Good morning, and thank you to those joining us in person on this cold New York morning. An equally warm welcome to those joining us virtually. My name's Keyur Parekh, and I head investor relations for Roivant. Before I hand over to Matt and the rest of the Roivant management team for the more exciting stuff today, just a bit of context to today. This is our first Investor Day since 2022, and we've indeed made tremendous progress on this journey. Matt and the rest of the team will talk about this a lot more in detail, but I'm truly excited about the journey that we are on today, and I do hope that most of you will join us, not just for this Investor Day, but also as a part of our shareholding group for the journey ahead. Lastly, and before I hand over to Matt, a few small housekeeping things for me to flag. One, I would 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've filed with the SEC for more information regarding these forward-looking statements and related risks and uncertainties. As you can see from the agenda for the day, there are going to be several opportunities for Q&A during the course of the day. May I please request that you state your name and affiliation before asking the question, and that you limit yourself to one question at a time so we can get through as many of you as possible? If you could also kindly limit your question to the topic of discussion, that would be very appreciated. We will be taking questions from both people in the room and those joining us virtually. If you're joining us virtually and would like to ask a question, please just type it in your webcast browser, and we will get to it straight away. Several members of the Roivant management team will join us for an informal lunch at the end of today's proceedings, and I do hope that you'll be joining us for that. So with that, let me pass it over to Matt. Thanks, Key. Thank you all for being here. It's great to see everybody. Those that know me well know this is not my most natural setting, so I'm doing my best. And the Rabbi at my Bar Mitzvah told me I set a land speed record, so I'm going to try and speak slow, but I'm not sure I'm going to make it. Look, I'm super excited to be here today for a bunch of reasons. It's been an incredible year for Roivant in terms of what we've done, and I'm excited to talk about where we are, where we're headed, and to lay out what we think is a vision for the business that's as exciting as it's ever been. I'm also excited because, as you know, one of the decisions we've made is that all the IR activities are concentrated in the Roivant management team, and I get to offload a little bit of the work today to some of my colleagues. And so you'll be hearing from a number of folks on the management team, including the CEOs of each of Priovant, Immunovant, and Pulmovant. So looking forward to that also. Cool. So look, what do we want you to walk away from today with? I think there's sort of four main things. One is we are a changed business. We've been a business that we've been proud of this entire time, but our next decade is just going to look different than our last decade. It's going to be simplified. It's going to be focused on development and commercialization of programs that we think are awesome and that at this point have reached the stage where they require a lot of attention in the best possible way. So that's the first thing, is that we're sort of starting off a new decade here, and I think it's an important moment to mark. The second thing is we're executing well. I'm just really proud of where the team is. We've moved forward a number of clinical milestones this morning. I'll hit them in detail, but I think those are all helpful for highlighting the level of clinical execution and focus that we've been bringing to the business. The third thing is we have just huge opportunities in front of us that each of our pipeline programs has multiple indication potential. Each of those indications has multi-blockbuster potential, and we think we can do something really exciting in terms of the scope of the franchise that we can build with that in mind. And the final thing, and obviously we're opportunistic, we will do all kinds of interesting things in the next 12 months and beyond, I'm sure, but we see a very high premium right now on executing on the opportunities we have in hand, and we think they are the kinds of programs that can carry us to extraordinary heights. So look, I think we are a pretty unique place. First of all, and this is important for biotech, we are very well capitalized. We have, as of our last reporting, $4.4 billion in cash and cash equivalents. We're funded into profitability as a business, which is something that very few of our peers can say, and it's something we're proud of. I'll talk more about it in a minute. The second is I think we have a track record at this point that highlights that we're good at science. It's humbling, so it's always a joke on its side, but we're good at developing drugs. We've had 12 + phase III studies. We've generated eight products approved by FDA, or eight approvals. We have three commercial launches coming. We've had over $10 billion in exits against that backdrop, which have enabled us to be this well capitalized, have funded this existing pipeline, and I think we've been good stewards of investor capital. We've repurchased $1.5 billion of stock since going public at $10 a share. We have an additional $500 million authorized. We are laser-focused on generating the kind of value we think we can generate in a shareholder-efficient way. What makes us unique? Look, the left side of this, and we've had some internal debate about whether investors even care, but I do think we have a talent model that is fundamentally different than many of our peers. We have homegrown leadership. You'll hear from a number of people today who are the CEOs and people executing on our big programs, executing well on our big programs who have come up from within Roivant. Roivant is, in many cases, the first place they've worked within the industry, and they've learned how we want to develop drugs. They've partnered with experts who have done this for a long time and have built a sort of unique hybrid DNA that I think is pretty important. We have a dynamic organization. We change things quickly when they need to be changed quickly. That is maybe common for biotech. And then I think we have an entrepreneurial mindset, and we have very carefully worked to align the incentives of the people working on projects with the success of those incentives. You'll hear from Ben. Ben's fate and fortune rests in the success of brepocitinib. You'll hear from Eric. Eric's fate and fortune rests in the success of the FcRn programs. We think we're good at creative product development. Obviously, the indications that we've chosen for Brepo at this point, we are incredibly proud of pioneering a series of different indications for a target that's pretty well understood biologically, but where we found, in our view, a completely new swim lane that is enormously valuable. We'll talk about a number of those opportunities. You know, Graves' disease is an indication. When we started working on Graves' a few years ago, it was a backwater. No one talked about Graves'. Investors that we spoke to were skeptical of the opportunity, but we knew from talking to patients, from understanding the biology that this was a huge patient population with a high unmet need and imitation is the finest form of flattery. There are now a number of other people working on programs in Graves' disease, and we are years ahead. We understand that documenting that patient population better than anybody, and then, you know, with mosliciguat, we took a program that had been studied in lung disease, in pulmonary arterial hypertension, had shown really great promise, and we got it at just the right moment where we could pivot to PH-ILD and be the first non-prostacyclin in PH-ILD. So again, a really exciting opportunity, and then we're laser-focused on execution. This is something that's always been true, but it's something I think we've invested particularly heavily in the last 12-18 months, is making sure that we run clinical programs the way we want to run clinical programs, that we put people in charge of those programs who are going to be relentless and aggressive in figuring out how to enroll them, get good data, get good data quickly. And I think you'll hear from the teams today, and you'll see my enthusiasm for that. And you can see a number of both in the past and in the future execution milestones that we feel really great about. Today, specifically, there's a number of really good updates on that. First, we're pulling forward the guidance on the DM NDA filing. We now expect it by early 2026, so really soon. That is a function of really hard work by the Priovant team. The NIU phase III study is fully enrolled and therefore will generate top-line data in the second half of 2026. That's earlier than it’s about six to eight months earlier than we had originally guided and is due both to incredible enthusiasm and a lot of hard work by the Priovant team. The cutaneous sarcoid study is also fully enrolled and will read out early in the new year in the first half of 2026. That was also previously expected for the back half of the year. Again, a faster-than-expected enrolling trial. Additionally, at Immunovant, the difficult-to-treat rheumatoid arthritis study came in about six months. That data is now expected in full in 2026. So previously, as you may remember, that's a randomized withdrawal study with an open- label run-in period followed by a randomized period. The period one data was expected in 2026, and the randomized data was expected in 2027. That's now all coming in 2026. That is, I think, a sign again of two things. One is enthusiasm in the late-line RA setting for new options, and we'll talk more about that. And the other is just really strong performance by Eric and the new management team at Immunovant and really focusing on getting these trials moving quickly. And I hope it's a sign of more timeline improvements to come there. And then PH-ILD trial is enrolling well, and we're going to get that top-line data in the second half as planned. And that's a pretty confident guidance at this point. Cool. Over the next 36 months, we have a lot to do. We have three plus commercial launches across DM, NIU and Graves. We have four NDA or BLA filings. Add myasthenia and Graves to that list for Immunovant. We have eight pivotal readouts across six indications, at least, and three proof-of-concept study readouts across multiple indications. And again, there will almost certainly be more to come there. This is just in the stuff that we have already announced that we're doing. And then I'm going to talk a little bit about this thematically in a second, but our commercial opportunity here is focused in the kinds of things that biotech companies have been good at lately. These are tractable, high-value indications, which fit sort of in this, in our view, very sort of useful, important sweet spot between the ultra-orphan stuff that's maybe a little bit smaller than we're focused on, and then the stuff like, bluntly, the biggest indications in cardiometabolic disease, where we're certainly excited about them, but we think it'd be much harder for us to succeed. These are indications that we feel in every case we are able to execute on successfully. Okay, a couple other things from a framing perspective, and then we'll get to the substance of the day. First of all, we're just proud of our capital efficiency. And I think there's very few companies that can actually make all three of the following claims at once. We have net returned cash to shareholders since going public. We have increased our cash balance meaningfully since going public, and we've doubled our share price since going public. And I think the combination of capital efficiency, again, it's something that we're all supposed to do and think about every day. And I can't promise that every period is going to look like this one, but it's something that we're very proud of in terms of being a part of our DNA. Okay, so a couple of thematic points, and then we'll get to the programs themselves. First of all, we are at a unique time in biotech. There was sort of a drought for a period in terms of graduates from biotech into biopharma. And actually, if you look historically, there are some great examples in the distant past before 2000 with the creation of modern biotech. In the early 2000s, there were a few really important people who entered that graduating class. You can see some of those logos here. Since then, in some ways, there's been a little bit of a gap. The market turned more to M&A. There were some structural factors that made it harder. One of the things that we are incredibly pleased about is that we get to now follow in the footsteps of a new class of graduates that have clearly made this jump. You look at the Insmeds and the argenxes and the Alnylams of the world. They have successfully commercialized programs that rhyme with ours. These are, we've got some stats on here, but we've gone from a sort of short the launch private public market environment where launch stocks were meaningfully underperforming to a public market environment where launch stocks are overperforming. And we think we have a lot of opportunity there. That breaks out into a couple of categories. It's probably less true in the last few months, but there was a period where M&A had backed off a little bit, and that opened up the possibility that, frankly, companies just made it longer and got to see their own success better. This says the rapid rise and influence of China biopharma. Really, there's just been a commoditization of certain discovery stage activities that make access to programs different for big pharma, different for us. And I think our creative development is now at a premium, and it's something we feel like positions us well. The capital markets are fickle. They're good right now, but that's been an up and down. And then there's just been sector themes from a macro perspective. There's been obviously changes from a government perspective, changes from a regulatory perspective, and we're watching all of that, and we think our portfolio, where it is from a stage perspective, sets us up pretty well to weather that storm. You know, we think commercial launches like the ones in our near-term future have been successful for a variety of specific reasons. They've obviously generated meaningful shareholder value, but they've also been the kind of launches that have outperformed everyone's expectations for them. They represent new therapeutic options, as our programs do, with good diagnostics. They represent significant need. There's been rapid adoption. There's sort of a handful of common themes in that recent graduating class: drugs that serve high unmet medical need, opportunities with tractable commercial execution, focused prescriber bases, prevalence in the, call it, tens of thousands or maybe low hundreds of thousands, not millions of patients, where biotech company can really make it work. Often diseases treated at specialty centers and by specialty physicians, companies building specialty dedicated patient access support and organizations, and frankly, programs with limited competition at launch, and I think you'll find that our commercial opportunities manage to hit basically all of these boxes across the board, and you'll hear about that from the leaders of each vent as we talk about these programs, so our pipeline is familiar at this point. I don't need to say very much about it, but we're incredibly proud of our latest stage drugs here. We think we have a pretty unique portfolio that fits together, hangs coherently, and has the potential to underwrite a new graduate, if you will, from this biopharma class. So I'm going to move on now to talk about Brepo. I'm going to introduce the section. I'm then going to hand it over to Ben Zimmer, the CEO of Priovant, to take you through those programs in detail. And I'm really excited. Ben has been at Roivant for a long time. He first worked on clinical development under Larry Friedhoff, who's actually sitting right there, one of the first developers at Roivant, and has since done a whole bunch of things, culminating in now the success of the brepocitinib program and DM. And I'm excited for you all to hear directly from him. I just want to talk a little bit about brepo first, though. Brepo is a bear of a drug. It's an amazing drug for us. It is a unique mechanism with dual inhibitor of JAK1 and dual inhibition of JAK1 and TYK2. We'll talk about that more in a second. We're focused on indications that benefit from both of those levels of activity. We have some great indications. The NIU treatment paradigm is clearly wide open for new opportunities with uptake across different market segments. That data is now, as I said, coming in the second half of this coming year, so pretty soon. There are no approved therapies in cutaneous sarcoidosis, an area that's been difficult for drug development and where we think the choice specifically of cutaneous sarcoidosis is going to benefit our drug and has some nice homology, as Ben will discuss, with uveitis, among other things. Then our DM data, I couldn't be more proud of this data, but our DM data gives us an opportunity to redefine a standard of care for DM patients where the current paradigm leaves patients poorly controlled, dissatisfied, and frankly, uncomfortable and sick with a very high steroid burden. So that NDA filing is expected by early 2026, and we are actively preparing for a commercial launch. Ben will talk a little bit about some of those details as a reminder that I think relatively few people in this room probably need. So the JAK -STAT signaling pathway is involved in signaling a whole bunch of cytokines in the inflammatory systems. There are four human JAK isoforms: JAK1, JAK2, JAK3, and TYK2. And both individually and really pairwise, they signal different cytokines. And so we're focusing on diseases that match the cytokines covered by the signature of our specific drug. JAK1 and JAK2 give us a lot of flexibility and area to run. From the JAK1 side, specifically, we get interferon gamma and IL-31. We get IL-2 and IL-21. We get strong inhibition of IL-6. From both JAK1 and TYK2, we get interferon alpha and beta, IL-10 and IL-22. And the interferons in particular are relevant to a lot of the diseases we're studying. And then from JAK2 and TYK2, from the TYK2 side alone, therefore we get IL-12 and IL-23, which is also an important channel that many of you are very familiar with. So we get pretty broad activity against an important group of targeted cytokines. We are focused at indications that are at the intersection of our capabilities here: mid-high, tens of thousands of prevalence, both either JAK1 or TYK2, clinical proof of concept of some kind is important to us, high unmet need with few approved therapies, and they're biologically suited for dual inhibition. Obviously, our current indications, DM, NIU and cutaneous sarcoidosis, more to come, and we're actively working up some additional late-stage programs. The other thing I'll say, which is easier for me to say because I'm the one on the stage, is just to highlight the Priovant team here has done an incredible job, and the successful execution there has set us up for success. The positive readout sets us up for the NDA filing. The enrollment of the CLARITY program sets us up for the fast-track line data. By the way, we significantly over-enrolled that study. We have 370 patients in that study, and it's still enrolled well ahead of schedule. That data is now coming in the second half of next year, and then the enrollment's completed in the proof of concept study for cutaneous sarcoid as well, so with that, I'm going to invite Ben up on the stage. Thank you so much for doing this, Ben. I'm excited for you all to hear directly from him, and he's going to take you through each indication in turn, and then we'll do some Q&A after. Thanks, Ben. Great, thanks. Great to see everyone and to be with everyone online as well. With brepo over the last few months, we've obviously had a lot of focus on DM and the DM data, and I'm going to talk more about that a bit later. But I actually wanted to start with some of our other indications. We've made great progress, as Matt mentioned, over the last few months on both our NIU and cutaneous sarcoidosis trials. That data from both of those programs now is coming out next year. I imagine for many of you, that's not been necessarily a primary focus. And so I just wanted to start by going through those two indications, providing a bit of background on the diseases, our studies, looking ahead to the readout. So starting with NIU, this is an ocular inflammation. It occurs in many cases idiopathically, but also it frequently occurs in combination with a variety of different other autoimmune diseases. Across all of these etiologies, the pathobiology though is consistent in terms of T-cell infiltration into the eye, and there's multiple different anatomical regions within the eye impacted by NIU as well. The most common is to be only in the anterior chamber of the eye, and that's generally treatable by local therapy, but in many cases, patients also will have intermediate or posterior involvement or panuveitis, which can include anterior inflammation, and that almost always requires some form of systemic therapy. You'll notice the prevalence numbers here have a pretty wide range, and that reflects different data sources. The academic literature, there's not that much academic literature on prevalence. Most of it's around 10 years old -1 5 years old. That comes into the lower ends of these ranges here with intermediate posterior panuveitis being in the high tens of thousands of patients. But we've actually been doing our own claims analysis looking at more recent data, and that shows significant growth over the past decade. Now looking at potentially just under 200,000 patients who have some involvement beyond anterior inflammation. I would again, just since this may be a newer indication to many of you, note also that another feature with the claims data is that many patients may sometimes initially be diagnosed with anterior NIU, but then go on to be determined to actually have panuveitis. We see sometimes patients who may initially have an anterior NIU diagnosis who ultimately go on to get systemic therapy. The unmet need here is very high, as you can think about with ocular inflammation and vision. In a lot of autoimmune diseases, physicians and patients will sometimes have tolerance for low levels of inflammation, and it's really only moderate to severe disease that draws a sense of urgency and moving aggressively to advanced therapeutics. In NIU, that's not the case. Even small amounts of inflammation, if not controlled, can lead to significant vision loss, and over time, if not adequately treated, can actually lead to blindness. NIU is one