I'll turn it over to the operator for Q&A.

[Operator Instructions] Our first question comes from David Risinger with Leerink Partners.

So I have two questions. First, for LPP, Slide 8, I don't know if you have these details, but could you talk about background therapy in the 13 brepo patients and the 3 placebo arm patients and whether that might have impacted the results of that study that was shown on Slide 8?

And then I know that Graves' disease is actually a comorbidity in a meaningful percentage of LPP patients. which obviously is a positive indicator for potential success of your new program given the Graves' disease results that you've previously disclosed. But could you talk about that and any other comorbidities that we should be aware of with respect to LPP? And then actually, I have one more after that, if that's okay.

Thanks, Dave. I appreciate the questions. So the first one for -- the tangible answer to that question is that meds were washed out pre-baseline in that IIT. That said, in general, I want to highlight LPP patients are polypharmacy patients who are on a whole host of background meds. And one of the things the Priovant team has thought very carefully about is management of, call it, polypharmacy background and concomitant meds in the Phase IIb/III program simply because these are very sick patients and poorly managed. There are a ton of comorbidities with LPP. These patients are sick in a variety of ways, including with Graves. As a reminder, the Graves study was obviously on the FcRn side and the study is with brepocitinib JAK1/TYK2. So I think the ability to effectively access and treat Graves patients is probably a useful indicator of a sick patient population. But obviously, in terms of the actual pathobiology, probably not as much direct read-through. But nonetheless, look, I think excited about what we're going to be able to do for these patients. And frankly, look, I think brepo is a great drug for patients with a lot of comorbidities because of the broad anti-inflammatory activity.

David you said, you have one more question?

Yes. Thank you. So obviously disclosed that the subset of hyperthyroid patients in the TED study showed similar response rates of thyroid hormone normalization to those seen in the batoclimab Phase II in Graves. So how did batoclimab performed in thyroid eye disease in that subgroup relative to the rest of the study participants?

Yes. I think the answer to that question is somewhat better in the hyperthyroid population in general. And we saw the most recent cut-off that I looked at in detail was in only one of the studies. So I don't have the full pool data on the top of my head. But in general, the answer is we did better in hyperthyroid patients than in the general population on proptosis.

Our next question comes from Yasmeen Rahimi with Piper Sandler.

This is Liam on for Yas. So I guess just in regard to the TED study, do you think there's an opportunity to transition any of the TED sites to the ongoing Graves pivotal program? And then if you could just provide an update on how enrollment is progressing across those 2 trials as well?

Yes. So first of all, specifically in the Graves program, we're focused on Graves patients, and we've excluded the more moderate and severe TED patients. And many of the sites in the TED study were more Opto-focused sites and sort of TED-focused sites, whereas obviously, we're focused on endos and the sort of Graves III physicians. That said, I'll say also, we are not particularly thirsty for more sites in Graves right now just because enrollment is generally going well. We're reaching as many docs as we can, and we will certainly increase site numbers over time in studies. But in general, I'd say we're happy with how enrollment is going in Graves and seeing a really enthusiastic reaction from the doc community there. Again, we expect both Graves studies to read out next year.

Our next question comes from Sam Slutsky with LifeSci Capital.

This is Kate on for Sam. Yes, we were curious just regarding the TED study, how much of a difference in proptosis response was there in the first 12 weeks versus the final 12 weeks? And I guess, did you see any similar numerically better trends on the secondary endpoints? And I also have a follow-up.

Yes, great. So -- I'm sorry, I didn't quite follow the first question. I think it was -- the difference between first and second -- first 12-week and second 12 weeks. I didn't quite catch if you asked on the primary or on the endpoint that we showed in the deck. The answer in either case is there was degradation in both numbers as between the first 12-weeks and the second 12-weeks. The proptosis responder rates, like I think in one of the -- in the blended across 2 studies, the proptosis responder rates in treatment arm were like low- to mid-20s, maybe low 20 precent, and the placebo arm was sort of high teens. And so there was some degradation, but the numbers are relatively -- the numbers of responders were relatively small. In general, we saw trends supporting better performance in the first 12-weeks and the second 12-weeks. I think the proptosis -- like the proptosis improvement measure that we showed was something like -- I'm trying to do math at the top of my head, which is always dangerous, but like 20% to 30% better at the end of week-12 than at the end of week-24. But did we get the exact number with a better thing. And the answer is yes, it was consistent across both the primary and multiple secondary endpoints that people perform better at week-12 than at week-24.

Okay. Great. And if you don't mind if I squeeze one more in. For the subset of hyperthyroid patients, any anecdotes of how they're doing off treatment and whether they're remaining in thyroid?

It is a great question. I don't have any anecdotes from that population right now, but it's a good question. And honestly, I hadn't thought to ask in the last couple of days, but we'll take a look.

Our next question comes from Brian Cheng with JPMorgan.

Just catching up on your comments around LPP AI being noisy. How should we think about the correlation of the endpoints that you have mentioned on the slide here and also the primary endpoint that you'll be using for the Phase IIb/III? And then I have a follow-up.

It's a great question. IGA-01 is generally just a much higher bar than LPP AI. But Ben, do you want to talk a little bit about endpoints and where we're at?

Yes. The LPP AI, it's a composite endpoint that includes a bunch of different symptoms. Some are physician assessed like erythema and scale and some are patient reported. The biggest problem with the endpoint in addition to just combining all of those, like all composite endpoints can have noise is that there's no definitions in the LPP AI. Each of the symptoms is rated 0 to 3 with no guidance or definition for the raters on what would be a 0, 1, 2 or 3. So generally, just like a highly noisy measurement. What we've done instead is really try to break it up into much more precise measurements. So our IgA measures erythema and scale with clear definitions consistent with the rigor that goes into an FDA supported IgA. And then through different secondary endpoints, we'll be assessing each of the different other burdensome symptoms for patients like pain, itch, et cetera, through, generally speaking, NRS scales. So I think, in our view, a more kind of less noisy and more clinically meaningful to physicians and patients' way to assess benefits.

Great. And maybe just a follow-up on the TED data that you presented today. Can you also give us some color on the proptosis improvement that you saw once you step down to the 340 mg second portion? Particularly was the proptosis impact quick to see deterioration once you pull back on the dose? And how does that proptosis reduction change once the IgG also start to see lowering once you switch to the step-down dosage?

Yes, thanks. Look, I think the answer -- and I don't have the number in front of me. I've seen it in the last couple of days, but the answer is the proptosis improvement that we showed in the deck gets worse at week-24. And I think it's about 20% to 30% worse at the end of week-24 relative to at the end of week-12. So that's about what it looked like, specifically on the improvement. So that's -- yes. And I don't have a time scale of like how quickly it degraded. But in general, IgG falls over a period of a couple of weeks to the lower level. And so I think -- and then proptosis obviously lags further. So I think it takes some time to get worse roughly. Yes.

Our next question comes from William Pickering with Bernstein.

So on LPP, can you just confirm that the primary endpoint for the Phase III portion is IGA-01 responder rate? And kind of what are your expectations for effect size there? And then could you talk about how you're going to be handling background therapies in the study?

Yes. Great question. First of all, I'll just say, and I'll hand it over then to Ben. I think, first of all, the primary of the Phase IIb portion is IGA-01. I think part of the reason the study is designed this way is to make sure that we're aligned with the FDA on the Phase III primary. And so I think our hope and expectation is that there'll be identical endpoints in the Phase III. But obviously, until we've finished the Phase IIb and had a conversation with FDA, we probably don't know 100% for sure. And in terms of background meds as well is just to confirm my understanding there and anything else. Ben, do you want to answer those questions?

The general approach is going to be to wash patients out of background meds ahead of the enrollment quite aggressively, which is consistent with how we've approached a number of other trials like cutaneous sarcoidosis and things should set it up for success. And yes, I think our base case is that the primary endpoint in the Phase III will be the IGA-01 with 2-point reduction. That's obviously generally the gold standard derm endpoint for inflammatory conditions. But as Matt noted, part of the, point of the -- this is an endpoint that's never been actually used before. So part of the value of the Phase II portion is to get a sense of the behavior of the endpoint, including even just on a blinded pooled basis before we read out the Phase IIb just to confirm that thinking ahead of starting the Phase III.

And if I could just squeeze in a follow-up. What do we know about the efficacy of off-label JAK use in this indication?

Yes. I mean, look, I think -- among the things we know about the efficacy of the use of JAKs and drugs like ours, obviously, is what we showed for the [ IIT ] for the use of brepocitinib. There's a lot of case reports as well. I think in general, you'd see across the board, like broad support for mechanisms like these JAK inhibitors, TYK2s and certainly JAK1s and TYK2s combined in improving these patients. I think they're not like -- in my sense, not like super widely used off-label, but they seem to work based on case reports.

Our next question comes from Samantha Semenkow with Citi.

Two for me. Just another on the IGA-01 endpoint. I think, Ben, you mentioned that this was -- this will be the first time you're using this endpoint in LPP. Can you just talk a little bit about some of the powering assumptions in the Phase IIb and what kind of placebo response you're sort of expecting to see or designed maybe around to see?

And then, Matt, you outlined in the start of the call some criteria for assessing indications for brepo. Just wondering what your capacity is for nominating even more indications going forward? And is it reasonable to think that you might stick within the rheum-derm sort of inflammatory space for those additional indications?

I'll take the second question because I can answer on Ben's behalf and put pressure on Ben, which is, look, I think we are almost endlessly enthusiastic for the breadth of opportunity for brepo. I think there's a lot of value to the relationships we've built in the rheum-derm context and frankly, a long list of indications in the rheum-derm context that we like. So I think that you will see us do more there. I also think we are excited about indications that go beyond that context, and you may very well see us go kind of outside of that area as well. And I think we want the Priovant team to succeed in everything it's doing. But certainly, this will be the second additional pivotal study we're starting this year in addition to the cutaneous sarcoid one. So we're looking at now, assuming everything succeeds at least 4 launches over the next couple of years, and I hope we can add to that list.

Ben, do you want to take the question on IGA-01 powering?

Yes. So as a general matter, we've looked at the kind of precedents we've used, if you look at kind of how these instruments work in general, the IgAs, particularly those that are developed in partnership with the FDA and used for registrational programs, the placebo rate in general across them tends to be extremely low. We saw that in our own Phase II sarcoid study recently, particularly requiring not just a 2-point reduction, but 2-point reduction, [ 2.01 ] tends to be a very high bar for placebo. So our general ingoing assumption is that we would hypothesize the placebo rate would not be high, but we'll have to see what the actual results are. We think that on the basis of looking at effective therapies in other inflammatory skin disorders and kind of how the IgAs there have behaved that this Phase IIb portion should be very well-powered to detect the difference. But again, ultimately, to Matt's point in the opening, from a clinical confidence perspective, I think we would have been happy to just go straight into a Phase III program without doing a Phase II piece. But I think that just given we're pioneering a new indication here, part of the point of the Phase II program is really to learn more and inform the Phase III and ultimately, we'll see the results of the Phase II and use that to repower the Phase III if needed, which is what will ultimately be the portion of the study that we rely on to support potential registration.

Our next question comes from Yaron Werber with TD Cowen.

This is Sarah on for Yaron. Just two quick questions from us. So on the brepo study, which of the 7 other successful Phase II studies give you conviction in LPP, mainly on the -- beyond IgA-01, which I know you've just discussed a bunch and maybe on the secondary endpoints? And then just a follow-up beyond that.

Yes. Perfect. Look, obviously, alopecia and CS, which we highlighted in this deck are both sort of very much the same phenotype from an inflammatory perspective, they're both sort of really sort of Th1-driven diseases. I'll say personally, I also just take a lot of comfort from the overall breadth of clinical evidence at this point in inflammatory disease across -- you look at the interferon drivers of LPP, et cetera, like I just think like it's pretty clear, and you can see it in the IIT on the sort of biomarker data. It's pretty clear that we sort of hit a lot of the right biology here. And I think that gives us some comfort. And then there's many of the other indications, significant components of these same inflammatory drivers. And so I think almost all of our studies contribute, probably the ones with skin components most of all, but not uniquely, but alopecia and CS are probably the two most important ones.

Got it. That makes a lot of sense. And then on the TED study, are you also taking forward the 680 mg and 340 mg dosing in the Graves study? And maybe just if you could just provide a little bit more color on what read-through that might have on the trial design for the Graves study?

Got it. And as a reminder, so the equivalent doses of [ 1402 ]. So the TED study we were out here was in batoclimab, which is not the drug we're studying in Graves disease. We're studying 1402 in Graves. The equivalent doses in Graves are 300 milligram and 600 milligram versus 340 milligram 680 milligram. Our Graves programs have both 300 milligram and 600-milligram dosing arms as between the 2 studies, and we're carrying forward both of those. As a reminder, based on our Phase I work, our expectation would be that 300-milligram would have competitor-like suppression of IgG and 600-milligram would have IgG suppression that is similar to what we saw at 680 milligrams in the batoclimab study. And I think all of the data we have is small end, et cetera. But the short answer is that our best expectation is that the Phase III data is heavily informed by what we saw in the Phase II, which is to say the high-dose arm outperforms the low-dose arm and that we see sort of adjusted for differences in endpoints and populations and other things, similar results at the high-dose arm in the Phase III to what we saw here.

As a specific reminder, the longer 52-week 2502 study is 600-milligrams only and then the shorter 2503 study, the 24-week study is 600 milligram versus 300 milligram versus placebo. So that's the difference.

Our next question comes from Thomas Smith with Leerink Partners.

First on the TED results, did you comment on what you observed on the TRAb levels in the study over time and how those compared to the Graves' disease data set? And then can you clarify, were the hyperthyroid patients in this study committed to titrate or ATD dose? And if so, did you have any patients that were able to down titrate or discontinue their ATDs entirely either over the course of the 12-weeks or the 24-weeks? And then I have a quick follow-up, if I could.

Yes. So -- on the TRAb levels question, I guess like the first thing I'd say is like on -- the data was just like unsurprising and matched what you would expect from these studies. So I'd say, yes, that's probably the best thing to say about TRAbs. On ATDs, the answer to your question is no. In fact, they were not permitted to titrate ATD. So these patients were required to stay on a stable ATD dose for the duration of the TED study. So unfortunately, we don't have evidence of clinical practice around ATD titration here. In fact, not only they were -- they effectively weren't permitted to titrate ATD. So we don't even get a look at what they would have done organically with these patients. Now as a reminder, and I think in some ways, the following is comforting and helpful. These were different hyperthyroid patients than in the Phase II Graves study and the criteria required patients to be relatively close to hyperthyroid. And so these patients were less sick hyperthyroid patients than the hyperthyroid patients in the Phase II. And I think the fact that they continue to respond at a similar rate is encouraging in so far as it highlights our ability to treat a pretty broad range of Graves patients at this point.