of the leading causes of blindness in the United States among the working-age population, so really a quite devastating disease. As you can see on the left hand of the slide here, that vision loss really can be driven by inflammation in all of the different segments of the eye, again, speaking to the importance when you move beyond just anterior inflammation of systemic therapy. I also think as we think about this indication and think about potentially in the future having an approved oral therapy, I think the kind of market and prescription environment here is going to be different than thinking about an indication like AMD or a lot of other ophthalmic indications. I think starting with the left-hand side of the slide, there is in the United States and globally a small group of uveitis specialists who are ophthalmologists, but are really pretty distinct profiles from your typical ophthalmologist. Many are double board certified in internal medicine. Even those who are not will do at a minimum one year, often multi-year fellowship focused on just treating these patients. That obviously involves a lot of interdisciplinary work with rheumatology and otherwise, and there's a significant portion of the NIU population concentrated at these centers, and these ophthalmologists are willing to move very quickly to systemic medications, treat very aggressively. Today they're using not only a lot of Humira, which is the only approved therapy, but a lot of off-label therapies as well, like tocilizumab and others, as well as off-label TNF inhibitors, and so we really see this as a group of prescribers that at launch with no behavioral change will be very eager and excited about a new approved therapy, then there's also many patients who are treated at your more classic community retina doctors. Those physicians, as you would expect, are really focused just on local therapy. When they see a new patient, they will start by doing several, usually, steroid injections in order to try to get it under control. With non-anterior disease, that most of the time does not work and systemic therapy is needed. At that point, they will loop in a rheumatologist. It's actually the rheumatologist who does all of the prescription of any systemic medication beyond sometimes oral steroids. The retina doctor and rheumatologist will partner where the retina doctor monitors the eye, the rheumatologist does all of the systemic prescriptions. In this case, the patients would generally follow a more conventional rheumatology ladder through systemic medication. I think it's important to note here though that none of these medications, as we'll get to in a minute, work that well. And so within this cohort, you see many patients ending up on TNF inhibitors and many patients going on to fail TNF inhibitors. And so even just in a more focused way, looking at rheumatologists and their partnered retina doctors who are using TNF inhibitors today for NIU, that provides an additional prescriber base at launch, I think would be very excited about potentially rapidly adopting a new oral therapy without any behavioral change needed. Obviously, over the longer term, if the medication is providing benefits to patients, I think there are opportunities for kind of more broad behavioral change as well. But I think we don't really need that to be successful. And certainly at launch, that would not be our focus. I would again just to kind of build off of the point I was just making. There is a significant amount of use of systemic therapy for these patients today. This data here does not even include DMARDs, which are also used frequently along with oral steroids. This just shows more advanced therapies in terms of Humira, again, the only approved drug. Other off-label TNF inhibitors and infliximab is used pretty frequently, and then other off-label therapies. And you see this is an analysis that IQVIA did with us several years ago. And through 2022, nearly 50,000 patients with NIU on one of these therapies. So this is even just looking at the market on TNF inhibitors today, pretty significant market. And I think notably, the TNF inhibitors don't work that well. We've seen in the VISUAL I trial, which was the registrational trial for Humira, 50% of patients failed on Humira within the first six months. And then in the open- label VISUAL III trial, again, over the course of one year, only around 50% of patients were able to achieve a quiet eye, which is a slightly different definition, but basically the same concept as treatment failure. And so you see both in the placebo-controlled setting, but even in the open- label setting, over the course of a year, only around half of patients being well treated with Humira. And I think that's why you see from the last slide significant uses of other TNF inhibitors as well as other off-label therapies because there really is this kind of zero tolerance for inflammation among these patients. So then moving on to brepocitinib, very excited about the potential here. As I mentioned before, the disease is characterized by T-cell infiltration into the eye. One of the great things about TYK2 /JAK1 inhibition is in a pretty distinct way, we're able to address both Th1 and Th17-driven inflammation. I think this is a nice slide both for NIU, but I think it also just brings to light some of the points Matt was making about our indication selection overall in terms of how dual TYK2 /JAK1 inhibition can be distinct from other medicines. In terms of starting with Th1 inhibition, both interferon gamma and IL-12 play a major role in that. Only by addressing both TYK2 and JAK1 are you able to hit both of those cytokines. Same with IL-6 and IL-23 on the Th17 side. I think the mechanistic rationale, not only for JAK inhibition in general, but for this particular mechanism is very well suited to the disease. And then we do have phase II data here in the indication. This was data that came out in early 2024. Some of you may remember that, but I'll do a brief reminder. This was a study. It did not have a placebo control, but did have two doses and was double- blind within those two doses. And the structure of these NIU trials, this was how the Humira trials were done. This trial, as well as our phase III, is given, again, given kind of the zero tolerance for inflammation. All patients who are eligible for these trials need to be treated immediately. So across both the drug arm and the placebo arm, all patients get a two-week 60 mg per day steroid burst. Then that's rapidly tapered down to zero. And then the clinical endpoint assessed is treatment failure. Even with that taper, do you fail or not? Notably in our taper, or sorry, in our trial, the taper was six weeks, which is more rapid than previous trials conducted. And the data we saw, obviously a small study, so we're excited to have the phase III data coming out next year. But certainly for a small study, very encouraging data, both on its own and in the context of the VISUAL I trial. Our protocol was modeled very closely on that VISUAL I trial, the registrational study for Humira. The main difference is their taper was 13 weeks while ours was six. So actually our study was designed to make it harder or easier for patients to fail, harder for the drug to prevent treatment failure. Patients in both arms did quite well, very clear dose response between brepo 45 mg and brepo 15 mg. Certainly sets us up potentially with data similar to this or even data that's not quite this good, but still strong to be clearly the leading therapy in this indication if the phase III goes well and the drug's approved. I would also want to highlight some of the biomarkers that we looked at. These are very important to ophthalmologists treating these conditions. The gold standard biomarker for NIU and particularly for posterior segment inflammation is a wide field fluorescein angiography measuring vascular leakage in the retinal area. You can see here improvement in a dose-dependent way between brepo 45 and brepo 15 mg. Notably improvement, particularly in the brepo 45 mg arm that increases from Week 24 to Week 52. In the brepo 45 mg arm, no patients worsening, while in the brepo 15, several patients worsening and really a distribution more centered around a lack of change. I think looking at this measurement, which ophthalmologists will tell you is not extremely noisy, even in a smaller study can carry a lot of meaning. You see the patient-level data here, I think a pretty compelling story that gets us excited for the phase III. Then the other biomarker I would highlight is Central Subfield Thickness, CST. Again, we saw improvement here in the 45 mg arm sustained out to a year without worsening even as the taper went on. This is an area where Humira is known to not provide a lot of benefit. We're excited to see what the phase III shows here. That brings up the phase III study. This is what we'll be reading out now in the second half of next year. So first, just to highlight that timeline, that's about a year after the VALOR trial that recently read out. So if all goes well and the study's positive, we're looking at a potential approval and launch in NIU just a year after DM, give or take, obviously. And so thinking about the early commercial launch, early revenue growth potential of the drug, early patient impact of the drug over the first few years, I think NIU is something that's very important to take into consideration along with DM. I would also note Matt made this point before, but the enthusiasm from the physicians and patients was really very striking. We enrolled this trial in one year while significantly over-enrolling it. And over 50% of patients were enrolled in the United States. So I think, again, speaking to that enthusiasm there, the study is going to read out as two distinct sub studies, CLARITY-1 and CLARITY-2. So they were different sites, different patients in each of these studies. So we'll read out as two distinct parallel trials with identical protocols across the two. Very similar design to the phase II NEPTUNE trial, again with a two-week steroid burst, six-week taper, and then the primary endpoint time to treatment failure. We'll also again be looking at some of the same biomarkers and patient-reported outcomes that we, in the case of the biomarkers, discussed for the NEPTUNE trial. So very excited about this readout coming out next year. Next, I'll move on to cutaneous sarcoidosis, where, as Matt mentioned, and I'll walk through in a minute, we actually have a much smaller study, phase II, but that we'll be reading out quite soon in the first half of next year. A bit about this disease, first just starting about the clinical manifestation of this. This is a skin disease with a particularly high urgency to treat. It's characterized not only by erythema, but also by scaling, ulceration in the case of bad scaling, as well as induration and depression. And as a result of that, can pretty quickly lead to permanent skin damage, as well as in some cases even damage to cartilage, so it's compared to many cutaneous inflammatory conditions, very high urgency to treat, get the disease under control quickly. And then thinking about this market, obviously can't really think about cutaneous sarcoidosis without the broader context of sarcoidosis. This is an indication many of you may follow primarily in the context of pulmonary disease and pulmonary sarcoidosis. It's a multi-organ systemic condition. Pulmonary disease obviously is the most common manifestation, but cutaneous disease, which we're studying here, and ocular sarcoidosis, which is part of non-infectious uveitis, are the next two most common organs impacted by sarcoid. And pulmonary disease has proven a pretty challenging area for drug development. Roivant itself, along with many other biotech companies, including with some recent readouts, have experienced that. And so at the moment, there's no approved therapies, there's no therapies in phase III. There are some phase II trials ongoing in pulmonary disease. But I think it's going to be, it has been, and I think will likely continue to be a challenging place to bring new medicines to market. And so if we are successful in cutaneous sarcoidosis as well as ocular sarcoidosis, we would really be the only approved therapy for any form of sarcoid, and with our two on-label indications covering a very meaningful portion of the overall patient population. So I think thinking about kind of the synergies and overlap between NIU and sarcoid, I think something that's valuable to think about as we look ahead to a world where this drug is potentially approved for multiple of these indications. And that kind of relates to how we think about the cutaneous sarcoidosis population alone. There's around 40,000 cutaneous sarcoid patients in the United States, so slightly still within that category of kind of large orphan indication Matt was talking about earlier, but certainly smaller than NIU and smaller for that matter than DM. But really our view is all of these patients would be very strong candidates for therapy if the drug's approved. Just under 50% of them have minimal to no involvement of other organs. Not all patients with sarcoid have pulmonary involvement, and even many who do, for not all of them is it severe enough to really be driving treatment. Then for slightly over 50% of patients, there would be significant non-cutaneous involvement. And there the other organ systems certainly would play a bigger role than the skin. Obviously, if you have really bad lung disease, that's going to take precedence over skin. Really bad eye disease will also take precedence over skin. Again, well, for really bad eye disease, that's where we have our NIU development program, and then again, I think within pulmonary disease, the unfortunate reality is that there's no approved therapies there, and I think at least for the near to medium term, there's not an obvious path to there being an approved therapy, so I think at least in the early part of launch, we would really see a lot of these patients being candidates for therapy with cutaneous disease alone, so I think sarcoid obviously is a complicated multifaceted indication, but we really see a significant opportunity here, both as a standalone indication, as a nice add-on to NIU and DM. A lot of these prescribers in cutaneous sarcoidosis are academic dermatology centers of excellence that have some overlap with DM. But then also really along with NIU as a nice beachhead into the sarcoidosis population overall and really thinking about brepocitinib as a treatment for multiple organs within sarcoid. So very quickly, just to wrap up this section, the study that we have again reading out quite soon. This is a small proof of concept study. Obviously, we'll have to see what the data says before getting too excited about the indication. But this is a three-arm study, brepocitinib 45 mg, 15 mg in placebo, 31 patients randomized 3:2:2, U.S. only, a shorter 16-week trial. Given it's a cutaneous endpoint, we would expect to be able to see improvement over that timeframe. The primary endpoint is the CSAMI Score. I'll walk through that quickly on the next slide. And the mean change in baseline difference of brepo 45 compared to placebo. CSAMI Score, this is an assessment that's very similar to the other area and severity indices used in inflammatory dermatology like the CLASI, CDASI, PASI. Similarly, it breaks out into activity and damage. Our focus will be the activity score, which again, as I was saying before in the opening, reflecting this disease measures not only erythema, but also induration and surface change. So we're excited to see the results of this trial. Obviously, a small study, but I think if the results are compelling, this will be a really exciting additional indication to add on as we think about the brepo potential. Terrific. And then I'll wrap up now last, but certainly not least with dermatomyositis. This is an area obviously we have a tremendous amount of excitement about. I think even if we were not doing anything with brepocitinib other than dermatomyositis, this would be a really incredible opportunity to make a very important impact in the lives of tens of thousands of very sick individuals and also make a very valuable franchise around the drug in the process of doing that. So excited to walk you through that. One of the things that over the last few years has made me so excited about this disease, or not about the disease, but about the potential to treat the disease and the indication is really spending a lot of time engaging both with clinicians who see these patients as well as patients themselves. I wanted to start by sharing a short video that we've put together with some patients talking about their story and experience with DM. It was just everywhere. It was very painful, very itchy. I found it so difficult to use my arms and to get up from the seat. I was like, "What is happening?" Then suddenly I started having joint pain. I was getting really red on my chest, my face, my hands. And we couldn't understand why. I had always had a very smooth, brown, creamy color kind of complexion, never got sunburned or anything. And then if I went outside for five minutes, I looked sunburned. The skin symptoms kept going on to the point where I had these sores in my scalp and they were bleeding inside my ears. I developed this rash across my chest, my face, my back, my arms. It was waking me up at night. I was clawing my skin off. I lost 35 lbs of muscle in an eight-week period. So I went from heavy yoga physical practice to needing help getting out of bed. I was just in excruciating pain. Every joint in my body hurt. My muscles in my thighs and my upper arms were hurting. And I was trying to drive to work and I couldn't grip my steering wheel. When I first went into the hospital, I'll never forget, they were rolling in a neighbor, my new neighbor. I remember hearing her say, "She can see me," because my eyes weren't even open. Like you couldn't, they were, I could see out of them, but if you were looking at me, you couldn't even tell. I started having some shoulder pain, some aches, a frozen shoulder. And I got the, you know, it's menopause, it's hormones, here's some estrogen. When I would try to explain this to them, it was all, "Well, you've got anxiety and it's probably that and it's probably you're just tired. It's probably asthma." And everything just kept getting brushed off because the blood work never showed anything. I got the call that I was diagnosed with lupus, but she still wasn't convinced. She really pushed through the door of trying to get into a specialist and quickly helped me get into a rheumatologist. One of them actually rejected me because my blood work was normal. I went to a rheumatologist. He spent two hours with me and went over all the stuff and just said that he could not figure it out. He just had no idea. They pretty much told me they didn't really know how to treat it. Their best guess was giving me prednisone and I would be on prednisone for life. The prednisone had so many side effects. I gained so much weight. I had blood pressure issues. The medication is the hardest part, especially during the IVIG portion. That was the worst. When you have to live on pain medication and the side effects that causes and the myositis medications and the side effects those cause. It was just a surreal experience. I started on the maximum doses of immunosuppressants, the high doses of steroids, and then a variety of other medicines that have been used that I had to stop because they just made me too sick. We take a lot of pills and don't feel better. We have to gauge everything, how are we going to do this? All of the different treatments that have been introduced and moved around and fine-tuned, I mean, it's a full-time job for me. Asking my doctors all the time, "How long do I have to keep taking all this, doing all of this?" And their answer is that they don't know. My illness looks invisible, which is another problem that we have. This is just a disease that nobody knows about. They don't understand it. I'm sorry. And I think a lot of people feel this way. You're constantly in fear of what's coming next. Because even though today you might feel well and things are going great, there's always tomorrow. And you do not know what tomorrow is going to bring. Thanks. I hope that was helpful for people to really try to bring to life a bit some of what these patients are living with and dealing with on a daily basis. And obviously that was an anecdotal set of five to 10 people. But I think what the stories and messages that you hear them delivering, we really see reflected in broader aggregate data around the disease. And I'll walk through some of that now, hopefully with the context of kind of seeing the real human element of it to bring even more understanding. I think the first thing is, as you saw several of the patients talk about, when patients are initially diagnosed, they are really loaded up with steroids. This is something that we see in the data as well, in claims data with average number of days on steroids in the first year of diagnosis of 128, and very notably an average steroid dose of 18.6 mg per day. An extraordinarily high steroid burden. Over time then, again, as was reflected in the video, patients end up on polypharmacy because there really is no actually approved efficacious treatment here other than IVIG, which has many limitations. We, again, see that reflected in claims data with nearly 2/3 of patients receiving two or more therapies a year on polypharmacy and over 1/3 of patients receiving three or more therapies. Primarily these are high-dose steroids and immunosuppressants, but also IVIG and off-label therapies. I think in spite of the fact that patients are getting all this polypharmacy, their steroid dependency and even their high-dose steroid dependency doesn't go away. We see that among patients receiving ISTs, off-label biologics or IVIG across. You're kind of looking at all patients, whatever the other set of drugs they're on, but if you're getting one of these, then you fit into that category. You can see that a vast majority of these patients still require steroids for a significant portion of the year. A vast majority of those are getting very high-dose steroids of 10 mg per day or more for a significant portion of the year, so really a very high steroid burden for these patients in combination with the polypharmacy of these other medicines. It would be one thing if these drugs were working, but they're really not. There's continued need in terms of significant symptom burden for patients. There's a significant amount of data on this. I'll cite some various statistics from different patient advocacy group surveys, different cohort studies conducted at various centers and other research data. But around 2/3 of patients are dissatisfied with current treatments and say they're only partially controlled. Notably, again, you heard some of the patients talk about this in the video, that 60% discontinue therapy due to either side effects or lack of efficacy or both. And really