Got it. That makes sense. And then just one quick follow-up, if I could, on -- looking forward to the D2T RA results later this year. Just wondering if you could provide any updated expectations for that readout? And also any clarity on whether you expect to report both the Part A open-label and the Part-B randomized withdrawal portion simultaneously or if you're thinking that will be more of a staggered approach?

I don't have updated guidance to give on either of those questions right now. We're still working through our analysis of the sort of best criteria to run the Phase III. And so I say that work is happening actively, and we'll share our thoughts on it as soon as we're ready. But we're excited about it, too.

Our next question comes from Dennis Ding with Jefferies.

This is Anthea on for Dennis. We have two. First, the investigator study looked at other scarring alopecia like FSA and CCCA. It seems like there were promising signals there, but curious what your interpretation of that data is and why you chose to go into LPP specifically?

And then second, on LPP specifically, how does disease activity fluctuate over time? And how are you planning to capture brepo's efficacy within 24-weeks? And if there are any sorts of enrichment that you plan to do?

Yes. Thanks. I appreciate both questions. On the first one in terms of breadth of indication, first of all, both across subtype -- other like inflamous-related diseases as well as other potential scarring alopecias. There's lots of interesting data available across different studies, et cetera, that suggest opportunity, including in the IIT, as you mentioned. LPP was pretty clearly to us the initial greatest unmet need and a well-circumscribed orphan population that, among other things, the regulators were excited about as well. So it just felt like a nice clean opportunity all around. But if your question is, are there even more indications in which brepo might work based on the IIT and otherwise? You're never going to get an objection to that question from me. And over time, there's a lot of different things we could study.

LPP tends to have a fairly steady unremitting course. These patients -- look, the disease is ultimately irreversible in a lot of the ways it affects people. And so these patients just get worse. And so there's a high desire to treat quickly, which is something that's sort of interesting about the disease, again, because it's sort of -- it's effectively viewed as an emergency. It's an urgent condition, and it tends to be irreversible.

Our next question comes from Corinne Johnson with Goldman Sachs.

This is Erik on for Corinne Johnson. We have one question regarding TED. So how should we think about the implications this clinical failure has on how physicians and payers think about utilizing 1402 in Graves' given the overlap in this indication and that TED is downstream of Graves' disease?

Yes, it's a good question. Look, I think the easy answer for me to give is, overall, I think there's going to be a lot of excitement for Graves. And I think the data that this study showed on improvement in proptosis as well as the data that this study suggests to me we will show on the same in the Graves study, I think will ultimately be encouraging for the use of these drugs in Graves. And as I think the limitations of using FcRns in TED, mostly stemmed from catching the patients too late at a time where FcRn therapy is simply not sufficient to treat the -- at that point, presentation of the disease. But I think there's plenty of evidence in this data to suggest we're going to be able to benefit proptosis in Graves patients and catch it early. Look, obviously, at some level, if this study had been extraordinary, I would be here telling you how great the read-through was to doc enthusiasm for Graves. And so yes, I think it probably would have been even better if this study had shown better proptosis response rates. But I think in terms of our ability to improve proptosis in Graves patients, overall, I would call the evidence from this study net encouraging. And I think in the fullness of time, docs will see it as such.

Our next question comes from [ Dina Makadi ] with Guggenheim.

So on LPP, you described it as a strategic fit with dermatomyositis given the overlapping prescriber basis. Can you quantify the extent of that overlap between rheumatologists and dermatologists treating DM versus those treating LPP? And how does that inform your commercial infrastructure build-out?

Yes. Great question. Yes. So look, I think the short answer is LPP is mostly treated by derms and especially hair loss and scalp experts. But there's a lot of overlap at the centers. So many of the centers that are sort of big myositis treatment centers are also big centers treating LPP. I'll tell you, and Ben should feel free to add anything to this than he has.

Our focus on commercial build-out right now is succeeding in dermatomyositis and making sure that we have enough breadth and enough coverage and enough relationships to succeed there. I don't think we are changing anything about our DM commercial strategy in anticipation of CS or LPP or anything else. I think in the fullness of time, the relationships that we have at these tertiary centers will definitely be helpful with the subsequent build-outs for the other indications treated at overlapping centers. But we're going to take each of these launches as the opportunity that it is to make sure we invest fully in it. Ben, anything you'd add there?

I'd just add on DM specifically, there's a combination of rheum derms and neuromuscular specialists who all will be potential prescribers, and we're focused on all three of those groups as appropriate. As Matt mentioned, I think there's overlap. Obviously, the clearest overlap is in the derm subset of that DM prescriber base, but also even a lot of the rheums and neuromuscular physicians, not all of them, but many are at tertiary centers of excellence where there's often multidisciplinary myositis clinics and myositis specialists, especially in the rheum derm space, but also involving neuromuscular experts. And so I think there's, in addition to specific prescriber overlap, the overlap in terms of overall institutional engagement and collaboration that is important.

Got it. That's very helpful. And maybe if I may, another question on the -- whats your -- on the LPP, what's the internal bar for success in Phase IIb to progress to Phase III?

Yes. So the short answer to that question is we are going to enroll patients in the Phase III before we read out the Phase IIb. So we're really not viewing this as a -- like run the Phase IIb, get the answer, run the Phase III. We're really [indiscernible] this like a continuous study. And I think the reason for that is, as Ben said, clinically, I think we have plenty of confidence to go directly into a registrational program. We're just making sure we have all the information we need from a regulatory and process perspective as well as to get the right powering assumptions and so on for the Phase III portion of the study.

Our next question comes from Alex Thompson with Stifel.

Appreciate the update. I guess for batoclimab, I think, Matt, you alluded to maybe sharing some more data from the study in the future. I was curious if you could elaborate on to whether we should expect to see more data from MG or CIDP in particular in the future?

And then as a follow-up to that, curious about your thinking on whether MG and CIDP data or even some of this TED data could help support ultimate 1402 filings in the future?

Look, I think never say never in terms of publishing MG or CIDP or other data. I mean we have an interesting treasure trove of things there. That said, like the 1402 MG program, for example, reads out next year. And I think at that point, everyone is going to be much more interested in the ins and outs of that data set than anything about what we saw in the batoclimab study. CIDP, there's a little bit more time between now and when the studies come out, and there might be interesting things to say there. So it's certainly possible. We're obviously principally focused on 1402. I don't think we will need any of the MG or the CIDP data to support the regulatory filings. I think the 1402 data will be sort of sufficient in and of itself. Obviously, the FDA is aware of all these studies, has seen safety data and everything else from these studies. And although I'm not sure the FDA would like publicly declare that they take great comfort in sort of cross-mechanism comparisons of things, obviously, the body of evidence suggesting safety and efficacy for FcRns in those diseases is helpful to us in our interactions with the agency, and I suspect helpful to the agency in making approval decisions. Obviously, the CIDP trial design is different for 1402 than the Phase IIb was. So that's something to take into consideration.

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

I'm just trying to understand the sequencing on the LPP Phase III study. It sounds like this is going to be sort of continuous enrollment from Phase II to Phase III. I guess I'm just trying to understand at what point you are going to validate the data and engage with the agency just in terms of finalization on the primary endpoint?

Yes. After we've read out the Phase IIb when we have the data to share with them is the answer to that question. Probably along the way as well after we read out the Phase IIb.

Okay. And so there will be patients who, I guess, you'll just be insured or just in terms of making sure you're collecting everything that is necessarily needed to input into some kind of composite endpoint if some kind of change or tweak is needed?