they're kind of living, DM is a disease where the severity of it, there's always some level of inflammation and burden, but it does ebb and flow in terms of how acute it is. And that leads to this kind of perpetual fear about worsening of disease, where even if at any one given moment the level of disease burden is moderate rather than severe, the patients live in this constant fear of getting worse. And that fear is reflected in the reality of their experiences. Around 3/4 of patients report experiencing a flare in a given year. Many of those flares end up resulting in hospitalization. And pain, as you heard some of the patients talk about, is a really prominent feature of this disease. And actually we see both in our own claims analyses as well as multiple different sources in the published literature that opioid use is quite significant among DM patients. Again, reflecting the amount of medication and really toxic medication that is needed to get patients to even a medium level of control where they're at a minimum not ending up in the hospital, and although with the kind of heavy treatment regimens they're on, patients are able to stay out of the hospital and sort of have the worst aspects of flares treated, the overall daily living activity burden on these patients is very significant. From the muscle disease here, you see in patient advocacy surveys, 2/3 of patients are unable to climb a flight of stairs, 35% of them requiring the use of mobility aids, so the muscle disease is very debilitating for daily living activities, and the skin disease is extremely bad as well, often covers large portions of the body, can lead to alopecia and hair loss, extremely itchy, extremely debilitating in terms of daily activities. DM is incredibly photosensitive. Patients really can't go outside almost at all unless they're completely covered from head to toe. Patients report really bad psychosocial burdens and emotional burdens of skin disease in terms of social life. Physical intimacy is heavily limited, and so really significant burden from the skin disease along with the muscle disease. We see this notably even in specialized myositis centers. This is a publication that came out of Stanford, which is really one of the top three or four dermatology centers of excellence in the world for DM. Even there, they were very open about the fact that only around 15% of their patients in the course of a year were able to get to clinical remission. That's even while those patients, again, heavily treated both with steroids, but also reasonable percentages with IVIG and then significant portions with DMARDs. With all of these medications, and particularly steroids, they carry significant adverse health effects of their own. There's large numbers of comorbidities associated with dermatomyositis, including heart disease and malignancy. Some of this relates to the disease itself. DM is a, it actually starts with inflammation of the vasculature in the skin and muscles, and that can impact other organs as well, including the lungs. But also a significant portion of this adverse event burden comes from the chronic high-dose steroid use. We see that documented in a large number of studies. Notably, as we think about the different adverse events that matter a lot to DM patients, and kind of look across published literature of different categories of drugs, we have here steroids, JAK inhibitors, as well as DMARDs. You see steroids really across these at the upper end, and in some cases real outliers with several multiples more incidence rate than we see from these other categories of drugs. Then we also see the DMARDs across most of these in line with or even with greater incidence of these events than we have with JAK inhibitors. Thinking about this set of comorbidities as well, we have to think about that not only in the context of the disease itself, but also the heavy treatment regimens that these patients are on, including steroids. We think some of this is actually reflected in the VALOR data, which I'll walk through in a minute. I think just to summarize this before I get to the VALOR data, there's a very significant unmet need here. These patients are very sick. They're heavily treated with polypharmacy, including high-dose steroids. They're not happy with that, constantly changing treatment options, continuing to experience flares in pain, significant daily living activity burden and quality of life burden. And then on top of all of that, you have the side effects of their existing medications, particularly steroids. So I think a real opportunity here for a new medicine that can deliver rapid and sustained efficacy benefit to these patients while also bringing them down in significant ways off of their steroid burden. And the VALOR trial resulted in data that we think sets precedent about potentially to have a product profile that can really do those things that patients need. I won't spend a ton of time going through the data. Obviously, happy to talk about it in the Q&A, but we've presented on this, I think, a few times now. Don't need to overrepeat ourselves. But again, I would just remind a few key things about this study. This was a 52-week placebo-controlled study. The trial was the first ever 52-week placebo-controlled trial in DM to read out positively. This also was a DM-only trial. Many of the myositis trials that have been conducted in the past or ongoing are pooled across multiple inflammatory myopathies. Our view, which I think is a consensus view, it's just a fact, is that the pathobiology of these inflammatory myopathies are not identical. There are important differences. We really wanted to focus our program on where there's the tightest alignment with the TYK2 /JAK1 mechanism of action and also deliver a data set that's maximally impactful for patients and physicians that is kind of directly relevant to the patients who we want to be using the drug. So the baseline data, I've been through this before. The main thing I would highlight again here is this is a real-world population, mild, moderate, and severe patients included. And then looking at these medications at baseline, we did not, your patients had to have tried and failed one prior DM therapy, but they did not have to be on any background therapy. And some of them were not on any background therapy at baseline. But just reflecting the real-world reality of these patients, you see heavy use of background therapies with 80% of patients on two or more DM medications. And for about 3/4 of them, corticosteroids was one of those with a mean dose of around 11 mg-12 mg per day. So very heavily treated with background medications. I'd also highlight these two lines at the bottom, again, reflecting the real-world nature of the population. Around a quarter of patients having previously tried and failed IVIG, and also I would note that this was not a study where we were overly exclusionary in terms of patients at risk of comorbidities. We really wanted to include real-world risk of a real-world patient population, which includes patients who have issues and challenges beyond just skin and muscle disease. This is true in terms of cardiovascular risk factors, significant numbers of patients in the trial with diabetes, obesity, hypertension, hyperlipidemia. As you saw from the videos, those things are frequently side effects of steroids, and we saw that on the previous slide as well, and then I would highlight here that around 15% of patients had experienced a prior benign or malignant neoplasm. Obviously patients with active malignancy were excluded from the trial, but patients who had experienced that in the past or may have had some risk for that were allowed in because that's reflective of who DM patients are in the real world. The data, we've been through this before, but we were really excited by this. We found out that we'd hit, we had primary endpoint nine ranked key secondary endpoints in the SAP. When I found out that we had hit on all of them, I was kind of blown away in a positive way, obviously. I think this is reflective of both the statistical robustness of the data, but also one of the reasons we ranked so many endpoints in the hierarchy is this is a heterogeneous, like the clinical manifestations of this are heterogeneous. You have patients where the muscle disease is worse. You have patients where the skin disease is worse. You have patients where the steroid burden is the thing that is bothering them the most. And I think we really wanted to assess the totality of these factors that impact disease burden. And by hitting on all of these endpoints, we were really able to show benefit across skin disease, muscle disease, rapidity of onset, steroid sparing. I think really a very exciting and compelling data set. In terms of the primary endpoint, Myositis Total Improvement Score, again, I think most of you are familiar with this, but statistically significant improvement from brepo 45 mg compared to placebo as early as week four, sustained at every single visit out to Week 52. Dose-response, I think, leading to the statistical robustness and meaningfulness of this data while also clearly establishing 30 mg once daily as the appropriate approval dose for this indication. Then achieving all of that while significantly bringing patients off of steroids. This simultaneous clinical improvement with reduction of steroid burden, I think, is one of the things I'm most excited about with this data set. As I mentioned before, around 3/4 of patients on background steroids and brepo 30 mg, mean dose of over 12 mg per day at baseline. Nearly 2/3 of those patients got to a minimal steroid burden by the end of the trial. Over 40% came off steroids altogether. Those numbers were about 2x the levels of reduction that we saw in placebo. So very excited about that. Looking at the TIS response thresholds, 40-point improvement moderate, 60-point improvement major. Again, very encouraging data. Just looking at the fact that over 2/3 of patients in the trial on brepo 30 mg experienced moderate meaningful improvement and nearly half experienced major improvement, and then when we look at the intersection of that endpoint with minimal to no steroid burden, we see still quite high levels of response within the brepo 30-mg arm and even higher placebo-adjusted differences, as you would expect, and the safety data, obviously something we were also very attuned to and focused on looking ahead to the readout, and I think also very encouraging data. SAEs were elevated in brepo 30 mg compared to placebo. That was driven primarily by serious infections, most of which resolved, and the patients were able to resume drug. And indeed, you see that AEs leading to permanent treatment discontinuation were actually higher in the placebo arm than the brepo 30 mg arm. And then of very high notable interest to us was the adverse events of special interest we looked at. And again, here we saw no increase in brepo 30 mg compared to placebo across these categories of AESIs, including cardiovascular events, thromboembolic events, and malignancy. In fact, the only two malignancies in the trial occurred in the placebo arm. And again, just to echo the point I brought up before, this data occurred against the backdrop of enrolling a patient population that had risk of these events. Of course, one of the many factors that can lead to risk of these events is high steroid burden. And so the placebo arm here is heavily treated with steroids and DMARDs. I think it's helpful to understand this safety data in that context. Again, I think that's the context in which we will be bringing the drug to market in the real world in DM patients. Obviously, the VALOR data happened. We're excited about it, but now onwards and upwards. The top priority at Priovant, as you can imagine, is getting the NDA in. We've been working on that seven days a week, many hours per day. I think we've been making really great progress on that. As Matt mentioned, we feel good about a filing, hopefully in the quite near term in early 2026. Then also really laying the groundwork for a successful commercial launch. I think we have the benefit here of having been working in this space for a number of years, working with patients, working with the patient groups, and working with the physician groups who treat these patients, and actually, even by the time of the VALOR readout, in our view, there's a little over 100 kind of key DM centers of excellence in the U.S., and we had a relationship with at least one key physician at each of those centers. Many of them were sites in the VALOR trial, which is how we built that, but many were not, and it was just a function of having been out in the medical community here at medical meetings, just being really actively engaged in this community to build those relationships. And now since the VALOR data, we already have a quite large field medical team in place working full-time on DM-related scientific engagement with the medical community. That's allowed us to significantly deepen our relationships within those key centers of excellence. Obviously, at many of these centers, you have five, 10, 15, 20 relevant physicians across multiple specialties. And then also going out to more of the community doctors, community rheumatologists in particular. Many DM patients are treated at community rheumatologists, not just the centers of excellence. And we've made great progress already over the last few months at deepening our relationships there. Same goes with the patient community. We have close relationships with the patient advocacy groups who are great collaborators of ours. They're very enthusiastic about new therapies for this condition and the need for that. And we also have a disease education website, dermatomyositis.com. This includes videos from patients, physicians, and caregivers, and we have several thousand patients and caregivers who have signed up and subscribed to this website and have a lot of great engagement there, as well as on associated social media platforms. So I think really working on building direct channels of engagement with these patients and raising awareness about the disease. There's actually remarkably little I found about DM online. And part of the, I think, reason patients have been excited about this is we actually have a lot of great content on this website, including not related to brepocitinib at all, that I think people have found quite valuable and actually meets its own real unmet need in the community. And then finally, laying the groundwork for the operationalization of the launch in real ways, all of the things needed to do to get ready for a launch, really kind of adopting a strategy and approach here that I think is consistent with other successful launches in analogous indications over the last few years. We'll be using a limited distribution network of specialty pharmacies and supporting that with an in-house Priovant hub. And significant progress has been made around the selection of our partners there, as well as the operational buildout of the hub. So really excited about all the progress we've made there. Really excited to hopefully get the drug approved as soon as possible and have a successful launch. So yeah, with that, I'll wrap up. This is the timeline chart thing. We've been through all of this already. Key points, DM, NIU, and cutaneous sarcoid, we're excited about all three and think all three have great potential. Thanks so much. Thanks, Ben. Right, right, right. Good morning. I'm Richard Pulik. I'll be moderating today. It's better than it was, yeah. Sorry, that's Eric Venker's mic. Can we turn that one off? It's me, Frank, and Ben who need the mics and Richard. You'll have plenty of opportunity to hear from Eric later. That's right. Up on stage, Frank Torti also joined us, who is the Vant Chair. So I'll be taking Q&A from the room and also from the webcast. And I know that some people were asking for the Wi-Fi. There's no passcode needed. And the Wi-Fi is Pen2. First question, Corinne? Actually, could you bring the mic down here, please? And can you introduce yourself? Corinne Jenkins, Goldman Sachs. Maybe on NIU, you mentioned that 50% of these patients have comorbid autoimmune disease. So what portion of the patients are kind of already on background JAK inhibitors? How are they treated in the trial? And what can we learn from their patient outcomes as you think about the mechanism of action? Yeah, thanks, Corinne. Great question. Ben, do you want to take that? Yeah. Yeah, I mean, in terms of background for the trial, like patients on kind of other advanced therapies were needed to wash out of those prior to enrollment in the trial. Obviously, anyone who enrolled in this trial, whatever therapies they were on, were not working for their NIU because they were experiencing active disease. I think JAK inhibitors are not used off-label for NIU as much as they are for DM, candidly. There was the phase II study of filgotinib that showed pretty strong data, not as strong data as our phase II study. But I think there's very kind of strong evidence around JAK inhibitors in DM, or sorry, in NIU in general. But I think it has not been actively used off-label as much. In terms of patients with the comorbidities, I do think for patients with bad eye disease, it is unlike something like cutaneous sarcoidosis where the other organs would take precedence over cutaneous disease if they're really bad. Patients who are experiencing active NIU, I mean, they're at risk of going blind. That really does tend to be what dominates the treatment of the disease. Certainly, whatever therapies they've been on for these other indications have not been working to control the NIU. From what we've seen in the claims data, it's a lot of TNF inhibitors that the patients are on with NIU, including patients with comorbidities. Next question, David Risinger up there in the back, please. Thanks very much, Dave Risinger from Leerink Partners. Thanks so much for hosting this session today. So my question is on the brepo launch in DM. Could you just talk a little bit about the prevalence of patients? What percentage are in the different buckets of disease, including severe disease? And could you talk about transitioning patients off of IVIG or other therapies? How quickly you think you can start to convert patients, which will obviously play a big role in the ramp upon launch? Thanks very much. Thanks, Dave. Great question. That just reminded me of one comment I intended to make earlier, which is we've said the NDA is going to go in by early 2026. We're probably not going to comment on the actual filing of the NDA. So the next you'll hear from us about that is when it's been accepted and we have a PDUFA date. On the commercial launch and segmentation, look, I think it's a good question. I think it's a little bit hard. I think our belief is that almost every DM patient is eligible for therapy and that a lot of them are quite sick on high steroid burden. So it's a little bit hard to sort of talk about how deep in. And indeed, when you talk to DM physicians, as many sell-side analysts have done, you get an answer that a very large percentage of patients would be on therapy. So I think we view a lot of eligible patients. And frankly, I think IVIG switches is a relatively small piece of the overall market just because IVIG is not that widely used in DM now. It's only about 13% of the patients are on IVIG. So I think we have a lot of flex. Ben, anything else you'd say about the breadth of the landscape there? No, I mean, I think in terms of the prevalence, I think the latest data that we've seen ourselves and that others have been seeing as well is high tens of thousands of patients, like 70,000 or more with DM in the United States. I think there's still real underdiagnosis of the disease as well. You heard some of the patients talking about that in terms of. I think there's a lot of patients who get diagnosed with lupus who actually have DM, and I think as more therapies get approved, as we've seen in other diseases, I think that will become reflected in the prevalence. I think in terms of mild, moderate, and severe, a very significant portion of those are in the moderate to severe category. But also even those in the mild, who may be mild in the sense that rating their skin and muscle disease at a given moment in time, they show up as mild, that is because they're receiving high-dose steroids, like their level of muscle inflammation and muscle impairment at one moment in time may be rated as mild because they're on 15 mg a day of steroids, and that carries with it its own whole separate set of problems, so I think I would just kind of echo what Matt said. In our view, obviously, it'll be a patient-by-patient, physician-by-physician determination, but in terms of what is kind of the eligible population who should at least be considered for therapy, we would really see it as the full DM market. Next question, Yaron. Up front here, yeah. Yaron Werber from TD Cowen. Thanks for doing really a great session. I have three quick questions. Maybe the first one for DM, is there any chance to get priority review when you file? I believe you have an orphan designation, so hopefully you can get a priority review. And then for the CLARITY study, you don't technically need to be refractory to a previous drug, right? You just need to be active disease. So is there a chance that you can have frontline patients and can you get a broad label? And then I have a quick follow-up on CLARITY. Is there any chance you can share what's the powering in the study? Thank you. Thanks, Yaron. All good questions. On the first one, I'll take it and I'll say, yes, there is a chance we'll get priority review. Look, obviously, we won't know until we have the conversation with FDA. On the two questions on CLARITY, Ben, do you want to take those two? Yeah. So the first is it includes obviously all patients enrolling in the trial are getting steroids as part of that initial steroid burst, but wide variety of patients coming into the trial, including a meaningful number who have tried and failed TNF inhibitors, but also a meaningful number who have not. That's not a requirement for entry into the trial. And we have a significant number of patients in both of those categories. I think as far as the powering goes, it's highly powered to detect. With the Kaplan-Meier curve endpoints, those are actually pretty robust statistically. We over-enrolled the trial, the VISUAL I trial. With over-enrolling the trial, each of our two sub-studies is around the same size as each of the VISUAL programs. And so we feel very good that any meaningful difference could be detected. Thanks, Yaron. Brian Cheng, next question, please, right there. This is Brian Cheng from JP Morgan. Just thinking about the groundwork that we need to do here for cutaneous sarcoid here, given the heterogeneity of the disease phenotype, which of the activity or morphology item do you think will see the most impact, just given the JAK1, TYK2, MOA here in the BEACON study? Is the trial power to show stat sig on primary? And can you give us a sense of what we should expect on the placebo arm? Thank you. Those are all each individually difficult questions to answer. But thank you. They're good questions. Look, I think I want to be clear. This is a proof of concept, a signal-finding study and an indication where there's some validation from open-label studies of JAK inhibitors, but we're trying to learn here in order to design a phase III program. So look, I think we're going to pay a lot of attention to the data and look for signal in a variety of different aspects. And I don't know that necessarily finding stat sig is the main goal of the study, but I think we're excited to see what we find. Yeah, I would agree with that. I think, yeah, it's a proof of concept study. One of the reasons we're doing it is to kind of get a sense of where we see the benefit across those. There's not been, Matt kind of talked about, creative development, pioneering new indications. This is one where there's really not been a lot of studies done of any therapy in cutaneous sarcoidosis. So we're excited to see the result, but it's an exploratory phase II. And then on the back of that, we'll have a lot more insights for the phase III. Really, maybe just to hand it to Frank for a second. Just look, sarcoidosis is obviously an area we've had some history and maybe a little bit of the thinking that went into cutaneous and some of the overlap with NIU and what we learned from the pulmonary program. Yeah, I mean, I think there's a lot that can be taken from what we did previously in sarcoidosis and thinking about how maybe you expand over time into broader kind of reaches of sarcoidosis and get beyond cutaneous. I think we're going to look for those signals in this study and kind of I think our ambitions for this study, if it's really positive, are both to go fast on this study and to kind of look more broadly into sarcoidosis. Now, that's all data dependent, but I think there's a real opportunity to both think faster and more expansively on the back of this data set. Next question, Umer. Hi, guys. Thanks for taking my question. Two, if I may. First, as it relates to the data set and congrats on the data, obviously, but when I look at the 31% versus 46%, the primary endpoint in VALOR, I'm not necessarily blown away, but I look at your responder data and it looks very intriguing. So could you speak to clinician feedback on the responder data at the higher thresholds in VALOR? And I ask because it has direct implications for your price, especially considering, which is the other part of my question, if GSK hits their study in polymyositis and dermatomyositis with a molecule which is in the market for a very, very low price point, how does that change the commercial reality of your gross net and the pricing integrity 2027 onwards? Thank you. Yeah, look, thanks. Those are both good questions. On the primary, I guess the one thing I'll say, and Ben talked a lot in his presentation about steroid taper and steroid burden for these patients, and I think the data have to be looked at in totality. I think one thing that was sort of interesting to us when we first saw the data is that we had spent so much time thinking about the steroid taper as kind of a risk mitigant on separation between the arms that we probably didn't give enough forethought into just how impactful the steroid taper would be as effectively an additional sign of clinical benefit. I think, and Ben can talk about the direct experience of the docs, but I think in general, the doctor who looks at this data and is in fact blown away by the performance on the primary, in part just because, to be honest, I mean, again, there's so many failed studies in this area that it's a big benefit. But then also they look at it in conjunction with the ability to deliver a very significant reduction in steroid burden at the same time. I think that's a real driver. So I think that plus the very good performance on the responder rates, the speed of action as well. For example, efgartigimod had a study that in phase II took, I think it was about 100 days or a little bit more than 120 days to reach and was a moderate response on average. And we took, I think, half that basically. So I think both speed, magnitude, and conjunction with steroid burden are all really important endpoints for us. On the commercial side, look. I think it's hard to comment right now both on price points and on the evolution of price points over time. We believe we have a pretty healthy lead here as a first-to-market option. Obviously, if FcRns enter, they will be at a still higher price point probably. So look, and IVIG is expensive in the indication. So I think there's good precedent depending on what other later market entrants show. And obviously, there's an anifrolumab study, for example. The market will evolve over time, but we get to paint that picture first and early as argenx, for example, did in MG. And I think that's going to give us a strong initial position. Anything either of you would add? I would just add on the first question, I encourage anyone to talk to as many DM doctors and hear from them directly. Their feedback, my conversations with them and ours has been extraordinarily receptive and enthusiastic. It's important to, again, contextualize this in the context of DM drug development and what the TIS is. The TIS is a composite endpoint that is somewhat noisy at the patient level. To be able to get that clean result on it, hitting with such a low p-value at all in meaningful difference is, I think, speaks to the fact only a drug that's delivering a lot of benefit to patients could do that. There's never been any other trial to show any improvement on TIS compared to placebo at 52 weeks. So I think, and then the responder data, as you point out, is quite impactful and is in some ways really a more, in terms of clinical meaningfulness, a more kind of interpretable result because it's like, okay, what percent of patients achieved moderate or significant improvement? So I say all that even before getting to Matt's point about the steroids, which I couldn't agree with more. I wouldn't minimize the level of clinical improvement that we're seeing amongst these patients in terms of their core myositis symptoms. And then you add on top of that the steroid reduction data. I think it's really a very exciting data set, and that's certainly been all of the feedback that I've received. Yeah, and I'd just add to that. I think, look, it's an extraordinarily limited set of competitive options right now. And I think that has a lot of homology with things that we like broadly. If you think about, we'll talk about Graves later in the day, another place where there's really limited innovation, really limited success. And I think if you think about commercial launches that have really worked well, launching into old generic competition with very limited efficacy really sets you up well in the physician community because they're really hungry for that next new thing or really the first new thing they've seen in a long time. We really hear that echoed a lot in the physician community of doctors we've spoken to about this data and more broadly. I'm going to have to cut it off here. We'll have plenty of opportunities for further questions, but we'll have a quick break and come back at 9:30 A.M. for those on the web. Thanks, everybody. We'll see you in five minutes. All right, we're going to get started again trying to keep things as close to on schedule as we can. So thank you, everybody. So we're going to move on now to the next section here, which will be first we'll talk about our FcRn program, especially IMVT-1402, where Eric Venker will lead the presentation. And then we actually have a great presentation from a physician in the field as a part of that. And then we'll talk about mosliciguat just after. So I want to start with just a little bit on IMVT-1402 to set the stage. I know most of you are familiar broadly with this program. But look, first of all, we obviously love FcRn as a field. It's an important field. We think it's evolving quickly in important ways. We think we have the best drug in the field. 1402 delivers deep dose-dependent reductions in IgG. We think we get to about 80% in terms of IgG reduction, which is as deep or deeper than any of our competitors go. There's significant evidence that we've generated across studies that deeper IgG reductions are associated with better efficacy. There's now been eight different indications in which that relationship has been shown. It also just makes good intuitive sense. We see an absolutely huge opportunity in Graves' disease. We have pioneered that indication. We think it's an enormous step forward for those patients. We sort of got there initially by way of studies in thyroid eye disease, but now we are all in and very focused specifically on Graves and what we can do there. We have generated disease-modifying data in our proof-of-concept study, and we expect registrational data in two different studies in 2027 with a multi-year lead, and we think we'll have best-in-class efficacy. We'll talk a lot about that with Eric and with Dr. Lupo. 1402 will be first, and we think best-in-class in Graves. It's potential to be first and best-in-class in difficult-to-treat late-line rheumatoid arthritis. We'll talk more about that study. It's now moving a little faster than expected, and in CLE, we think we have an opportunity for a best-in-class drug in the established FcRn indications, MG and CIDP, as well as in Sjögren's. The top line, as I said, for the difficult-to-treat RA study is now expected in 2026. That'll be great. Look, FcRn antibodies are killing it as a field. As I said, there's now $7 billion in cumulative revenue in MG and CIDP within the first four years of launch. We're excited just to be a part of that field in general as well. We think we have a best-in-class drug. Obviously, the main sort of leg of that stool, the top of the pyramid, is we think we have the potential for best-in-class efficacy. We think deep IgG suppression will win the day in terms of clinical benefit across a range of indications. We also have great administration. We have a simple low-volume subcutaneous autoinjector. That is the format that is being tested in our clinical trials. So we feel great about that, and it sets us apart as well. And then finally, FcRn's one of the maybe unsung great facts about the FcRn class is how easy it's been for physicians to use. The safety has consistently been clean. These patients are really benefiting. They've been easy for docs to write. And so we have a safety profile with 1402 that we think is commensurate with the other great drugs in the class. I know that not everybody agrees with the headline here, but we believe the deeper is better debate has largely been settled at this point, that deeper IgG suppression yields better clinical benefit. We've shown that in our own data in three separate studies at this point. In our Graves phase II-A study, in each case, we've cut the data based on less than 70% or greater than 70% IgG reduction. One thing to note, we think the vast majority of patients on our drug will be over 70% from an IgG suppression perspective, whereas our competitors' average IgG suppression in many trials is in the, call it, mid-60s, so in the Graves study, we showed over 60% of these patients were off any thyroid drugs as responders, compared with just over 20% in the below 70% population. In myasthenia gravis, we looked here at minimum symptom expression, which is sort of like a measure of disease remission in MG. Over half of our patients with the deeper IgG suppression had this minimal symptom expression endpoint hit, whereas only 30% in the lower case, and again, sort of double the number, double the percentage of responders in the CIDP phase II-B study at the deeper IgG suppression versus at the lower level, so again, this data we've shown before. We're not going to hit the point too hard today, but we do feel like we will continue to be able to outperform from an efficacy perspective given the depth of IgG suppression we deliver. 1402 is well underway from a development perspective with eight potentially registrational data sets coming in the next 30, sorry, with five potentially registrational data sets coming in the next 36 months. Obviously, first-in-class and best-in-class indications, Graves, RA and CLE. Graves is the elephant in the room there, and we'll be talking a lot about it today. In Sjögren's, we think we have a potential for a best-in-class program that will be neck and neck maybe within a year of the other programs from an FcRn perspective in Sjögren's in a rapidly evolving field that we think has high unmet need. And then obviously in CIDP and MG, well-established FcRn classes. We're playing from behind from a timing perspective, but we think there's real upside there from our clinical profile. Wide variety of risk and commercial potential across these indications, ranging from something like MG, which is extremely well validated for the class, extremely well validated for our programs, but a more competitive indication, something like Graves where we've actually generated phase II data, which is highly de-risking, big commercial opportunity, all the way to the other side of the spectrum where we've got indications like D2T RA and CLE, not yet heavily validated for the class, potentially big opportunities, especially in late-line RA where there's a huge amount of patient demand that we're seeing come out of the woodworks if we can deliver a clinical benefit to that recalcitrant patient population. We like having a diversity of risk and opportunity across the portfolio, and we're continuing to evaluate opportunities in different parts of this spectrum. This is just the beginning for the FcRn class. We are not the only company to put up a slide like this. There's a lot of other companies out there working in the field or a handful of other companies out there working in the field. But really, we're just at the tip of the iceberg in terms of this biology. We are sort of through a set of indications where there's FcRn proof of concept and in development in a bunch of indications where people are either ourselves or others are working. But there's also a ton of opportunity in FcRn land kind of beyond the existing indications. You can imagine we are spending a lot of time and effort continuing to evaluate where we think the field is going and figure out places where we can play, where we can continue to expand upon the profile of what we've done. There's also just as true in terms of the metrics of what's happened over the last handful of years here. We've gone from in 2020, a handful of indications across about 700,000 addressable patients in development now to millions of addressable patients, 20+ indications in development, and obviously just a lot of commercial validation for the class behind us. There are other classes that have followed a similar trajectory. These are not chosen at random. But look, obviously both the TNF class and the JAK class were broad biology, lots of applicable places to go, both classes that were early pioneered with molecules that were subsequently succeeded by better kind of best-in-class molecules. And we just want to point out both the way these markets have evolved in terms of the number of therapies approved, but also the role that the best-in-class molecule ultimately played over time in each of these markets was significant. And it wasn't about who came first. It was about who delivered the best drug and the best profile. And over time, that's what carried the day. And we hope we have an opportunity to do something similar in the FcRn space. 1402 alone is now looking at markets with over 600,000 patients. Obviously, that starts with MG and CIDP, which are well established. Graves' disease is an almost unfathomably large patient population for a mechanism of this kind, but also excited about late-line RA, excited about Sjögren's, excited about CLE. It adds up to a lot of addressable patients, which obviously at the price points that people are talking about for FcRns or using for FcRns is a really big opportunity. So I'm going to end my intro kind of overview there and hand it over. I'm going to introduce Eric Venker. Eric has been at Roivant for a long time, was previously president and COO of Roivant, and is now president of Roivant and CEO of Immunovant, is leading these programs since April, is going to take us through some of the near-term opportunities, and then we'll get into a longer discussion on Graves. So with that, Eric, thank you very much. Yeah, take it away. Great. As Matt said, yeah, I've been at Roivant for a long time, almost 10 years, and I've moved into the Immunovant CEO role just eight months ago earlier this year. Yeah, my first focus, really the first six months, I think we're there now, I can say with confidence, but was just getting the clinical execution trains on the tracks. This is an enormous amount of clinical activity for a company of Immunovant size to have this many studies start in parallel. At the same time, we had not asked this team to do this much in parallel. There are very few biotechs of this size doing this much work in parallel. So that's been my sort of maniacal focus. I think the first thing on this slide here on the left-hand side demonstrates how that has been effective in that we're able to bring forward that difficult-to-treat rheumatoid arthritis top-line data set from 2027 forward several quarters into 2026. I'll make a little note about that fact, I think, which is a testament to the Roivant model as we've been doing it for several years. It offers us pretty outstanding advantage to be able to divide and conquer and have excellent people spend the right amount of time on the right things. As an example here, there are not many CEOs of public $4 billion companies that do not spend a lot of time with investors. I spend zero time with investors, and I work a lot. That means that I can spend all my time working on this stuff and driving these programs forward. By having Matt able to take the brunt of that work for Immunovant, it's just an incredibly successful execution model that has worked for us. So I'll walk through these three first here. We'll talk about rheumatoid arthritis. We'll talk about CLE. We'll talk about Graves. We'll hand it over to Dr. Lupo, who is a longtime Immunovant advisor, a thought leader in Graves, has a large practice here in Florida. We'll then do a fireside chat with Frank, who's the Chair of our Board at Immunovant, with Dr. Lupo. And then I'll come back on to talk through kind of how I think about the commercial positioning for Graves' disease at more detail before we round out the rest of the portfolio. So this is a slide template you'll see for every indication that I talk about today to orient you. We're going to talk about the kind of target patient population we think we're going after, that we think 1402 is going to be a great option for. We'll talk about the rationale, and all of these are smartly designed, and indication strategy revolves around the likelihood of something working with 1402, and that is principally that it's autoantibody-driven, usually with an IgG subtype being predominant. And then, as Matt said, we always have the angle of deeper is better, and we think efficacy we can win basically everywhere. And when we're first, we're going to be first and best. So for RA, I think the thing to think about here that's important is lots of drugs approved for RA, still a meaningful unmet need out there for late-line patients. When we say refractory to therapies, what we mean and what we've studied in our phase II proof of concept study here is patients that are fourth or fifth line. So they've had multiple exposures to TNF, JAK, a typical earlier DMARD, so very late line. This is actually different. I I think it's an important distinction. We're going to have this data set out next year, so you're going to look for it. And you'll look at the nipocalimab data from J&J that came out. That was an earlier line patient population where only 25% of the people in that study were fourth line or later. So that's in contrast to 100% of the patients in our study will be fourth line or later. So I think our bar, which we'll do work to understand what we think good looks like, but almost any clinical benefit is going to be meaningful to these patients. And as Matt said, when you think about 70,000 patients as the group of people that need this medicine, that are excited about a medicine like this, that can enroll in a trial at varying speeds depending on a lot of factors, like how many other trials are ongoing with competitive agents, etc. But the pace at which this enrolled is a testament to the execution for sure. I don't want to step away from that, but it's also a testament to the unmet need and the patient demand and physician demand for this. To pull a study of this size forward that much demonstrates just how much people need another option after they've been on so many agents. This is a classic autoantibody disease. The ACPA is an IgG positive antibody. We're enriching our study for that. You have to have an IgG positive ACPA serotype to get into our study. It has to be elevated well above the upper limit of normal. So I think we're enriching for a group of patients that will respond there. As we think about the patient group build in a little more detail, RA is a big disease. There's 500,000 people in the U.S. who have severe RA, even more, over a million who have RA generally. But if you, again, circle that Venn diagram down a little bit more narrow and say who has positive autoantibodies, which is a likely responder for our therapy, and who has been refractory to treatments, that number gets down to a tighter 70,000, which is kind of a sweet spot for us in terms of market size. Moving over to CLE. So CLE is a little bit different. And as Matt said, I think this has got risk attached to it without a whole lot of proof of concept data in mechanism. Not none, though. We ourselves have demonstrated in an open-label CLE study with 1402 that clinical response has been seen in patients after 12 weeks of dosing. But this is another classic autoantibody disease. It's got a nice population base, about 150,000 people total. Half of those people do pretty well on the topicals and antimalarials that have been approved like 50 years ago. But that leaves half of the patient population that needs something new. And our agent, I think, is well positioned to deliver that. Again, it's an IgG autoantibody-driven disease, so it should tee up well. This is the patient build similar to what you saw for RA. It leaves us with about 75,000 people who need a medicine, who need a second-line agent that can work for them. And this, with the dermatologists who treat this, kind of the profile that they tell you they want to see in a product actually lines up really well with what we have in 1402. They want a targeted biologic because the therapies available today are not targeted. They want rapid mechanistic onset of action for