Yes. The short answer to that question is, yes. I don't think we are anticipating like major changes to the way the endpoints are structured and things like that. Obviously, there's a fair amount of knowledge about this going in. It's mostly about sort of validating assumptions that we're going in with.

Our next question comes from Dina Ramadane with Bank of America.

First is maybe to clarify an earlier point. Given there's considerable overlap between the TED and Graves populations, and it looks like you guys had a strong responder signal in TED patients with elevated thyroid levels. How do you plan to apply these learnings to your pivotal Graves program? Just curious what your thoughts are on how you're thinking about the inclusion of patients with ocular symptoms and if you think there's still an opportunity in the Graves program to show a benefit on proptosis and maybe a subgroup population?

And then just on the subgroup data you presented in TED patients that were hyperthyroid at baseline, could you provide just some additional color on how this patient population compares to the Phase II Graves in terms of kind of disease characteristics that define severity, maybe baseline T3, T4 levels or length of time uncontrolled or hyperthyroid on ATD?

Yes. These are all great questions. Thank you. Look, I think the first answer is, although this comment may read as glib, the quality of the response in hyperthyroid patients in the TED study mostly just validates our view of where we're at in Graves that this is across multiple sites, a broader population in some ways, like continuing to show like very strong performance in treating hyperthyroidism in these patients. But the Graves -- TED study was designed to exclude severely hyperthyroid patients. And so the reason that only 20 out of the 100-some-odd patients in the overall combined program on drug had sort of hyperthyroidism is because mostly the patients who came in were controlled. Now many of them were controlled on moderate doses of ATDs and things like that. But nonetheless, like these were mostly not hyperthyroid patients at baseline. So I think like from that perspective, they were less sick than the patients in the Phase II study. I think we expect to show benefit in the Graves study on ocular symptoms, and we think it will be incrementally helpful. But it's not obviously the focus of the Graves program. And the Graves program excludes moderate to severe TED patients who've already progressed to more significant ocular symptoms.

And our next question comes from Chi Fong with Bank of America.

I just have a quick follow-up on brepo. So given the integrated trial design and you mentioned parallel enrollment as well earlier in the call, how do you plan to handle the Phase IIb results once you have those on hand? Could you or do you plan to top line or publish the Phase IIb results? Or would the disclosure be more go or no go, or tweak or no tweak? And ultimately, the Phase IIb data would be kept in-house until you have unblinded the Phase III data?

I don't know that we have a super well-formed view on what we'll say publicly about that data. I think our pretty strong expectation -- at some level, the biggest possible version of the impact of that data is like some kind of futility analysis basically, where like, obviously, if we saw something super unexpected, it could cause us to like change our conviction. I think that would be pretty surprising given what we know. And so I think that's sort of the sort of basics, whether we will say something about it once we have it or not, I just -- to be totally honest, I just haven't thought that much about it.

I'm showing no further questions at this time. I'd like to turn the call over to Matt Gline for closing remarks.

Thanks very much. I appreciate it. Thank you, everybody, for dialing-in. Obviously, a lot of good questions on both LPP and on Graves' and TED. I'm sorry if we missed anyone in the queue. Look, I want to say thank you again, first of all, to the Immunovant team, to the patients and the investigators in this TED study. Obviously, always disappointing when a study doesn't work out. I hope one of the things you walk away from this call with is we learned a lot from that study that has been helpful. We learned even more that we haven't shared today because it's competitively valuable and will set us up to win in Graves. So we're excited for all of those learnings. And it's just a herculean effort to get these things across the line. And then excited in advance from the same commitment that we're going to get from the LPP community who are deeply in need of new therapies and really excited about the possibility of something new. I have great confidence in the Priovant team to run a good study there and to take advantage of all the relationships we've built and the work that we've done and excited to just continue to add big bricks in the wall that is the brepo opportunity. So looking forward to having a call similar to this one again in the not-too-distant future to talk more about new indications for brepo, at least on that side of it. Thanks, everybody. Thank you for joining this morning, and we'll talk again soon.

Thank you for your participation. You may now disconnect. Everyone, have a great day.

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.

Good day, and thank you for standing by. Welcome to the Roivant Second Quarter 2025 Earnings Call. Please note that today's conference is being recorded. I will now hand the conference over to your first speaker, Stephanie Lee. You may begin.

Good morning, and thanks for joining today's call to review Roivant's financial results for the second quarter ended September 30, 2025.

I'm Stephanie Lee with Roivant. Presenting today, we have Matt Gline, 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 investor.roivant.com. We'll also be providing the current slide numbers that we present to help you follow along. I'd 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.

Thank you, Steph, and good morning, everybody, and thank you for listening. I appreciate all your dialing in. So not at all a quiet quarter for us and that we put out both the Graves' data and obviously the Phase III data for brepocitinib in DM, sort of a tremendous moment of transformation for the business, but a relatively quiet earnings call as we're looking forward to getting everybody together in December for a more fulsome telling of where we are as a business, more about the future on our Investor Day on December 11. That registration link is live on our website to look forward to see you all there.

Today, we'll be more of a review of what's happened in the recent quarter. And then we'll talk much more about the future when we get together in December. So we're looking forward to that.

I want to start out on Slide 5 just by taking a short victory lap because it's been a pretty wild year for us. Obviously, starting with and probably most notably, the VALOR data for brepocitinib in DM, which hit on all 10 ranked endpoints and just a phenomenal data set that we think is going to transform lives of DM patients. So that NDA filing remains on track plan for the first half of next year, and it will be the first novel oral therapeutic in DM if approved.

We also put out data in this quarter from the durable remission sort of portion of the Graves' disease trial for tomab. which sets us up for the future there in our 1402 grades program. That demonstrated disease-modifying potential for 1402 and then we think earlier this year, we put out some data in MG and CIDP, we did do a pretty nice job of validating the deeper is better idea for FcRns from an gene expression perspective. We also have initiated an Immunovant this year, potentially registrational trials in Graves', myasthenia gravis, CIDP, it true RA and Sjogrens as well as a POC trial in CLE. So some really exciting progress there with IMVT-1402, which we hope will take us to a first-in-class in many cases and best-in-class in we hope all in all indications, potential.

We got a favorable marketing ruling this quarter for Genevant in the Pfizer case and just overall continued progress in the LNP litigation with the jury trial and the Moderna case scheduled for March of 2026. And our capital position remains very strong with $4.4 billion of cash, cash equivalents which will get our current pipeline to profitability and support pipeline expansion and potential additional capital return, including the $500 million that we have currently authorized.

On Slide 6, and we've been showing this slide for a while, but it feels realer and realer with each passing quarter, just a late-stage pipeline that we are really excited about with 11 potentially registration trials and indications with blockbuster potential. Obviously, the first to comment my side is now behind us, but many more to come setting us up for a slide that we've been showing since June on Slide 7, which is just a stacked 36 months ahead of us. between multiple registrational data sets, first EM and NIU and BPO and then the beginning of a long list of them in 1402 lining up for a series of launches, again, first and Bret and the NI and BPO and then very shortly thereafter 1402 across multiple blockbuster indications, including Graves'.