us. That's IgG dropping quickly within a couple of weeks, a strong reduction there. And they want to see that the disease can be modified longer term with remission and a well-tolerated drug. So 1402 hits that bucket for this indication as well. All right, so before we get into Graves' in total, myself, I'm going to have Dr. Lupo come up. He's going to walk through how he views this disease and the unmet need. And like I said, he's been a great collaborator for us and a thought partner and a leader in the Graves' community. So Dr. Lupo, excited to have you on board. Thank you. All right. Thank you, Eric. All right. It's a pleasure to be here as a clinician to share my thoughts about Graves' disease over the last 22 years of having treated these patients. The talk is, why are we treating Graves' disease like it's 1950? And by the end of this talk, hopefully you'll understand why I titled it this way. These are my disclosures. I'd like to call out that I'm a consultant and speaker for Immunovant. So a little bit about my practice. I established the practice in 2002 in Sarasota, Florida. It's an independent center focused specifically on adult thyroid and parathyroid disease. There are three endocrinologists, and we see hundreds of patients with Graves' disease. And as we look back, a lot of these patients, over half, are still on antithyroid drug therapy. So of our hundreds of patients we see and follow per year, many of these patients are still on methimazole primarily. When I think about patient phenotypes, we recognize that Graves' disease and thyroid eye disease is very heterogeneous, meaning these patients present in different ways. They respond differently to therapy and sometimes predictable, sometimes unpredictable. If we look at how they present, first, we diagnose Graves' with a measurement of TSH receptor antibodies because that's what we think is mediating and driving the process. And then in our practice, about half of them are relatively mild presentations with small goiter, either suppressed TSH like a subclinical hyperthyroidism or mild overt hyperthyroidism with high T4 and high T3. These patients may have no evidence of thyroid eye disease or mild thyroid eye disease. They have a modest elevation in TRAb levels, and they have usually a predictable response to antithyroid drugs. About 35%-40% are in that moderate category. You see more goiter, higher T4/ T3 levels, more symptomatic. They are more likely to have mild or moderate thyroid eye disease. The TRAb levels tend to be 3x-5x normal. You end up having to change the antithyroid drug a lot more frequently. You can predict that from the beginning based on that initial presentation. Severe cases, which is about 10%-15% of our population, large goiter, very high T4/ T3 levels, a lot of symptoms of tachycardia, insomnia, anxiety, very high TRAb levels, often 5x normal. They sometimes will have thyroid eye disease that's quite severe with diplopia and a lot of pain and other symptoms. They have high antithyroid drug requirements with an unpredictable course. With each of these, there are other factors such as age, less than 40, male sex, or tobacco use that increase the probability of relapse or persistent disease. Clinicians rely on TSH receptor antibodies, not only for diagnosis, but for management. This graph kind of plots out three typical trajectories of TRAb levels over time that kind of mirrors what I just talked about in terms of mild, moderate, and severe disease. If we look at the top line, the smoldering, that's about 20% of patients in this pretty well-documented cohort that was published a few years ago, they have a remission rate of 20%. These patients have persistent high TRAb levels and are very difficult to treat. Just under that is a typical autoimmune disease phenotype. These are patients that relapse and remit. TRAb levels look like they're improving. We take them off antithyroid drugs, and they come right back. It's very frustrating for clinicians, very frustrating for patients. They're on a roller coaster that looks like this kind of waning sine wave that you see in the middle. That's about 38% of patients with about a 38% probability of remission. The bottom line is how we want patients to behave. Those are the mild cases with predictable response to antithyroid drugs. That's about 40% of patients, very high remission rate after cycle one or one 12 months-18 months of antithyroid drugs of 90%. As a clinician having done this for 20 years, if I can see some of these patients in the top two curves be shifted to a predictable response curve, that would be a paradigm shift for the way we manage and treat Graves' disease. Why do we care? What's the consequence of uncontrolled Graves' disease? The primary thing we think about as endocrinologists is cardiovascular. Atrial fibrillation. Everyone here knows about atrial fibrillation, either personally or with a family member. So we know there's a higher risk of stroke and death with atrial fibrillation. We don't think about it as much, but we clearly see with hyperthyroidism, high output heart failure, which can lead to morbidity and death, and increased clotting factors, which increases the risk of strokes and blood clots, pulmonary embolism, etc. So high stakes there. Bone loss, which can cause osteoporosis and fractures, especially in postmenopausal women with hyperthyroidism. Thyroid eye disease, so vision threatening, that would be the most severe form of thyroid eye disease. But these patients have severe proptosis, diplopia, a lot of psychological stigma, difficulty driving, difficulty working. Other quality of life impacts that we commonly see are anxiety, insomnia, muscle weakness, tremor, infertility. Often these patients are treated for anxiety or depression well before their diagnosis of Graves' disease is made. Looking specifically at atrial fibrillation, this was a large registry data of almost 600,000 adults with previously no atrial fibrillation, previously normal thyroid function, looking over time by TSH level. This goes from left to right. As the TSH goes down, the incidence risk ratio of atrial fibrillation increases. The increase for subclinical and mild subclinical and overt is in that 1.2-1.4 roughly risk ratio or hazard ratio. That's pretty consistent with what we see with other cardiovascular risk studies in patients with hyperthyroidism. 20%-40% increased risk there. This may be more impressive: fracture risk. Looking at this meta-analysis with a high number of patients looking specifically at any fracture for a TSH less than 0.1, twofold risk of any fracture, and then at the bottom, lumbar or spine fracture, a TSH of less than 0.1, the risk is three- to fourfold the regular normal population. This is high stakes for these patients. We need to think about how we're treating them. Why are we treating them like it's 1950? Because it's been 75 years since we've had an approved drug for Graves' disease. That's when methimazole was approved by the FDA in 1950. Reviewing the three treatments, we can give antithyroid drugs, which inhibits thyroid hormone synthesis, or we can destroy the thyroid, either surgically remove it or give radioactive iodine to cause thyroid dysfunction or destruction with radiation. These are our tools that we've had for 75 years. That's why we're treating it like 1950, because same toolbox. But as we look at clinician surveys on how we use these tools, there has been a big change over the last 35 years. This is a survey sent out to endocrinologists saying, how would you first-line treat a patient with Graves' disease? In 1990, about 70% would respond with radioactive iodine. That's when I was in med school. That's how I trained, was radioactive iodine. But as you start seeing this shift, you see 90% first-line therapy. Now the preference is antithyroid drugs. Surgery is always an option, but stays as a low percentage of patients being treated first-line. But if you look at that shift now in 2023, and 90% of patients being treated with first-line antithyroid drugs, and as we'll talk about, the remission rate's about 50%, you end up with a larger pool of patients who have not had definitive therapy like they did in the 1980s, 1990s, and 2000s. And now they're on these cycles of antithyroid drugs, often with a non-predictable response. So we've seen it in our practice. More and more patients are not interested in destroying their thyroid with radioactive iodine or surgery. So more of them end up on long-term methimazole, but over half of them still don't achieve a durable remission. When we talk about definitive treatment discussions, this is usually a discussion when patients are not tolerating the antithyroid drugs, either due to side effects or rash or whatever other issues they have, or they have a very unpredictable response or requiring high dose, or they get tired of it. After a few cycles of antithyroid drugs, they say, "Enough is enough. Just take my thyroid out and let me be on levothyroxine." The options for knocking out the thyroid would be radioactive iodine, but we have concerns with that. We see an increased risk of thyroid eye disease. We see increased TRAb levels, especially in reproductive-age women. That can be an issue because those high TRAb levels cross the placenta and can cause fetal and neonatal thyroid dysfunction. Radiation exposure is an issue with a slight risk of increased solid tumors down the road and permanent hypothyroidism dependence on medication like levothyroxine. Thyroidectomy, there are certain indications. If we have a thyroid cancer with Graves' disease, it makes sense to take the thyroid out or a large goiter or patient preference. But interestingly, when you look at the data on thyroidectomy for Graves' disease versus thyroidectomy for goiter or low-risk cancer, we see a higher probability of hypoparathyroidism, which is very difficult to treat, low calcium in the absence of parathyroid hormone. We see higher risk of postoperative bleeding, hematoma, higher tracheostomy requirements. So this really demands a high-volume surgeon with expertise in Graves' disease. So this is a high-risk proposition to send someone for thyroidectomy. Certainly, there's a scar, which is concerning, and again, resulting in permanent hypothyroidism. I don't see permanent hypothyroidism as a cure for Graves' disease. You're trading one problem for another. Quality of life after definitive therapy. Hypothyroidism, no matter what the cause is, Hashimoto's autoimmune or destroying the thyroid, these patients consistently report a decreased quality of life compared to general population. Of course, we have the treatment-specific complications that we talked about. In general, one in four people feel unwell post-definitive therapy despite having normal thyroid labs. They are out of sync with their clinician telling them, "Your TSH is normal. You should feel fine. I don't feel fine." This is a conversation we have with our patients every day. One of the larger studies looking at long-term outcomes was 2,400 patients with Graves' disease. Over half followed for a mean of eight years. With antithyroid drugs, the remission rate was 45%, with radioactive iodine 82%, surgery 96%. And for patients who failed first-line antithyroid drug, if they went on to a second course in this study, a 29% remission rate. So once you fail course one, you're setting yourself up for a lower probability of success with future cycles of antithyroid drugs. And if you focus more on antithyroid drug population, 50% had a chance of avoiding definitive treatment. So that's why we sometimes use antithyroid drugs is to avoid definitive treatment. That was flipping a coin. And 40% have a chance of achieving a chronic euthyroid state. And overall, 25% did not feel fully recovered long-term, no matter how they were treated any of these three ways. So thinking back about that survey, that reminds us that now 90% of patients are being treated with first-line antithyroid drugs. The question is, why are we choosing that? Well, it's hope for remission and avoidance of hypothyroidism. That's what the clinicians are wanting. That's what the patients are wanting. But the reality of that remission question is we know that 50% of patients with Graves' disease relapse after stopping medical therapy. So you stop medical therapy, we follow for two years. And at the end of that two years, 50% after stopping first cycle antithyroid drugs, those patients will relapse. So what happens to them when they relapse? Most of them will go back on antithyroid drugs, again, increasing that pool of patients who are on cycles of antithyroid drugs with a somewhat unpredictable response and inconsistent quality of life and health. So looking at this in a different way, a kind of claims-based data, this is over 46,000 patients with a diagnosis of Graves' disease. These are from November 2017 to October 2023. These patients had a diagnosis within three years before or two years after. So the idea was to try to find first diagnosis of Graves' disease, first prescription of methimazole, and then follow them for two years and say, "What does that journey look like?" So this is the journey. And this is a Sankey diagram. So if you're not used to seeing these, it looks a little confusing. But the idea is to take those patients at time zero. They all get started on some dose of methimazole, high, moderate, or medium-low doses, and then they get followed over time. And so following them over time, you see clearly a lot of movement. So that movement reflects the lack of predictability of response to therapy. That movement to the patient means that they're changing doses, they're having more labs, they're coming back to see people like me more often than they want to, and there gets to be some frustration there. These are patients who really are not consistently healthy, and they don't have a lot of other good treatment options. So after one year, 46% of patients are still on moderate or higher doses of antithyroid drugs, or they have had ablation or total thyroidectomy for their disease, and then so when we look at this, the thing for me for this Graves' is that the top 4%-6%, so 10% of patients are still on 15 mg or more at the end of one year. And if you look at the 35% that stopped after one year, we don't know a lot of those were going to end up resuming after in second year, but 25% of those, another almost 10%, end up with definitive therapy. So at the end of one year, we're seeing 20% of patients still on high-dose antithyroid drugs or who have committed to definitive therapy. So this is a frustrating journey for patients and for clinicians. When we look at current recommendations for the management of Graves' disease by the American Thyroid Association, we usually give antithyroid drugs for 12 months to 18 months. We measure TRAb levels. So TRAb is central to the way we make decisions on managing these patients. If TRAb is normal and they're euthyroid, we stop antithyroid drugs. But remember, half the time they're going to recur. So if they relapse, then they end up, most of them going back to long-term therapy, cycling on or off, or radioactive iodine or surgery. But if after that 12 months to 18 months, they still have positive TRAb levels, then they stay typically on cycle two or continued antithyroid drugs. So arguably, there's an unmet need in Graves' disease. We know that the standard of care is to destroy the thyroid or to slow the thyroid down. In other words, we're targeting the innocent gland where the underlying pathology is an autoimmune problem. So we know current therapies do not target the underlying autoimmune disease. A significant portion of patients respond to antithyroid drugs. Up to 25% are unable to complete their initial course due to side effects or unpredictable response to therapy. And 50% remit after stopping antithyroid drugs. And positive TRAb levels are highly associated with relapse rates. So these TRAbs are driving the process, and it makes sense clinically to lower TRAb levels to help these patients hopefully have a higher chance of remission and be able to come off antithyroid drugs. So the rationale makes sense for treatment with an FcRn blocker for Graves' disease. So these are pathologic IgG autoantibodies of stimulating the TSH receptor. And the FcRn blocker would then, instead of escorting for recycling, the FcRn is blocked. So then those TSH receptor antibodies can be degraded in the lysosomal process and therefore lowering pathologic TSH receptor antibody levels in the blood and then therefore decreasing the stimulation of the thyroid gland. So clinically, this makes sense. It's an unmet need. And doing this for over 20 years, and it's exciting to see potential future options for these patients. So I thank you for your time. Hey. Hey. Thank you. Okay. Okay. We've got a nice fraopportunity now to just have a little discussion with Dr. Lupo and kind of give us a little bit more informally some of his insights from the field. I wanted to start with kind of an easy one, but you've mentioned that there hasn't been anything since 1950. What's your feeling about, when you talk to your colleagues, the excitement for a new mechanism and their kind of view of that? Yeah. It's interesting. I mean, there has been some complacency of independent thinking. We can treat Graves' disease fairly well. But as I learn about new options for Graves' disease, the enthusiasm and engagement over the last year or two has been really dramatic. I mean, we've known that TRAb is the driver here. And the fact that we have an opportunity to potentially lower TRAb is a huge shift. So I'm seeing with my colleagues and a definite engagement and interest here that's kind of not something I've seen before in thyroid disease. It's exciting. Yeah. That's great. Yeah. Give us a little bit more of the patient perspective. How are these late-stage patients really doing? How do they feel? How often are they in your office? What's that experience like? Yeah. They're frustrated. I mean, so the ones who the only ones who are really happy are the ones who've tapered off and stay off, and that's that 40%, give or take 50%. But the ones who keep coming back, I have a patient who's a neurosurgeon, and he has Graves' disease. So he's texting me his TRAb levels and with little emojis that are not happy emojis saying, "Why is my TRAb still high?" So patients are getting their labs tested every two to three months. Usually, they're coming back to see me. We're adjusting methimazole doses up and down. So that can be quite frustrating. And certainly, if they've had definitive treatment with the permanent hypothyroidism, they're generally not completely happy or satisfied with that response to therapy. Yeah. Great. And one of the things I noticed when I first started talking to physicians about the indication, and I called some referral academics about this, is they said, "Hey, look, if I treat with super high doses of methimazole, right, I'm going to get people into remission." Right. And does that really happen in real life? And kind of how do you think about those really, really high methimazole doses? Yeah. The idea of driving patients into remission with very high dose, just we haven't seen that play out. So first off, the doses that people maybe state when they have that comment, that 30-mg to 40-mg dose or more, I almost never see anyone starting that. I almost never start that. So usually, the doses are less than 20 mg. So no one's using that. And the studies have not shown that higher-dose antithyroid drugs drive these patients into remission. You may be able to control their hyperthyroidism, but they have more side effects. So higher antithyroid drug doses have more specific side effect probability. So it actually becomes more dangerous to be cavalier with that concept. Yeah. And I think that's a nice segue maybe into just thinking about these side effects. And we see them in the label, right? There are black box warnings for a lot of side effects, and these are old drugs. But what's your real-world experience, you and your colleagues, of these severe side effects? Yeah. Let me anecdote about a colleague. I have one colleague who had a thyroid-only practice, and he had one young patient with agranulocytosis. That's our most severe side effect for antithyroid drugs. This was with methimazole. That means your ability to fight bacterial infections is zero, almost like a chemotherapy patient. And that patient died because of that. Then categorically, he would never give antithyroid drugs, which I understand. But I've seen that happen as well. I've had patients hospitalized for low white blood cell counts and have to get G-CSF to stimulate the white blood cell count production. And those are very nerve-wracking situations. These are real issues with antithyroid drugs, especially if you start using higher dose. That percentage goes up to almost 1.52% at high dose methimazole. And that's a big deal for those patients. Also, liver toxicity is a big deal. With PTU, it can be irreversible. It can lead to hepatic failure and death. With methimazole, usually it's reversible, but these are real major side effects that we have to discuss with patients on a regular basis. Yeah. Good. And as we think about where this might be used clinically, how do you think about it kind of sitting in front of thyroid eye disease? And kind of what is the relationship you see between Graves' and thyroid eye disease? Yeah. Thyroid eye disease is an extrathyroidal manifestation of Graves'. And the way we look at it pathologically is that that means that the TSH receptor crosstalk with IGF-1 causes thyroid eye disease. So if I can lower TSH receptor antibody levels, then more likely than not, I will probably impact thyroid eye disease, especially in patients who currently don't have thyroid eye disease or have mild to early moderate. That will probably change the course for them. So I see, if you look at my phenotypes that I presented, if I have a fairly symptomatic moderate or severe patient with high TRAb levels and thyroid eye disease, and some of these patients will present with tachycardia or atrial fibrillation, I need quick control. So I think having a newer option for quick control would be very welcomed. Yeah. Great. And maybe talk about both quick control, but also kind of long-term control. And again, kind of back to that patient experience, but is this really happening? Do you feel like you get patients into good long-term control? Yeah. So. Yeah. So. Especially in this kind of population we're talking about, right? The second-line patient, and I think it's for the group important to distinguish between the front-line patients who come in and get rapidly controlled and then kind of second-line population, which is really our focus. Right. So the rapid control I meant for life-threatening kind of arrhythmias, things like that, mediated by thyroid, but for the second line, so yeah, these patients are not consistently well controlled, so only in studies that are very closely engaged with patients can you get a long enough long-term antithyroid drug therapy where your remission rate goes down significantly. In the real world, what's happening is these patients are coming on and off antithyroid drugs with a lot of unpredictable response. So I don't think that even with some of the data on long-term antithyroid drug looking good, the reality in the average community practice, the average patient is not getting that tight control, is not following up consistently, and so I don't think we're back to that 40%-50% control rate. Yeah. Good. And And then you've had an opportunity to present this data in the clinical community, especially kind of coming out of ATA and showing some of that off-drug remission. Yes. Can you talk about just qualitatively, how was this perceived before that data? How was it perceived after? And how are people thinking about it? A game changer in terms of the audience engagement. So when you talk about we might have something that can lower TRAb levels and maybe we can get some patients off antithyroid drugs, at least for the short term, it's like, okay, there's some excitement there. But clinicians always want to know, is this durable? Is there going to be a remission? So when the ATA data was released on a short remission with these patients, the engagement shifted completely. Because now you take and we're not talking about the average Graves' patient. We're talking about hard-to-treat Graves' patients, and you're getting them off antithyroid drugs and off therapy and still in remission six months plus down the road. That's a very enthusiastic acceptance from the community. So we want to see more of that as clinicians. Great. And then just thinking forward then, if that data were to be replicated in the pivotal studies, how do you think about in these kind of hard-to-treat patients, where this would fit into your treatment paradigm, where you'd use it, and kind of what patients you'd kind of start with? Right. So I think I'd use it first line for the higher-risk patients potentially. And then certainly would use it for patients who have failed first-line therapy of antithyroid drugs. As we've talked about, the appeal of definitive treatment with surgery of radioactive iodine has really gone down both with clinicians and patients. So I think there's going to be a lot of interest in patients who are now on cycle two or three of antithyroid drugs saying, "I need to do something different." And then I've got multiple patients on cycle three, four, five who I think would be excellent candidates for it as well. So if I look at my population who I have a small amount who've had definitive treatment, most of mine either went into remission in that 30%-40%, or they're still on antithyroid drugs. And I look at the burden of disease, even above five or more milligrams of methimazole. Those patients, once you're on more than five, I know they're less predictable than the patients less than 5 mg. So if I've had someone on 7.5 mg- 15 mg, for example, on cycle two, three, I would certainly want to offer them something different. Great. Yeah. Good. Well, thanks again for your coming to speak to us today. And I know it's a nice opportunity to meet some of these investors and engage in this forum. We really appreciate your insights and willingness to help. Thank you. Happy to be here. And you're welcome. Thank you. Thank you. Thanks, Dr. Lupo. Appreciate it. Thanks, Frank. All right. Thank you, Dr. Lupo. Thank you, Frank. That was great. So I will make up a little bit of time here, probably. We're a few minutes behind, but most of my content is new. There's a few slides that will be redundant to Dr. Lupo, so I'll kind of move through those more quickly. So this is one of those. The punchline for this slide is Graves' disease is not fine. It's not okay at all. It's beyond Graves. You have other complications. You'll develop morbidity, mortality. It's a bad disease that leads to worse diseases down the line. So there's a huge unmet need. On the right-hand side of this slide, TED is talked about. You're probably very familiar with TED, with TEPEZZA doing great. TED is on the spectrum of disease of Graves' disease. I think that sometimes is missed. You don't get TED without Graves' disease. Okay? That is how this works. You have bad Graves' disease for many years, and you develop TED. 40% of people with Graves will develop TED in the course of their life. So this is if we can control Graves' disease upfront, oh, wait, a step in front of that actually and have it be a huge impact on patients' lives down the line. So this, I think I want to hit again. Dr. Lupo hit on this a little bit. This is let's just walk left to right here. This is a patient journey with Graves' disease. Okay? I'm a 40-year-old man. I get diagnosed with Graves' disease. It's a peripheral blood test. I feel like crap. I went to my physician, TRAb positive. I have Graves' disease. What happens is, as Dr. Lupo said, no more are we doing huge percentages of surgery, thyroidectomy, ablation. Most people, 90% +, are starting on antithyroid medicine. For some percentage of those people, that is just fine. They do well. They're able to get off antithyroid drugs. They go into remission, and they're okay. The bottom right here, this is the red line, the red dashed line. This is our patient target population. Okay? 25%-30% of these people after that first line do not do well and need something else, and Dr. Lupo mentioned that extensively, so that's the group I want to double-click on for the next few minutes and really explain kind of what's happening with that group, so this is what that group is dealing with. Okay? They've been on antithyroid drugs for a couple of years. It's not going well. They're not controlled or they're relapsing and flaring like Dr. Lupo said. Dose changes, labs are out of whack. We have definitive therapy as an option, as he mentioned. I just find it hilarious that we talk about that like it's a reasonable option. You have hyperthyroidism, and so your solution is that you're just going to destroy the thyrocytes, take it out of your body to sentence you to a life of hypothyroidism forever then. You're treating one thyroid problem for another, and it's the same situation. You take levothyroxine. If you don't know about how that's managed, there's 20 doses of levothyroxine. You do the same thing. You go in with your thyroid function tests. It's a little bit off. You tweak it. You're taking 88 mcg. You're taking 75 mcg. You're taking 108 mcg. It's a mess. It's all the same, and the patients aren't doing well. So that's not great. Okay? So no one's picking that, and we know that. The chronic ATD use issue in the middle bucket is you can stay on this stuff forever. As Dr. Lupo said, the patients who are not responding well upfront tend to need longer duration and higher doses of methimazole to get their Graves' under control. Then the risk-benefit calculus shifts away from something that you're interested in, and it doesn't make sense. You want another option. The only option we have right now is that definitive therapy on the left pillar. And that's bad for all the reasons we talked about. So that's the issue here. And on the right-hand side, you got to do something. These patients are going to get sick. They're going to have cardiovascular disease. They're going to have bone health problems. They're going to have issues. There's a huge unmet need here, and we are sort of positioned to totally deliver it. This is a slide that I want to focus again. We're double-clicking here to understand who is the patient population that we have that is going to be a great candidate for 1402. This is a five-year look and a snapshot in time. On the left-hand side, what patients do first when they're diagnosed. You can see there's a lot of people on methimazole, some are high doses to get started, medium doses. Five years in, what has happened to those patients? The top red dashed bucket is a different version of the red dashed bucket on the slide before. That is the percentage of patients that had to revert to a thyroidectomy or ablation, are still on uncomfortably high doses of methimazole at that period of time, who are going to be again recommended to consider definitive therapy. This is the group of patients that Dr. Lupo and his colleagues, and I'm in the field every week meeting our investigators in person and talking to docs at conferences. This is who they're saying, "1402 is going to work for these guys. I want to offer them this as another option." It's a big group. So this is just kind of a funnel building to think about the patient population. It's like any disease you think about, you got to think about the incidence market. That's new patients getting diagnosed every year. That's on the left-hand side, and then the prevalent pool, right? Graves' is a little unique. It's not insanely unique. There's a couple of examples of this in the last 25 years. But when there's been no innovation and no new agents approved in three, four, five decades, there tends to be a very large prevalent pool that is sitting there ready to receive the new therapy you have available. That will rhyme with things that you've experienced in the past, things like Hepatitis C. So we have a huge group of patients here that's just sitting here, but it's not everybody, right? There's a million people, 880,000 people in the U.S. with Graves' just sitting there. That group, though, some of them will do okay on ablation. Some of them will do okay with their methimazole. We whittle that down to a few hundred thousand patients who are just sitting there, coming into the clinic every month looking for something else. So that's a big ball of patients we'll be targeting in our first years of launch. On the left-hand side, this is what it looks like on a replenished annual basis. About 20,000 people are going to end up not doing well in the therapies that are available, including hopefully avoiding things like thyroidectomy and ablation and another 20,000 patients there for us that will be great candidates for 1402. All right. So this slide is what Dr. Lupo mentioned about this remission data we presented at ATA in September in Scottsdale. I was there with a lot of our investigators and key opinion leaders. So I'll walk you left to right through this slide. This is batoclimab data. This is FcRn inhibition data that we generated through the course of the last year and presented the right-hand side of this in September. So 25 patients came into this study. All of them had uncontrolled Graves' disease. That means they're on methimazole. They're still not controlled. Most of these patients had very elevated TRAb levels and really fit the phenotype of the commercial population we're thinking about targeting here. So what we did for this study, 12 weeks of high-dose therapy. Okay? The high-dose batoclimab is equivalent to the high dose of 1402 from an IgG suppression perspective. At Week 12, how did it go? It went insanely well. 20 out of 25 of those people were able to get their T3 and T4 normal. So they're euthyroid, and they did not have to increase their ATD dose, and many lowered their dose. I'll show you a slide on that. So that's a great it's an 80% response. That's just an unbelievably positive number. This study, we also wanted to probe the question, as Matt mentioned, is lower better here for us also. We've seen it in MG clearly. We saw it in CIDP clearly. We wanted to look at Graves' too. And so after 12 weeks of high-dose therapy, we stepped people down to the low dose of 340 mg, which is also equivalent to the 1402 low dose. Another 12 weeks of therapy at that lower dose and see what happens. Now, we lose two responders. You say two responders, 20 to 18, not that big of a deal. I think that's wrong. Okay? I think you got to think that number 20 was going to go up if you stayed on that high dose for another 12 weeks. So it's not a loss of two. It's a loss of greater than that. In any case, it didn't even maintain the level of response. After Week 24, this is what Dr. Lupo was talking about when the tone in the room changed. When you say, "Okay, that's great. You've got now six months of therapy, 12-week high dose, 12-week low dose. Let's stop the drug. Let's take the FcRn inhibition away, and let's see what happens to these patients." That's when everybody got really excited. 21 people entered that follow-up period, which was a six-month period off of batoclimab. 17 out of those 21 retained their response rate at six months, euthyroid, T3/T 4 normal, and no increase in their baseline methimazole dose, which is an outstanding level of remission. When you see something like this, what I do as a clinician myself is think, "Well, that looks great. I'd like to see some other data points and evidence that kind of throughlines that together in a way that makes complete sense." As Dr. Lupo kind of talked about, the next two slides will do that. This is the 17 people that did remain in remission at six months off therapy. What did they look like, though, underneath that? Half of them on the right-hand side of the pie chart, 8 out of the 17 were off of all methimazole in total. That really is like the remission standard that Dr. Lupo was talking about trying to achieve. There's guys not on drugs at all. He's not coming in to check his labs. He's in a functional cure at that point. In the bottom left-hand of the pie chart there, you see another 30%. We're on basically the lowest dose of methimazole we have is a 2.5 mg a day dose. So very, very strong, not only in the response rate with 17 people maintaining that, but half of those are able to be off drug at that six-month period. Now, this is the other evidence I wanted to point to. And this is we talked a lot about TRAb, so I won't repeat what Dr. Lupo said, but TRAb is the disease-causing autoantibody in Graves' disease, period. Okay? This is the same study we just talked about. 680 mg for 12 weeks on the left-hand side there in that purple color, stepped down in the salmon color to 340 mg for 12 weeks, and then all batoclimab taken away, FcRn inhibition taken away for another six months of follow-up. That solid line is IgG that tracks over time. We know this works. You guys know these other FcRn inhibitors. Drops like a rock. We get 80% reduction, consistent. When you take the drug away, we also know this. The IgG comes right back up to baseline. So at the end of Week 48 there, these people's IgG has returned. What is interesting here, obviously, and this points to how the mechanistic rationale is working for this achieved remission, the TRAb dropped like a rock also. TRAb, I think Dr. Lupo mentioned this, but it didn't. TRAb is an IgG antibody. It is about 90% IgG1 and maybe 10% IgG3. We do not have any sensitivity around IgG subtypes. We just suppress all IgG subtypes equally at 80%. So TRAbs come down like a rock here too, but when we stopped batoclimab at Week 24, TRAbs stayed suppressed. TRAb is the indicator for us that we think about when you're likely to go back into remission. Are you likely to or to recur? I mean, are you going to stay in remission, and this as a marker just mechanistically makes complete sense for us as we see why these patients are able to stay in remission and what is so exciting, I think. So look, this is kind of a recap of there's a lot of information. I'll just give you a recap of what I just said. So let's go through it quickly. First-in-mechanism data for Graves' disease generated by us earlier this year with batoclimab. Remarkable efficacy seen with 18 of 25 patients hitting clinical response in euthyroid after six months of therapy. Off of drug, an unbelievably high-quality remitted benefit shown here where, of the 21 patients that rolled over, 17 remained disease-free after six months off of batoclimab therapy. This is a disease-modifying thing. No one else had seen this. Of those 17 patients that were responders at six months, half of them were off of their methimazole and truly in the early stages of remission. One note in bullet four here, the step down for the batoclimab study was six months of or sorry, it was three months of 680 mg and then three months of the lower dose. Our pivotal studies that we're enrolling right now globally for 1402, it's just the high dose for longer. So I think the efficacy in those studies should even be better because you're dosing higher for longer, and we'll see that translate or we should. As I just said, we've got two registrational studies globally active now with lots of screening and enrollment happening, and it's off to a great start. Okay. That is Graves, which is super exciting. We're thrilled about it. Dr. Lupo, thanks again for joining us here. I want to pivot to the rest of the pipeline quickly. We have a lot going on. These are the places where we won't necessarily be first, but where we really do think we will be best. I'll talk through those. These three indications, most of them you'll be familiar with. MG, massive market as Matt said. CIDP also growing quickly with the FcRn class approved now. Sjögren's disease is one that has in-class data from J&J and nipocalimab. Not an approved agent yet, but I'll walk through each of these in turn with our similar formatting from before. Sjögren's is interesting, I think, and maybe one of the most interesting things about it is that there seems to be a huge amount of patient interest. This is an enrolling study for us, also enrolling ahead of our expectations in terms of timeline. It's a pretty bad disease, though. It's a classical autoantibody-driven disease. It's the lacrimal and the salivary glands that are unable to do what they're supposed to do when you think dry eye, dry mouth, whatever. Unfortunately, that's not how it works. You're going to have cavity problems, teeth problems. You're going to have eye infection problems. It's going to be bad for your quality of life. There's about 300,000 people with primary Sjögren's disease in the U.S. If you slice that as we always do, and I'll build the next slide, we'll build this autoantibody-positive people who are moderate or severe. That number is going to come down to about 90,000, which again is in that nice sweet spot for us. This is a classical autoantibody disease, as I said. And this is a place where actually we already do have in-mechanism data to support the deeper is better concept. We have not generated that ourselves. The slide Matt had up before was actually Immunovant data from Immunovant studies. But nipocalimab, the J&J data that put out shows clearly that deeper IgG responders lead to more autoantibody reduction and more clinical benefit. This is the build that you've seen, as I mentioned, I think a few hundred thousand people here. But if you focus on the most likely to respond to this therapy with positive autoantibodies as well as people who are moderate to severe, you get that patient population down to about 90,000. Sjögren's, look, there's a lot of things in development for it. There's nothing approved right now. Zero agents approved. It's still kind of high-dose steroids and really junky stuff. Moving to MG, I can be quick here. You guys know this market. It just works well clinically, we know. The one thing that I would say is that I do think the commercial picture is shifting from a physician expectation perspective around what is the unmet need, what do you want. This MG-ADL few-point reduction is no longer what the neurologists are talking about. They want to see MSE. They want to see really total symptom control. As Matt talked about, that's one of the cuts we did in our phase III studies for bato where we see just a much better rate of MSE achievement in that higher IgG reduction pool. I think we are going to come in with a best-in-class on efficacy, able to deliver where the physician community and the patient community is moving, which is to get MSE up and up and as the core measure of success. Won't do the build there because you guys have seen it. Then for CIDP, again, I mean, early uptake is great with Vyvgart. I think there's a huge unmet need here. There's not a lot of good agents. This is a tough disease. It's a smaller population, probably closer to 15,000 that we think are good candidates for 1402, but a meaningful population still driven by an autoantibody. Again, clinically very de-risked with the in-mechanism approval already and clear evidence that deeper is better here. You saw this before from Matt. I won't belabor it. This is just a very rich catalyst period. Every year now is going to be a big year for data at Immunovant. So it's exciting. And then I hit on all these points about 15 x. So I think I'll leave it there, and we can have a Q&A. Mark's going to join us up for this too, so later. Yeah. Yeah. Good. Great. First question goes to Yasmeen. Thank you so much for the great presentation. First question is for a physician with thoughtful remarks. You showed that beautiful curve where a patient who is on anti-thyroid medication sort of goes through these peaks and valleys of response and lack of response. That kind of creates a little bit of a fear among investors given this is a placebo-controlled study. So help us understand how could we control that to make that we don't capture patients who are at full response? And what would be an acceptable placebo response? We get that question a lot. And if I might squeeze one question we get also is the work that you guys have done in terms of understanding the TAM. A lot of times we try to get the repetitive question, is this really the market? And how do we know? I'll pass on the mic to my next colleague. Thanks, Yasmeen. Those are great questions. I'll hand it over to Mark to take most of them. Look, obviously on trial design questions, it's an Immunovant study. I can say I think we feel confident, but maybe Mark, you could speak to it as well. I guess even for those patients in the middle, maybe to reframe the question, how likely is it that those patients with kind of waxing and waning disease would be able to see normal thyroid hormone levels and get off anti-thyroid drugs as a part of regular way treatment? Right, so it's important. The inclusion criteria was set up to look at patients who were less likely to have those nadirs of TRAb levels and less likely to spontaneously go into remission because these are patients who had been treated for a long period of time with high-dose methimazole with high TRAb levels. So yes, you'll see a placebo response, and that might be in that 15%-20% range. I would expect, as a clinician, that has nothing to do with the data. We don't know that yet, and that would be maybe reasonable, but overall, it was designed to try to tease out that very question of by picking not all Graves patients, but patients who are harder to treat who are less likely to go into remission spontaneously. I know you had two other questions in there as well. I think the other question was just on TAM. Market size. Market size. Market size. Thank you. People say, "Do you believe those? Is it really that big? Yeah. Do you have those patients in the real world? Yeah. It's not what I think about every day as a clinician is market size. But if I look at my market and think about if we have 1,000 