So look, as I said, a moment of real change in transformation for the business. I think we recognize that we're excited to talk more about it when we get together in December. It's something that the team internally is excited about. It's exciting that I hear from investigators certainly and patients and docs in the DM landscape and from investors as well. So moving forward to the next leg of our journey here. I'm going to do just a brief recap of the 2 major data sets from the quarter. So I want to spend a ton of time on either of these because we've talked about all of them in this setting before, but they are rementioning just because of how how exciting both of them are, starting with the repricinibvaor data on Page 9. Again, we've gone through this all before, the our succeeded with really highly significant, robust and consistent data across the primary and all key secondary endpoints with a nice clear dose response that sets us up for 30 milligrams to be the optimal dose here. Responses were rapid, deep, broad, clinically meaningful across the board a statistically meaningful and clinically important delta to placebo on mean tift with deep responses offering quickly and across a range of endpoints, including muscle and skin. And as a reminder, on Slide 10, this is a patient population with a very significant unmet need. And this is a story that has been underscored over and over again as our team has been out talking to physicians in the field after this data, this is a patient population that is significantly underserved by therapeutic options. 75% of these patients are on only either steroids or ISTs and are struggling to get well controlled.

And many of them are requiring high doses of oral prednisone in order to be sort of be treated appropriately and are all looking for options or man, and we're looking for options. Only a relatively small percentage, only 1/4 of the market is currently on other therapies at all. And of the ones that are, some of them are on very demanding IVIG regimens, multiple days a month spent entirely in the infusion centers and others are on a series of off-label therapies, many or most of which have failed VM programs before but are used simply because there are no better options. So we're getting a predictably enthusiastic response from all of the physicians we've engaged with on this data already, and we're obviously looking forward to continuing that as we go through the registration process in the coming year.

Looking at Slide 11, again, a recap from before, but this is the primary endpoint. This is mean test. And this is a textbook picture from my perspective of positive clinical data. statistically significant at the high dose starting at the earliest time point, nice clear separation, nice clear dose response. And 1 thing compared mentioning, and we said this -- we put the data out originally, we had originally been focused on the steroid taper as a risk mitigant in order to make sure we saw a clear benefit from the drug against the background of not really placebo, but actually actively but actually actively manage background therapy. And we did that. But the other thing we were able to show is a real dose response on steroid reduction.

We were able to get a significantly greater portion of patients to lower steroid doses or off steroids on high-dose brepocitinib than on placebo. And I think that actually with the doc community has been enormously resonant in finding, it's something that the docs are really, really focused on getting these patients off high-dose steroids and we are very excited that we were able to show this in the study, including as a part of at least 1 key secondary endpoints. On Slide 12, more than 1/3, and this is the key secondary where we were able to really hit both the TIS improvement -- or the TIS, I should say. And a minimum in steroid but more than 1/3 of REP3 patients were able to get to both major TIS responses and minimal or no steroid burden at week 52. So that's just a really exciting finding across the board.

And more than half of patients were able to achieve the TIS 40 a moderate TIS response with very low dose of oral steroids at the same time. So just a phenomenal outcome there on the combination of endpoints. On Slide 12, again, without going through them all. Just a statistically data set, I'll say, with really low p-values across every secondary we tested benefit -- muscle benefit on skin, benefit on patient-reported outcomes like the happy questionnaire on disability. Just across the board outcomes here. In terms of what's next here, I think everyone is clear, the NDA submission, we're moving as fast as we can. The only erogating item here was drafting and it's ongoing right now. We expect to get a file in the first half, big readout from that proof concept study in CS that we have ongoing will be next year. In the NIU study, which is enrolling very nicely, is currently anticipated to read out. or say, guide into the first half '27 around the same time as potential registration of brepo and launch in DM. And then we submit the sNDA for NIU shortly thereafter with potential further indications and so on to come. So that's brepocitinip. I'm sure we'll get some questions about it. Like I said, we'll talk more about that program and what it could represent commercially on the suffice it to say, a tremendous quarter and something we're really excited to carry forward from here.

Next up, I'll just recap the grade disease remission data that we put out earlier this quarter as well. Starting on Slide 16, but just a reminder, this is a very large patient population with a significant unmet need. And there's been -- I think this is an important point as people are doing the work here, a shift away from ablation over time as patients don't want to go through the surgical procedure or the radioactive iodine, but really a lack of new medical therapies that's left something like 25% to 30% of Graves' disease patients who are relapsed uncontrolled on or intolerant ATD, just a very high proportion of patients who are unable to get well controlled. As a reminder, on Slide 17, this is a bad disease. These patients are at much higher risk of cardiovascular events, much higher risk to preecclampsia you have 4x higher risk of preeclampsia and a 7x higher risk of thyroid cancer than the general population. So these patients are are really set or at a high risk of developing severe comorbidities. They often go on to develop thyroid disease. About 40% of patients go on to develop these i symptoms, some of which get optic neuropathy and other issues that can be pretty significant for vision.

And then there's a bunch of other complications here, 16% are diagnosed with thyroid storm, which has thing with hospitalized as 16% or diagnose thyroid storm, which is a 20% mortality rate, again, potentially sort of very sick patients and again, a relatively high risk of thyroid cancer, including a high risk of progressive thyroid cancer. So disease that makes people quite sick. Again, more to come on the 11th, but I just wanted to highlight that fact. And then on Page 18, in addition being a severe disease, it's a disease affecting a lot of people. And so you've got every year call it, 65,000 newly diagnosed patients, of which 20,000 of those wind up in that sort of refractory bucket and then there's 880,000 diagnosed U.S. patients. So what's 330,000 in the prevalent population are walking around in that intolerant or unable to get well-controlled buckets.

So just a huge patient population with a significant unmet medical need. What we showed earlier this year in the batoclimab study is a pretty interesting result. We showed real disease-modifying benefit in these patients. Of the 25 patients who came in at baseline, as a reminder, the way the study work, patients were treated for 12 weeks at high dose batoclimab followed by another 12 weeks of low dose batoclimab and were then followed for another 24 weeks off drug entirely. And we saw is after that first 12 weeks, 20 out of 25 of those patients were responders to therapy. After dropping to low dose after another 12 weeks, 18 out of 25 of those patients were responders. And truly remarkably, after being off drug for a further 6 months, 17 out of the 21 patients we were able to follow up with we were responders to therapy.

So these are patients who were uncontrolled on standard of care at the beginning of the study and 17 out of the 21 of them that we were able to follow up with remain responders to therapy having good off drug for 6 months. So a pretty remarkable disease-modifying benefit. Of the off-drug responders on Page I'm sorry, the ones on Slide 20. Nearly half of them were fully off ATDs and over 75% of them were on only the lowest doses of ATVs are off ATDs, so not only were we able to deliver a disease-modifying benefit for patients who are uncontrolled on ATDs before, we were able to significantly reduce or eliminate ATD need for those patients.

Now this was underscored on Slide 21, not just by the sort of clinical data on T3, T4 and so on, which is obviously what's most important to the patients. But you could also see it in the TRAP productions on Slide 21. And as you can see, as you expect for FcRn therapy, these patients sort of rapid decline both in general IgG and in TRAB levels, especially on high dose the IgG levels came back a little bit as you expect during the lower dose period. And then what is maybe unique to Graves' disease or at least unusual among FcRn and indications, is while IgG bounces right back when you come off therapy, and the only time points on this graph are ready 24 and week 48. But by week 48, these patients we're effectively back at baseline from IgG.

The vast majority of these patients still had basically sort of reduced their TRABs. And that is a pretty remarkable finding around the durability of the benefit here. On Slide 22, the next period is absolutely stacked for us in 1402 with data coming in a variety of indications, D2T RA and CLE next year. the second part of the D2T RA study as well as Graves and MG in 2027 and then shorten CIDP after One small update, just a flag for today. The TED study remains on track to conclude this year, last patient last visit is very close to today. But we're going to hold off reporting the top line data from that first study in all likelihood until we see the top line data for the second study in the first half of next year, the evolving competitive landscape in TED and especially in Graves' disease has led us to take a more prudent path there. And so we're going to collect that data together and report it when we have it all.