patients with Graves' disease at any given time and the three physician practices that treat thyroid, we probably have 500 or 600 on cycles of anti-thyroid drug, and probably half of them would be candidates for this. I think the percentages align nicely with what we're seeing clinically in Graves' disease. Thanks, Dr. Lupo. The one comment I would make just about the placebo question too. I think the trial's designed, and this is in there, so you can read this, but we are pushing, and there's a grid guideline and phone calls and conversations to titrate down the anti-thyroid. Everyone will attempt to titrate down. If you really are a sick Graves' patient and we titrate down your meds, you are not going to be okay. So I think placebo could be driven quite low as long as we do that titration well. Next question is from the web. Thomas Smith from Leerink. Congrats on all the progress for Immunovant. Now that we're expecting potential registrational data for IMVT-1402 and difficult to treat RA in 2026, can you comment on how you're thinking about the path to registration in this indication? Particularly interested in your thoughts on FDA's recent comments suggesting a move to requiring one phase III study rather than the historical requirement for two in many settings. For Immunovant 1402, are you still planning to report period one data from difficult to treat RA study prior to full top-line results? And if so, can you help frame your expectations for the period one readout? Thanks. That's a great question from Tom. Look, I think first of all, I've gotten a lot of questions this year on how we feel about our ability to do things in light of the changing policy landscape, and my answer is always, I feel like all we know about the policy landscape is like a couple of tweets, and so the tweets just aren't completely clear on this point, but look, I think you can imagine we will be aggressively looking at any change in guidance to figure out whether the existing program allows us a faster path to registration, especially now that the studies come in. On reporting, I think I'll say we just haven't decided yet now that we're going to get the data within the course of 2026 whether we're going to change how we talk about the data, but we'll be thinking about that as well. I'll say on D2T RA, and Frank or Eric may have comments on this too. I'll say a piece of work that we are doing very actively right now is frankly setting our own expectations on what good looks like in a population that is very understudied. There are not that many studies in patients who have failed both TNFs and JAKs or TNFs, JAKs, and IL-6s, all three. So the response rates that people are used to looking at in other mechanisms for other categories of RA patients are not the relevant benchmarks. I think let alone your collective expectations outside of our four walls, we need to give some thought to just what we're hoping to see before we flip over that randomized trial card. Anything else, Frank? Just to add, I mean, look, I think back to the FDA for a second. First of all, we have a lot of respect for the people at the agency and the work that they're doing, and the idea that we could accelerate medicines to patients who need them is an incredibly exciting opportunity for us. I think if you think about these kinds of programs, whether it's very late-line RA treatment, whether it's Graves and we've got a 1950-era treatment paradigm, whether it's brepo coming into dermatomyositis, and we've got the longest, largest study ever done in that indication. In all of these things, I think we have the kinds of things to offer to patients and to offer to the agency for discussion that if accelerated paths exist, and that's an if, but if they do, we're going to avail ourselves of those. I think that we have the kind of clinical data and kind of unmet need that would put us in a good position for those conversations. Yeah. And I do think for the refractory RA group, specifically our fourth and fifth line, remember this is very different from what you've seen. This is not the second study. This is one of two pivotals that we have here. The second study, it's not going to be some 800-person massive. This population is small. This is the kind of population like can get breakthrough designation. It's that small and not refractory. So it's a different thing than what you've seen out in the marketplace for rheumatoid arthritis. This is a pretty refractory group, uniquely so. Great. Thanks, Tom. Great. Next question is from Sam Slutsky from LifeSci. Batoclimab versus TRAbs rebound. Any mechanistic hypothesis for why TRAbs stay reduced following treatment cessation with batoclimab versus rebounding? You definitely but yo u have this. Yeah, more. I'll take that one. So I mean, of course, it's reducing IgG and pathologic IgG antibody recycling. So that's part of it. And if you look at what accounts for the circulating IgG in the serum, most of that's recycling and protecting it from degradation. But so when I see those curves diverge like that and the TRAb is going down, that means that TRAb production has been decreased. So this is beyond a decrease in TRAb recycling. We're seeing a decrease in TRAb production. So we know the FcRn system in part plays a role in antigen presentation. So if you're having less TRAb cycling through, it's less TRAb or TSH receptor antigen presentation. So therefore, less plasma cell production of TRAb levels through that process. So I think there's an underlying secondary process that's keeping that blunt response of TRAb compared to IgG. And I do think, actually, probably less well appreciated, but it is in the public domain. You can see that we actually did reduce the volume of the thyroid gland in those studies until you can actually see a reduction in that inflammatory loop and in fact of the volume of that gland. And that's a gland where the life cycle of a thyroid cell is very long. They turn over 5x, 6x in a patient's lifetime. So if you think about the reduction and why would that gland get smaller, it's not because you're adjusting the actual volume of thyroid cells. It's really breaking that inflammatory loop. And so I think there's good evidence of us doing something fundamental to the biology that supports a long-term durable effect. Just one follow-up from Sam. Dr. Lupo, in your own practice, what percentage of Graves' patients do you envision ending up on a drug like IMVT-1402 commercially? And would patients with mild TED be a particularly interesting population given the difficulty in getting TEPEZZA reimbursed for mild TED? Yeah. I think independent of a reimbursement question, I think just mechanistically for mild TED in patients with active Graves' hyperthyroidism, something that lowers TSH receptor antibodies would be a first choice. So in percentage of patients, I still think we're in that 20%-30% of patients with Graves' disease would be in one of these boxes clinically that we've discussed that would be a good fit for specifically targeting TRAb levels, either due to stuck in this relapse cycle or risk of progression to TED or needing rapid resolution of hyperthyroidism due to AFib or other issues like that. I think that 25%, give or take. Great. I know we're running a little bit behind, so that's all the time we have for questions, and we'll move on to mosliciguat. You want to cut it off there? Great. Okay. All right. Great. Thank you. Thanks, everybody. Thanks, guys. Thanks. You're going to be up. So I'm going to hand it over to Frank, who's going to introduce the next section on Mosliciguat. Great. Matt, how do you advance the slide? How do you make it go forward? Green button. All right, so it's nice to be able to introduce our Mosliciguat program because I think it's a little bit less talked about in our portfolio of programs. But if you think about the potential value, and I think increasingly appreciated value in pulmonary disease franchises, this is a really nice place for us to be playing and complementary to a lot of the kind of thematic work we're doing across the portfolio here. To start with PH-ILD, well, this is a very, again, large actual unmet need, and I think these people with this interstitial lung disease, there's about 200,000 of them in the U.S. and Europe who can really benefit from something new, and this is really a differentiated mechanism of action. We'll talk a little bit more about that in Drew's presentation and also briefly on the next slide. We start with a drug that's already been shown to really meaningfully impact PVR, Pulmonary Vascular Resistance. And when you think about how these drugs work and the kind of physical manifestations of ILD and of PAH, the ability to kind of reduce that vascular resistance really offers an opportunity, especially independent of other pathways, independent of treprostinil and complementary to those pathways, to drive incremental and important efficacy for patients who don't get good therapeutic response. I think respiratory diseases in particular, if you think about the evolution of how PAH has been treated, but even if you go back to how COPD or asthma have been treated, really pave a way for combination therapies, right? These are diseases, whether it's a simple asthma or COPD patient, or even thinking about the way that people have layered on vasodilatory approaches in PAH, that there's an opportunity both for mosliciguat to provide independent standalone efficacy, but also really work well in an environment of combination therapy, and as we think forward to the way this field could evolve, I think we'll bring dramatic and important efficacy ourselves as a single agent, but also in the future work well with agents that are being developed in the class and exist in the class today, so our data is on track. The team has made great progress in that study, and we'll look forward to reading that out kind of later in 2026, but maybe just to give you two framing slides before we turn it over to the team, so what does this drug do, right? If you think about soluble guanylate cyclase, this is a key enzyme in the Nitric Oxide cGMP pathway. And in the existence of particularly ILD, you get kind of a lower oxygen environment. And why is that important? Because this is an activator. And so the activator actually works in a nitric oxide effectively independent way. And actually, in the cases where the heme binding pocket is altered because of that hypoxic state, it can activate the sGC pathway even in that kind of environment. And so that gives us a difference from a stimulator, different from other approaches, really the ability to work in the physiologic environment that exists in these kind of PH-ILD patients. And I think we're really excited about what that can do and how that can drive clinical effect. We've also worked on kind of some of the things that we know matter in respiratory diseases and that, do you have the right particle size? Are you getting distribution to the right parts of the lung? And can you bring the drug to where it matters? And we've already done that work and demonstrated that we can do that. And I think that's important. It's also important to just remind yourself if you're newer to this program. This is a dry powder inhaler. This is not a nebulizer. And so there's just a lot more patient convenience in patients who have a lot of medication burden to bring to them. But I think fundamentally what we want to bring to them is a treatment for a disease that is complicated. When you think about PH-ILD, it really exists in this intersection between lung parenchymal disease and vascular disease. I think Drew, again, will go into this, but I think the ability to focus on sGC activation allows you in this hypoxic state, in this state where you have inflammation, you have maybe some scarring and fibrosis, you have impaired gas exchange. But you also have the kind of vasculature effect that you see in some more traditional PAH. And in that intersecting disease state, to bring both activity and clinical response has been something both our investigators have been excited about. And I think mechanistically we were excited about from the get-go. So maybe with that, I'll turn it over to Drew to dive into the presentation. But we will start, as he's nicely reminded me, with a nice video to kind of lay the groundwork from the patient perspective. In pulmonary hypertension associated with interstitial lung disease, PH-ILD, chronic vascular constriction results from pathological inflammation and fibrosis in the lung parenchyma and surrounding vascular tissues. This can be driven in part by dysfunction of the NO-sGC-cGMP signaling pathway. The NO-sGC-cGMP pathway plays a critical role in vascular function by facilitating vasodilation, reducing inflammation, and reversing vascular remodeling produced by endothelial cells. Nitric oxide diffuses into vascular smooth muscle cells. Once inside, NO engages sGC in the presence of reduced heme, initiating activity and triggering the production of cGMP, a key driver of vasodilation and a mediator of antiproliferative signaling. Optimal function of the NO-sGC-cGMP pathway requires sufficient NO production by endothelial cells and the presence of reduced heme sGC, specifically the ferrous Fe2+ state. Oxidative stress associated with severe cardiopulmonary diseases such as PH results in reduced NO production and loss of heme from sGC, resulting in impairment of the NO-sGC-cGMP signaling pathway. Loss of the heme group deprives sGC of its ability to engage with NO, resulting in significant reduction in cGMP production and hindering vasodilation. Inhaled mosliciguat is a potential first-in-class sGC activator with once-daily administration via inhalation into the lungs. It is designed to directly target the lungs, minimizing systemic exposure and potentially decreasing systemic side effects. Unlike sGC stimulators, mosliciguat works independent of NO and heme by directly engaging the heme binding pocket to activate sGC and trigger cGMP production. Mosliciguat is believed to act by restoring the function of impaired sGC, resulting in cGMP production and vasodilation, even under disease conditions of NO depletion and shifts toward impaired heme-free sGC. Inhaled mosliciguat has the potential to be a first-in-class inhaled once-daily target-directed therapy designed to restore sGC function independent of NO and heme loss seen in the oxidative stress environments of PH and other cardiopulmonary conditions. It's hard to step up after such a great video like that. It's like a mic drop, but it's great to see you all. I want to thank Frank a ton for a great introduction to mosliciguat. At Pulmovant, it's our mission to transform the lives of patients with pulmonary diseases. I figured I'd start today with a look back at where we've come from and where we're going with mosliciguat, which was discovered by Bayer in 2012. Very rapidly after the phase I inhaled data was completed, we immediately in-licensed mosliciguat into Roivant in July of 2023 and rapidly built Pulmovant to be able to announce and unveil mosliciguat in Q4 or Q3 of 2024 at the ERS conference in Vienna. And then very rapidly thereafter, we were in a position to initiate our phase II PHocus study in PH-ILD. We are still completely on track to deliver data in the second half of 2026. We're also going to speak today a bit about our new PHactor study. It's our phase II PHactor study, which is going to be looking at mosliciguat in combination with inhaled treprostinil. I'll go into more detail there. I would just say here that we're so pleased with the speed and quality of what we've done here with this program. I attribute that to the Vant approach at Roivant and also our world-class team at Pulmovant. With mosliciguat's MOA and its overall profile, Bayer decided to move into a phase I study in healthy volunteers and PH patients. Now, I'll start by telling you a little bit about the five WHO group categories for PH organized by disease type, clinical presentation, and also therapeutic approach. Across that, in the phase I study, there were 170 participants. The first group was 132 healthy volunteers in SAD, MAD, and Bioavailability studies, single and ascending dose formats. And the takeaway was that mosli was extremely well tolerated in this group and also had a long 40-hour half-life. Further, the second group looked at in phase I was a 38 group PH set of patients in both Group 1 PAH and Group 4 CTEPH. And this was a single ascending dose format. Same punchline. Mosli was extremely well tolerated and also was clearly very potent. And so what would we expect? And let's just dive into the ATMOS data in more depth here. What would we expect effectively with a potent vasodilator in pulmonary hypertension? That would be the reduction of pulmonary vascular resistance. We saw that very clearly with mosliciguat. With one dose of mosliciguat, we saw PVR drop right out of the gate for the first hour and through the three-hour observation period. Thereafter, we also saw mean PVR reductions of over 30% and mean peak PVR reductions of up to 38%. When you look across single dose and repeat dose studies, it's very clear that mosli is a very active drug. Any way you slice it, it's an impressive PVR reduction, especially for a single dose study. Frank spoke briefly about the importance of cGMP in a couple of different ways, including vascular homeostasis and also vasodilation and the potential to exert antifibrotic and anti-inflammatory effects in the lung. Here again, with one dose of mosliciguat, we saw cGMP rise immediately and sustain at elevations through a 24-hour period. There were no clinically meaningful side effects systemic, including with blood pressure and heart rate. We actually attribute that to the inhaled approach to mosliciguat and the fact that mosliciguat has very low bioavailability in circulation. It's over 95% protein bound. So we would expect to see that localized effect of mosliciguat. Also, with cGMP production like this, we would also see other hemodynamic parameters kick into gear. We saw that with mean pulmonary arterial pressure and cardiac output. With one dose of mosliciguat, we saw mean pulmonary arterial pressures reduce up to 20%. With cardiac output and the strain coming off of the right heart, we saw cardiac output go up as much as 25%. I think what I would say here is all of this culminates into what you saw in the last couple of slides, a real intensive drive down of pulmonary vascular resistance, which is very important to the ultimate efficacy of these patients, and mosli was very well tolerated, as I mentioned before, both in healthy volunteers and PH patients and also across doses. We saw that the reported treatment emergent adverse events were mild to moderate across doses and patients. We know that cough is a major issue for PH patients, and in fact, we also know that the inhaled treprostinil drugs today can exacerbate cough in these patients upon administration. We did not see that with mosli in the ATMOS study, and further, we saw very limited systemic bioavailability, which ended up impacting very limited aspects of the periphery and in circulation. Again, blood pressure hardly being affected at all. And that's really important given understanding this entire environment. So with data like this, what do you do in phase II? Well, we were extremely focused on picking the right indication going forward. And we looked at a host of indications that lined up very nicely with mosli's attributes and also had a large population, but in particular with an unmet medical need. And if you look at PH-ILD, that came to the top of the opportunities over and over again as we were looking early and ongoing. The reason, the lung is the primary site of disease, high dosing burdens for these patients with treprostinil administrations today. Current therapies are not well tolerated. In particular, cough is a major issue. Last but not least, we have the lung parenchymal disease and the pulmonary vascular disease, which comorbidity becomes a very big challenge. Mosli lines up beautifully. You have an inhaled med once-a-day administration, well tolerated, especially not seeing that cough that we're all concerned about. And then with cGMP production, the ability to address both the lung and the pulmonary vascular side of the disease. To dive deeper into PH-ILD, it's got a huge medical unmet need, and I'll speak more and more to that. Up to 200,000 patients in the U.S. and Europe. We believe it continues to be underdiagnosed because of the limited treatments available to these patients, but also diagnostics and also treatment paradigms are catching up now to the treatment of these patients. These patients are fragile. They have less than a five-year median survival, and PH-ILD is a really tough disease. I'll also say that the comorbidity of PH and ILD is worse than PH and ILD separately and alone. So those two together create a real issue for the duration and the prognosis of these patients. And there are very limited drugs on the market. There are only two FDA-approved drugs. They're both inhaled treprostinils, and I've already gone through a little bit of that background, and we'll do that now. As we take a look at a bird's eye view of what's going on in the heart of this development arena, you can see the three light-colored boxes up on the top are three inhaled treprostinil drugs. Two are already approved, Tyvaso very recently, Yutrepia, TPIP just going into its phase III, and seralutinib, which is a TKI, very different kind of drug. I can have you look across this grid, and it'll bring your eye right back to mosliciguat, which is where we're heavily focused, and the reason is we're in a great position to differentiate from all of these other drugs over time, but in the end, with our mechanism of action, once a day, simple inhaled daily dosing approach, and then the tolerability that we have here, and also the PVR reductions, which over time will inure to the benefit of the patient via efficacy, we believe, is something that we believe will drive the standard of care in this arena, and the last thing I'm going to say about the PH-ILD market specifically is we've seen a market that's very nascent. Over the last three years, starting with Tyvaso being approved in 2021 as a nebulized formulation or administration, and then going to a DPI, we see the great demand here that has driven this one drug out of the gate to a billion-dollar blockbuster status. And again, I'll remind you, only inhaled treprostinils are available in this space. And I will say, and I don't know how often I'll say this, we really do agree with United Therapeutics that this is the tip of the iceberg for this group here. And I'll be clear that I think it's actually larger than even what they're saying. So this was a point where I felt and our team felt we could bring some real context to another market that we believe PH-ILD may mirror going forward. And effectively, that's the growth of an evolution of the market around pulmonary arterial hypertension. If you look at the key treatment pathways and median survival, and then ultimately the PH guidelines