Moving on to the -- briefly to just a reminder of where we are in the LNP litigation, which I know some people are following. In the Moderna case, we are in a pretrial process around the narrowing claims and defenses and around summary judgment, which is happening now, the judge is reviewing some of doesn't briefings in the sort of a calendar on the docket that we're hoping will take us through China in March. The trial is scheduled for March and the first international proceedings are also expected in the first half 2026. The Pfizer case is ongoing in discovery, and there was a favorable market ruling issued in September that certainly sets us up nicely for what we think we need to do from there. So I'll conclude before we go to Q&A with a brief financial update.

Overall, a straightforward quarter from a financial perspective, loss renting operations net of tax of $166 million and cash, cash equivalents of $4.4 billion with no debt on the balance sheet and obviously, a share count reflective of the significant share buybacks we've done over the last 18 months. So a strong position overall that, as I said, is expected to carry us through profitability. We've got more of our financials in here, and the catalyst sort of road map on Slide 28. But again, just a really exciting 6 months or 12 months behind us and a really exciting 12 months or 36 months ahead of us. So feeling great about where the business is, feeling great about it, just the significant transformation in our profile that we've been through in the recent months and looking forward to carrying that forward from here.

Once again, as a reminder, we have an Investor Day in New York City for those that can make it in person on December 11, 2025, that registration link is live. It's in the presentation we put up as well as on our website. I hope to see many of you there to round out the year and talk about the future. So with that, I'll say thank you again for listening again a relatively quiet earnings call, but not at all a quiet quarter. And I will pass it back over to the operator for Q&A. Thank you, everybody.

[Operator Instructions] Our first question coming from the line of Dave Risinger with Leerink Partners. .

Congrats on all the progress, Matt, and looking forward to the event on the 11th. So my question is, could you please comment on what we should be watching next with respect to Pfizer litigation? So specifically, in international in international markets and then in the U.S.

Thanks, Dave. I appreciate the question. And obviously, something that a number of people were watching. It's tough as always to comment on ongoing litigation. I have nothing to say about any potential timing of any kind of international cases. look, it's a busier moment coming up. I think there should be a sort of scheduling process for the Pfizer case underway, and we should learn more about the exact time line, including, hopefully, a trial date in the near future. And I think that's probably what I would be most watching out for in terms of what's public at this point is just getting that schedule together and progressing from here. Great question.

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

Just 2 quick ones from us. How do you feel about Argenx stepping into Graves' and whether that has any impact on your strategy of 1402 and that we have quick follow-up.

Thanks, Brian. It's a great question. And look, I think you heard my comment on the timing of the intended sort of production of the etokimab Ted data. Obviously, we're acutely aware of the competitive landscape in Graves' disease. And look, I think to make a gentle comment. Whatever imitation is the finest form of flattery. I think it's great to see others recognizing the importance of grades as a disease. It's great to see more people working on treatment options for these patients. Obviously, in our Phase II study, we studied both high and low batoclimab and we saw a great benefit to the higher dose batoclimab in the study. And then also we reported in the past data, breaking out the patients between that 70% cutoff below -- above below 70% IgG reduction. And we have 3x as many patients getting off ATDs at the above 70% group and in the below 70% group.

So we think we should have quite a competitive profile there. But most importantly, to be honest, it's a big patient population, there's a lot of sick people. And I think a rising tide there will lift all boats. And like I said, Argenx is a formidable company with a wide following and has done a great job of execution. And I know there's at least some people out there who find it, all those might be frustrating to us, validating of our strategy that they're following in our footsteps. And so we'll always take it.

Great. And just 1 quick one. So on the Investor Day next month, just curious if you can talk about what do you want investors to get out at the Investor Day -- is this more of a broader recap of your current strategy? Or do you think that there will be some unveiling of completely new data or new strategic direction at Roivant?

Yes, look, it wouldn't be a fun Investor Day if I revealed it now. But I think most importantly, this is just -- it's a moment of huge transformation for our business. I think the type of investors who are now along for the eye are different -- and obviously, a lot of other things about the bids are different. So I think we want to make sure we're telling that story fully that we're helping people see the course from a commercial perspective, from a patient need perspective in these indications that they can see at least the reasons why we are so excited about these indications about the certain nature of a blockbuster opportunity there might be some other new things we're able to share by then in terms of updates or other things, but we'll see where we're at in a few weeks here or a month. But I think it will be an exciting opportunity to get together and take stock of the business and to talk a lot about the future and the opportunities in front of us.

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

Just for Graves' when thinking about the remission data -- is there any way to keep out the impact of starting on the high-dose pitoxamab in that study? And how much that actually contributed to the remission rates you saw. Just wondering if there's anything that you could share that you were able to teed out from the data when you analyze it. So if we think about the competitive landscape?

Yes. Look, that's a -- it's a great question. And I don't think we're going to -- I guess I'd be a little bit careful about some of what we say here because of the evolving competitive landscape, and we're going to learn more about this from hyperthyroid TED patients and so on. in that study as well. But look, I think in general, remission is about TRAb getting normal for longer. And our view is that deeper at reductions are going to drive towards exactly that outcome. And so both in terms of the seed of responses that we saw in the BAT trial and the depth of responses that we saw on the bat trial in terms of 2 ad lowering, I think that's going to be a significant driver for us. So I think we feel good at this way about our level of IgG suppression in that program at high dose. That's a great question.

Next question coming from the line of Ron Werber with TD Cohen.

Great. Maybe a quick question -- we've been getting a few questions about the ongoing preliminary summary judgment against Moderna with respect to the U.S. government involvement in the EU -- I'm sorry, EUA and whether the government ever to control of the vaccine for distribution and whether that made them a commercial party and whether that impacts their involvement. And as a result, would potentially provide Moderna some venue to make an argument. Any thoughts about that, if you can comment at all would be great.

Again, as usual, it's difficult to comment in depth about an ongoing litigation and it's ultimately going to be the judge's decision on the 498 question. I'll point out that the -- 2 things that are just like worth keeping in mind. One is the Moderna case in the U.S., Moderna sales of COVID vaccines in the U.S. in total is a bit less than half of Moderna's total global COVID vaccine sales. and Moderna total global COVID vaccine sales are a bit less than half of the total inclusive of Pfizer. And so -- and then what Moderna has claimed in their own briefings is we asked for about $5 billion in damages in the U.S. case and Moderna has claimed a little bit less than half of those damages would be subject to 1498 in Moderna's view. And so I think you're talking about a little bit less than half of a little bit less than half or a little bit less than half of the total is the issue in summary judgment on 1498. Our position is pretty clearly laid out in our motions. And frankly, Moderna's position has also laid out in their motions. Obviously, we feel like we have a strong case to make here but it's hopefully going to be up to the judges to determine. But I just wanted to sort of scope out the magnitude of the question as well.

Next question coming from the line of Prakhar Agrawal with Cantor Fitzgerald.

Congrats on the progress in the quarter. Maybe firstly, on sugar disease. Recently, there has been a lot of excitement around Sjogrens market opportunity, especially with the recent data from Novartis is BAF drug, inelumab. Maybe can contextualize how FcRn differentiate on ESSDAhespecific endpoints? And do you think you could be first in class in this indication? And secondly, just quickly on Breo, do you plan to apply for FDA's national priority voucher for brepo?

Thank you. Those are both great questions. Look, I think on children's, we are also excited about the market opportunity. It's a large patient population with a very significant unmet need. And just a lot of people kind of going through it as it were. There have been a variety of therapeutic classes that have shown some benefit. Obviously, the in-class data was positive, and the J&J data, in particular, showed that lower is better. So we think we have a real shot at best-in-class. We are working to launch as close to first-in-class as possible. I don't think we're here to commit that we'll beat our competitors who obviously got a little bit of a head start on us, but I think we're trying to be kind of within a window small enough such that it shouldn't matter who comes first, and we can differentiate based on our profile.

And I'll just say, I think first of all, I think the Novartis data was positive, but probably less room for even better as I think have all of the Sjogrens data produced today. And I think the FcRn data to date has sort of been competitive with other classes of drugs. And so if our deeper IgG suppression yields a better benefit than other FcRns. I think we should have a truly important opportunity in the space. A lot of excitement about new therapies from KOLs and from our investigators, the unmet need is significant in the overall market is a significant number of patients.

So it's a great place for us to be in our view. And then sorry, you asked about the CMP program for Brepo. We haven't said -- look, this is a orphan population with high unmet need. So I think we're thinking through all of the different ways we can get through FDA and out to patients as quickly as possible and thinking about the puts and takes of them all, but stay tuned.

Our next question coming from the line of Corrine Johnson with Goldman Sachs.

Maybe following up on an earlier question about competitive intensity in Graves' disease. I think it goes beyond Argenx in terms of number of companies that have announced plans there. So how are you thinking about the kind of competitive clinical landscape that's evolving? And what do you expect to inform sequencing decisions in that space over time? And then maybe separately, just on business development. Curious if you could give an update on what you're seeing on that front?

Yes. Thanks, Corinne. Look, I think the first question, and obviously, we see the competitive landscape. Similarly, there's a number of people trying different things which is exciting. It's exciting for gray space is getting to be there. One comment about that is -- or I think we've watched the myasthenia gravis landscape play out, and there's a lot of competitive intensity and a lot of new mechanisms -- and also that FcRn has been, a, a pretty undisputed gaming so far; and b, that the first FcRn to launch for the quality of that data has been a tremendous head start. And we think we've built something similar in Graves' disease, which is a market, obviously, a multiple of the potential size of the MG market -- so we feel great about our position, both from a timing perspective as well as the mechanism. It's a well understood mechanism FcRn. And it's pretty exquisitely well suited to treating the biology of Graves' disease.

So you think about some of the other mechanisms outside of FcRns, I have something in common with ATD, which is that at high doses, they will cause patients to go hypothyroid, which is which is a measurable thing as well. And so I think 1 of the great things about FcRn biology is other than maybe for a very short period of time, because what you're really doing is getting at the root cause of the disease with these other antibodies, you're not going to like cause the thyroid to react in the other direction sort of directly. It's not like a TSHRturbrative mechanism or something like that. And so I think that will be a big benefit to FcRn. The other thing that I think is maybe underappreciated in some communities about FcRns is just how safe and well tolerated they are. And I think in a great patient population, that is going to be an important fact. -- that I think will be great for FcRn as a mechanism. So I think that those will all be sort of good guides towards FcRns being important and early line therapy for these patients who can't manage it with with standard of care today.

In general, as I said, I think lots of activity in the space is actually going to be good for everybody. These are docs who haven't run a lot of clinical trials, these are docs who haven't had a lot of new treatment options. I think the more voices that are out there talking about this stuff, the better we'll be able to get out to the patient population. So thanks, it's a great question. And then you asked for BD update. Look, we remain extremely well capitalized. We remain very excited about the opportunities for pipeline expansion, we are incredibly excited about the things we currently have in our pipeline. And obviously, you heard that in our voice. You see that in the way that we're talking about our data. Obviously, we're thinking about indication expansion for those programs and then always looking in the world for programs, especially programs that are of a size and scale that can move the needle against the backdrop of our existing pipeline. And I think we've got some exciting ideas.

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

We have to, if we May. Number 1 is on Poland. So you guys will a Phase II PH-ILD data in the second half of next year. I guess, how confident are you about the translatability from PAH to PH-ILD how should we think about that update and what's the positive delta on PBR? And secondly, on the LNP litigation, I'm curious if you've done any work on what percentage of the U.S. doses were given to actual federal government employees as we think about a middle scenario for some trust.

Thanks, Dennis. I appreciate it. Both great questions. Thanks for the question about pulling it. We're obviously super excited about mostly. Look, I think you have correctly identified the risk that exists in the mostly data and as we don't have data on the PHLV-patient population, and that's sort of the nature of this study. In general, PVRs have translated well and so I think that's an important backdrop fact between these indications. And where they haven't, it's mostly been, for example, because of the mismatch issues associated with with laser dilation in lung disease patients. And we think the format of mostly addresses that issue. So we are, I'd say, cautiously optimistic about that translation but obviously, I'll feel a lot better when that Phase IIb data is in hand. And my hope is that we see pretty significant PVR reductions and pretty significant clinical benefit in those patients.

So looking forward to that data in the second half of next year. That's another area where there's quite a lot of enthusiasm for the program and for new opportunities, especially with the overall growth from the prostacyclins in PHI leaving plenty of room for additional mechanisms. The the thing I'll point out is just the 38% PG election we saw on pulmonary hypertension, even if PVR-eductions are for some reason a little bit lower in PHLD. Obviously, there's still a lot of room for a very significant amount of assets for these patients.

Your second question, what percent of doses given to federal employees. I don't think our best estimates of that are in any of our motions, but I think you can imagine, as you think about the number of federal employees that it's a relatively small percentage.

Got it. And if I can break 1 more in about the Alpivation. Maybe remind us what's the status in terms of the OUS trials? We're not familiar with the OUS process? So I guess can you remind us on me cases you filed, which 1 is the furthest along? And can you get an initial decision in 2026.

Yes. So thanks. It's a great question. In the case of Moderna, we filed a number of OUS actions, including in the UPC in Europe as well as in Canada and Japan and a couple of other places. Those litigations are all ongoing. There are important hearings in 2026. And nice thing about some of these European jurisdictions is they can move quickly. So it is possible that we would get outcomes of various kinds within 2026 in some of those jurisdictions. And look forward to saying more, there's more to say.

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

Congrats on a great quarter. This is Dominic on for Yasmeen for me. We just had a question going into the TED data. Could you help us understand what you're thinking about with the expectations for the studies that are reading out here soon? And what do you hope to see to consider development considering the competitive landscape?

Yes, thanks. It's a great question. We're looking forward to having that data relatively shortly for sharing it next year. Look, I think the competitive borrow in TED is relatively high with IGF-1R as being pretty efficacious. That said, they certainly leave room from a safety perspective, et cetera. And so I think we're looking to see data that makes sense in the context of the competitive landscape there. The other thing that I think -- and this is part of the reason why we're focused on the sort of competition in Graves' disease. I think we'll learn a lot about hyperthyroid grave patients from this study as well as the possible ways in which Graves' and TED might interact with 1 another. And so I think we're looking forward to the data from that perspective as well. We'll obviously make a final decision on a launch in batoclimab once we've got the TED data in hand and in consultation with our partner. It's a great question.

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

I guess maybe as another follow-up on Grace and TED. -- as you referenced, the 2 diseases are obviously sort of interrelated with interplay I mean I guess when we think about our Gen day will potentially come to market with this are being both Graves' and TED. Obviously, you have a big type star with Fortune O2 in Graves'. So I'm just curious how you're thinking about potentially pursuing tag with 1402 versus as you just noted, potentially thinking about batoclimab and the sort of disadvantage or maybe sort of coming up those 2 markets with 2 different molecules.

Yes. Look, thanks. It's a great question. And a couple of comments about this. One is it's -- we'd be speaking in the abstract now. We're going to know a lot more about the TED data that will inform the answer to this exact question, and we will be in possession of more information than anybody else will have at this moment in time on the sort of overall treatment landscape and on what FcRns can deliver. And so I think that will just up really nicely to think about the possible options they're totally different pull point in terms of the physicians who treat these things. And there are different stages of disease. And so I think they get to different times in different ways. And I think being able to talk to endos who are treating Graves' patients about the benefit in first of all, in TED, for example, is an important potential thing to be able to discuss when we get to it.

In terms of thinking about the sort of TED versus Graves' market dynamics, I'd say let's just wait and see what the TED data looks like and then we can talk more about it. As a reminder, the Graves' population is meaningfully bigger and it's upstream of the TED population. And so I think there's a reason that was our first focus once we got into the clinic with 1402.

Great question. Okay. Great. And Matt, if I can, on a follow-up with Brepo, obviously, incredibly impressive results in. I'm just curious if you have given thought just given sort of somebody alluded to sort of the competitiveness in Sjogrens, have you ever thought of that as an indication because I think there is optimistic for ratna. And obviously, an oral option would be value.

I appreciate the question. Look, I think the short answer is we have thought pretty exhaustively about possible indications for Brepo. We have a number that we think are exciting beyond what we've talked about. I think if you look at the indications we've chosen so far they've been indications where we can really chart a market-defining course, and I think there are maybe more to do in that story. But the short answer is there's an embarrassment of riches in terms of the indication set available for Brepo, and we feel very privileged with the data we have in hand for what we've got. As a reminder, it has worked almost everywhere has been tested and so I think we feel like it's a great molecule and with a lot of great places to go.

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

This is Hal Colin for Derek Archila from Wells Fargo. I guess we have a question on repo. We were at ACR. So very positive feedback from all the KOLs. So question is about really the competitive landscape. I guess we're seeing this card having data next year and CAR-T is also starting their pivotal trials, how do you see the kind of the treatment paradigm evolve over the years? And Brepo, do you have also plans to explore in other subtypes outside is like IMM ASMS.

Yes. Perfect. So look, I think on the deal and competitive landscape, there's a similar comment to, frankly, my comment in Graves', which is that I think it's a great opportunity to be able to get out in front of it. And obviously, first and foremost, 1 of the easiest and oral is always going to have a huge place some, majority of these patients are on oral therapy now. And so I think just like the overall profile that makes us unique. I'll say, the CAR-Ts that's not, in my opinion, going to play for the same patients mostly that we are. That's obviously a much different sort of intervention. And there's still plenty of open questions about benefit there. Look, I think that's all sort of a little bit about that landscape. FcRn could be a compelling option. Obviously, IVIG is used. But I'd say, first of all, it's good to have what we think of as a multiyear head start in DM and we think the patient population that we have access to, given the nature of our therapy is really basically the entire DM patient population, which gives us a lot of room to go.

So we think, again, similar to VivbartenMG, we think we get to define that market and be the heart of it. And so I think that's all great. We also suspect that the data we have in DM specifically, maybe just the best overall, and that's the biggest part of the myositis market. Obviously, Argenx is studying in other subtypes of myositis as well and some of those may be more directly appropriate for an FcRn. As to your question about other subtypes of my sites for us, I'll just say again, we thought about a whole bunch of different places to go. There's a lot of exciting places to go, and we have an impartment of riches in terms of where we can take the molecule from here. Thanks for your question.

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

Just with respect to the TED program and the competitive landscape. Could you comment on some of the data we recently saw from the IL-6 class whether you think Satis approvable with that data set and sort of your expectations for batoclimab relative to those results? And then Secondly, is there any update you could provide from the overseas study that you're running with 1402? And any sort of timing guidance for when we might see data from additional indications from that study? .

Look, obviously, great questions. I'll say, obviously not our place to make comments on the approvability of other mechanisms. There was a notably high placebo response in the ALS study, which is something we've paid attention to. But overall, no specific comments on where that program goes from here. From a competitive landscape perspective, I think -- the competitive intensity in TED is real, as I said earlier. And the IGF-1R are efficacious, although they have safety and tolerability concerns associated with them. And so I think we're sort of focused on where we could play in Ted and then as we said a minute ago, thinking about Graves', thinking about Graves' and opportunity to impact the disease much earlier in its course. And I think that's an important thing the way that we are approaching that with 1402.

On the sort of second overseas study, look, I think we, obviously, at this point, have a number of large registrational programs running in 1402 that are big global studies. We continue to like the option of small, fast POCs overseas and feeding that information into bigger studies. If and when we have anything to share from those ongoing efforts, we'll share it. But mostly, it's being used to inform either indication selection or design decisions of the bigger studies. Thanks for the questions.

And our next question coming from the line of Brendan Fifth with Wolfe Research.

This is Brandon on for Andy. Have you provided any analogs for the DM launch? And I'm curious to know what to expect for the cadence out of the gate in longer term?

Yes. Perfect. Look, I think is an area with high unmet need, but also not a lot of novel therapies recently launched. So first of all, there aren't great analogs to look at specifically in DM. And second of all, I think the appropriate course for any public company is to guide cautiously on launch speed and to say that we're going to do everything we can to get this drug out there. and to get docs excited about. And the thing that we're most confident in is that the overall market opportunity is large that there is high unmet patient need and that when we get to fetpenetration, there's really a really big and exciting opportunity, exactly how long it takes us to get there. I think we're going to say is the answer, and we're going to do everything we can to make it as successful as we can. Obviously, the real value add is the stuff to get the long-term trajectory here, right. So that's probably how I think about the launch.

Next question coming from the line of Sam Slutsky with LifeSci Capital.

This is Gordon for Sam from LifeSci. So just a question on Graves here. Based on all the market research done to date, as you compare the uncontrolled Graves disease opportunity versus what FcRns have shown in the MG market, I guess how do you size these up? How are you thinking about the opportunity? Is it bigger, smaller similar as we think about MG for FcRns? .

I mean, look, it's hard to -- the MG market has been tremendous and -- so I think it's hard to call it 1 way or another. But obviously, there's a lot of uncontrolled graves patients and it's an exciting place to be. And I think we have a real opportunity to build something big. There's just lots and lots and lots of uncontrolled patients is the answer. The other thing I'll say is we'll talk more about the commercial opportunity in Graves' disease on December 11. And I think we're excited with what we see. And I think we can make the -- I think the most important thing is -- there are hundreds of thousands of patients for whom we could make a meaningful difference and a lot of different ways for us to get into that market and establish different toeholds in places. And so we're looking forward to all of that. we're also learning, and I want to highlight this as an important advantage that we have from being first so much about the Graves opportunity by being out there with these docs enrolling patients in the study, looking out at what we're finding. And I think that competitive benefit is going to set us up really well to make sure we've got the right product on the market as well.

There are no further questions at this time. I will now turn the call back over to Mr. Matthew Gline for any closing remarks. Thank you.

Thank you, everybody, for listening this morning. Once again, a phenomenal quarter for us in terms of the results we delivered and super importantly, looking forward to getting together on the 11th to talk about the future and address in further detail some of the very same questions we got on today's call. So I hope to see many of you there. And I hope you all have a great end to your year apart from that. Thanks very much, and have a good day.

This concludes today's conference call. Thank you for your participation, and you may now disconnect. Goodbye.