that supported all this, we started over 30 years ago with supportive care for these patients in PAH. It's ironic because that's exactly where we are today with PH-ILD. With very few drugs available across the globe, many of these patients move directly into supportive care or go on drugs that really are not giving them any benefit. Over the ensuing 30 years, we saw this evolution of drugs coming in from IV prostacyclins, then through numerous additional mechanisms of action, and over time, combination therapy came together as those mechanisms proved to be powerful also together, and at the same time, treatment guidelines kept pace and supported each of these stages of this evolution. But the great punchline here for patients is we went from approximately three years of median survival in the early days to now over 15 years of median survival for these patients in PAH. And as I stated, we're now at a large market. We have a $7 billion market growing at 20% year-over-year. There are literally 15 drugs approved, and it says something about the unmet need. It says something about the difficulty of pulmonary hypertension. But also at the same time, we've seen some of the earlier classes start to become generic. But yet, I will say we have not seen, or let me say it in a positive way, we've seen a very robust pricing environment. And the reason for that, again, is this is a hard drug to treat, a hard disease to treat. You need multiple mechanisms. Combination therapy is the norm, and the pricing supports that, and it continues to grow as I've described. The punchline here is 40% of patients begin today when they're diagnosed with dual therapy. By the end of that first year, 15% more of those patients will go on another drug and have triple therapy. And that is the norm. I understand that PH-ILD is a different disease. I actually believe it's a complex heterogeneous disease where this kind of increase in mechanisms of action and the need to do combination therapy over time will also become similar. But with a drug that has great single-agent activity, we're going to be in a great place in this early part of the market. So bringing us back to where we are today, we're looking at our phase II PHocus study. We're in Group 3, PH-ILD, just putting it back in the WHO group designations. Our phase II PHocus study, which we effectively initiated in the second half of 2024, is a study of mosliciguat in adults in PH-ILD. It's a placebo-blinded, randomized study, double-blinded study. When patients come in and they're screened by the investigators, the most important things that we look for here, although there are other inclusion and exclusion criteria, is a clear diagnosis of ILD, elevated PVR, and then limits on fibrosis and emphysema as seen by CAT scan. Once these patients are eligible, they move into the study and go through a rapid up-titration and get to stable dose, and then move forward to the 16-week endpoint analysis where we look at the endpoint of change from baseline PVR and then secondary endpoints of change from baseline 6-minute walk and NT-proBNP. These patients move on to Week 24, all go on drug if they were not on drug already, and move into an elongated long-term extension, which is a really important thing for these patients to get the opportunity to get on the drug. And then I mentioned earlier the phase II FACTOR study, excuse me, of mosliciguat in combination with inhaled treprostinil. This is just beginning to be opened. It's an open-label study in 20 patients with the objective of looking at tolerability and safety primarily as we put an eye towards the end of our phase II PHocus study in the second half of 2026 and thinking about the design of our study in phase III for mosliciguat. So to wrap up, we're really psyched about mosliciguat. I'm excited that Roivant brought it in. I think we have an excellent opportunity here. It's a very early market. As you saw with the PAH market, we're really on the front end of this market. This is a great opportunity for PH-ILD patients. Mosli may be the second drug approved after inhaled treprostinil formulations or administrations. And we keep coming back to mosli's overall profile with an excellent mechanism of action, a simple once-a-day inhaled administration, and then seeing that it's well tolerated in important things like cough coming out of the ATMOS study. And these deep PVR reductions will be an important element of how mosli evolves over the coming years. Top line, again, for mosliciguat should come in from our phase II PHocus study in the second half of 2026. I personally, and I think the team believes that this could be, with good data, a real de-risking opportunity, not only across the PH-ILD area, but given mosli's profile, much more across the pulmonary disorder arena. I believe we'll be in a position to really drive the standard of care in this area. I'll make one last self-serving statement. I really want to give a great nod to our team at Pulmovant. We built a world-class team, not only in the business functions, but we knew early that we needed to build a team very deep in pulmonary hypertension experience. It's really inured to our benefit as we've gone fast and we've built excellent relationships across the spectrum. I thank our KOLs, our steering committee members, our investigators, and most importantly, the patients for what they're doing for our study. And then, of course, there's Roivant. I do want to thank Roivant, one, for having a great investment team to find a drug like this, but also to give us their acumen in so many areas, and of course, allow us to keep our heads down and focus on doing the right thing for the development of mosliciguat without being at the sort of whims or ebbs and flows of the capital markets day in and day out. So thank you, guys, for that. And so I'll stop with that, and I'll be pleased to take your questions with my colleagues. Thank you. Thanks, Drew. So on stage, as Drew was saying, we also have Carlos Sanmarco. He's the Senior VP Program Lead at Pulmovant, responsible for leading the mosli program and overseeing CMC and business operations functions. Carlos has extensive experience working in pulmonary hypertension and was the global program lead at Acceleron, overseeing the sotatercept program in pulmonary hypertension from IND filing through phase III completion, which obviously led to the company acquisition by Merck for $11 billion. Yaron, first question. Thanks so much, and congrats on that really nice data. I guess the biggest question that I have, there's no question you have a very nice effect on PVR. Can you talk about the anti-inflammatory and the fibrotic effect and what you've seen maybe in preclinical models or biologically based with cGMP modulation? It's a great question. Thanks, Yaron. Drew and Carlos. Sure. I'm happy to take it. Yaron, nice to see you. It's been a little bit. I would say that there are preclinical models that actually demonstrate that this type of mechanism could have impacts on reducing fibroblast proliferation, collagen deposits, things of that nature. I know I can make the statement that there are more preclinical models in this world, especially coming also out of oncology, but it was impressive the way that was working. I think more importantly, we really do know that cGMP in particular has the opportunity to drive these anti-inflammatory and antifibrotic effects. So we'll see what's also happening in some of the other areas where we're, TETON is an example of that, where we'll see if they're actually driving antifibrotic effects or there are other reasons for that study doing what it's doing. That will continue to allow us to go further and deeper into which aspects of this broad set of opportunities we have with mosli that can drive antifibrotic effects. Carlos, anything you'd add there? Yeah, I don't know. I'll just add that it's clear that there is a cross-talk between the cyclic GMP and cyclic AMP as well. So the potential of having an antifibrotic and inflammatory effect in the sGC pathway is high and is proven in preclinical models. Thanks, yeah. Look, I think it's unclear to us whether the TETON data is a function of vasodilation and vascular remodeling or whether it's a function of more fundamental antifibrotic effect. I guess our general view is we're watching that program super closely, and we mostly feel like if they're able to do it, we should be able to do something similar. Thanks, Yaron. Great. Next question comes from Yatin from Guggenheim, PH-ILD correlations. How is the historical correlation between PVR and six-minute walk test in PH-ILD? What kind of signal would you like to see on the secondary endpoints? Yeah. In terms of correlations within PH-ILD between PVR and other measures of clinical benefit, I think there's a question about how many data points you need to actually correctly compute a correlation. We just don't have that many. In general, obviously, in pulmonary hypertension, there is quite a good correlation between PVR and measures of clinical benefit. But Frank or Drew, anything you'd add to that? Nothing for me. Yeah. I just think in this study, we're in phase II. We have a mechanism that we know is a very potent vasodilator. We wanted to really explore that in an appropriate way so we understood the attributes of the drug. We are looking at six-minute walk, but you'd have to power it in a much larger study, which we would do in the future. But I feel pretty strongly that there's a great opportunity for those things to correlate over time. And there are other data points we're looking at to triangulate. For us, we will really just be looking for some form of a trend here to give us some confidence alongside, I think, what will be other hopefully very positive data. Great. Thank you. Doug over here. Hi. Doug Tsao, H.C. Wainwright. Thanks for taking the questions. If we look at the data, we saw a very nice response for both the two and the 4-mg dose in terms of PVR. We really saw a separation for the 4 mg on cardiac output. I'm just curious if you sort of understood or had a sort of hypothesis on what we saw there. Thank you. It's a good question. Carlos, you want to? Yeah. I think it's interesting. This is like a single-dose study. When you think about the importance of cardiac output in pulmonary hypertension, that's normally what you'll be expecting from a really strong vasodilator. That's one of the reasons we believe there's something there related to the 4-mg dose. The expectation is that you may be able to see the effect on the right ventricle because of that effect as well. As Drew was mentioning, there was a difference in the patient populations. We had CTEPH and PAH. This may have played a factor in some of these results, but that's exactly what we're trying to investigate as part of the PH-ILD phase II study. And I think, as you know, but others may not be aware, our protocol calls for an escalation of patients to the highest tolerated dose. So our goal is to get as many people to four as can tolerate four. And we think actually the vast majority of them may well be able to do that. Great. Thanks, Doug. Corinne. Thanks. Maybe looking forward a bit, you highlighted a combination program as well. And so as you think about a registrational program, how would you prioritize monotherapy versus combination? And how do you anticipate kind of this market playing out with respect to polypharmacy? And then kind of a last one to that, what do you need to show for this to be sort of the frontline treatment and backbone of therapy in PH-ILD? Yeah, thanks, Corinne. I think Drew did a really nice job laying out some of this in the presentation today, obviously in parallel to PAH, where polypharmacy is the name of the game. I want to be clear, we are not ceding frontline to anybody else. We think we have, look, one inhalation once a day is a big benefit. The fact that cough is an on-target effect for prostacyclins, treprostinil is a downside to that mechanism. Obviously, it'll depend on what the clinical data show, but we think we absolutely have a path to frontline use. And remember that in a variety of geographies, treprostinils aren't even approved. And so I think it's important for us to have good, robust monotherapy data for global use as well as for frontline use. Obviously, the study that we're running now, which these guys can talk a little bit more about, will help us generate some data on top of Tyvaso. And I think our general sense is over time, there will be a lot of mechanisms in PH-ILD and that we'll wind up in combination with multiple of them. But thank you, Carlos. I don't think there's much more to say on that. You got it, Matt. Okay. Thanks, Corinne. Great. I think that's it for questions. We're going to go to a 10-minute break for those on the web. Great. Final session, we come back. Thanks, everybody. All right. Great. Okay, so this is the last section. So we're going to talk briefly about the LNP litigation, which I know is a topic on some people's minds. We'll wrap up with some concluding remarks from me and then a final Q&A. Thank you again for bearing with us. I know there's a lot of content here. We really appreciate all of you joining. I'm going to talk a little bit about the LNP litigation. I'm going to introduce Lindsay Androski who is the CEO of Arbutus and a special counsel to Genevant on the litigation, has been at Roivant for a really long time, done a whole bunch of different things with us. That's a pattern across our leaders these days, and we're really proud of it. One comment on this before I hand it over to Lindsay to speak, and again, I'll do a little bit of intro, is as we get closer to the trial, which is set for March, we're probably going to just be a little bit more sort of focused on how we talk about this and careful. And so we're not going to take Q&A on the litigation itself today. Look, in terms of overview here, this is a big and important moment for us in a part of the story that's a little bit peripheral, but also obviously a huge opportunity or something that could matter. Look, we believe that the Moderna COVID-19 vaccine and the Pfizer vaccine both infringe on multiple Genevant and Arbutus patents. There have been $145 billion worth of combined sales of the Moderna and Pfizer BioNTech COVID-19 vaccines. So there's an implication there on the overall size. We've now had marketing rulings in both cases. So claim construction is complete in the U.S. cases for both Pfizer and Moderna. I think we view those outcomes, Genevant views those outcomes as favorable. Probably most importantly, in the coming months, there's a U.S. jury trial now scheduled in the Moderna case for March. And so we're looking forward to and doing an enormous amount of work to prepare for that. We're looking forward to that opportunity. And outside the U.S. and the Moderna litigation, we initiated proceedings last year, earlier this year, and they'll begin having hearings and outcomes in 2026. So 2026 will be a big year for this, as Lindsay will talk about. So with that, I'll ask Lindsay to come up on stage, and Lindsay will take you through the state of this and where we're headed. All right. Thank you very much. Thank you, Matt. Hello, everyone. Good to see you all this morning. This story actually begins 25 years ago at a predecessor of Arbutus, where our scientists were pioneering the field of lipid nanoparticle delivery. Our inventions changed the landscape of biotechnology, and alongside our partners, proved that you could get nucleic acids into the body in a way that would be therapeutically useful. Seven years ago, Roivant got more directly involved in this space when it teamed up with Arbutus to launch Genevant Sciences, which freed up Arbutus to focus solely on its chronic Hepatitis B development programs. Today, Genevant continues both to pioneer in the LNP space with a large team of scientists and to partner with companies with proprietary nucleic acid payload technology to develop innovative medicines. There are a number of patents at issue in the pending proceedings against Moderna, globally, and Pfizer/BioNTech in the US. The patents in these cases fall into three categories. First, we have what you could call the particle composition patents, and you can think of those as the recipe you need to follow to produce lipid nanoparticles with optimal characteristics. We have asserted some of the particle composition patents in each of the Moderna and the Pfizer and BioNTech cases. Pre-COVID, Moderna admitted that it was practicing some of our particle composition patents, and it asked the U.S. Patent and Trademark Office to rule two of the patents on this chart invalid. Moderna did not succeed. Moderna appealed, and it did not succeed on appeal either. We've now asked the court to limit what Moderna can argue about those patents' validity at our jury trial, and we're awaiting the court's ruling on that. Second, also in both cases, we have an mRNA LNP composition patent, and you can think of that as an invention that protects the mRNA cargo that travels inside the LNP into the body, and third, we have asserted against Pfizer and BioNTech specific methods used to manufacture our lipid nanoparticles, so, as Matt mentioned, our U.S. Moderna trial is scheduled for March. This is a big case, and it's an important event for us. At the same time, the U.S. revenues for SPIKEVAX, which is the dark blue wedge in this pie chart, represent just 10% of the total global revenues for SPIKEVAX and COMIRNATY combined. In other words, 90% of those revenues are not going to be impacted by this first trial. The March trial is really just the beginning. I'm going to talk a little bit more detail now, specifically about the Moderna case. We filed a Moderna U.S. lawsuit in February of 2022, so we're now almost four years into that case. Our position then, as now, is that Moderna accomplished something incredible by developing the SPIKEVAX vaccine in record time. Our position then, as now, is that the reason Moderna was able to move so quickly in developing the vaccine is that Moderna had access to our LNP delivery technology, including through a pre-COVID license. It did not, however, have a license to use our LNP in the COVID vaccine, and unfortunately, it became necessary for us to protect our rights through litigation. A lot has happened since we filed this lawsuit. Initially, Moderna asked the court to dismiss the lawsuit as to a significant portion of the infringing sales. Moderna argued it had permission from the U.S. government to use our patents and that we should be required to sue the U.S. government for all sales that were made through a government contract. This is under a statute called Section 1498. The court denied Moderna's partial motion to dismiss. Later, the U.S. Department of Justice, during the last presidential administration, filed a brief weighing in on this issue on Moderna's side. The court reconsidered the issue, but it again denied the partial motion to dismiss. But the Section 1498 issue is not quite done yet. It's pending again before the court right now in a stage of the case called summary judgment. We have just concluded our summary judgment briefing and Daubert briefing, and I'll explain what both of those things are shortly. In early 2024, we received a claim construction ruling, which is when the court decides disputes between the parties over what certain terms in the asserted patents mean, and earlier this year, as Matt mentioned, we sued Moderna in many other countries globally. Now we are fully immersed in getting ready for the U.S. trial. Pretrial briefings will be due in January, and that includes things like voir dire questions, which you use to pick a jury, jury instructions, the verdict form that the jury will fill out at the end of the case, lists of witnesses who will testify, and lists of exhibits that might be shown in court. Trial scheduled for March. Later next year, we expect to have public hearings in some of the international cases as well, so summary judgment. Juries decide facts. When parties can't agree on the facts, it goes to the jury, and the jury effectively decides, "Here's what actually happened." Summary judgment is a stage before trial where the parties say, "Hey, we don't need a jury to decide this issue. We all agree what the facts are. You, Your Honor, you should decide this issue based on the law." And then we can save time at trial because we don't need to talk about it to the jury. There are a number of summary judgment motions pending before the court right now. I already mentioned Section 1498, which is the issue of whether we were right to sue Moderna or whether we should have to sue the U.S. government instead. There are several other summary judgment motions pending, and all of those deal with specific issues under the patent laws. We expect the court to rule on these motions before trial, but we don't know exactly when that will happen. After we receive the rulings, we and Moderna may have to adjust what we will present to the jury at trial. And in addition, though we initially filed suit on six patents, we were ordered to narrow our case for jury presentation purposes, which is customary. We currently intend to present infringement arguments on four patents. So turning to Daubert, we've also just finished Daubert briefings. The name Daubert comes from a Supreme Court case, and it basically set the rules for how judges should determine if expert testimony will be helpful and appropriate for the jury to hear. It is standard in these kinds of cases for each side to try to keep out the other side's most important expert witnesses through Daubert motions, and this case is no exception. So there are a number of Daubert requests pending, including to exclude both sides' damages experts, which are the experts who analyze how much money Moderna should owe Genevant and Arbutus if the jury finds infringement, as well as other experts who are offering opinions on various aspects of infringement and patent validity. So as one example, we have an expert who conducted fractionation testing on Moderna's vaccine samples, which involved separating out the vaccine particles to make it easier to determine the molar ratios of the particles in the vaccine. Moderna is asking the court to rule that the jury cannot see those test results. So what's going to happen from here? As I mentioned, we expect the judge to rule on Daubert and summary judgment motions at some point before trial. Then we're going to head to Wilmington, Delaware, for a while. Trial is scheduled to begin on March 9th, and we estimate it will be a two-week trial, give or take a few days. The way trial proceeds is that we first pick a jury, each side does its opening statements, then we present our case with Moderna cross-examining our witnesses. After we finish, Moderna presents its defense, and we get to cross-examine Moderna's witnesses. Once both sides have presented their cases, we'll have a chance to put on a rebuttal case where we can put on additional witnesses and evidence to respond to Moderna's defense. After that, there are closing arguments, and the jury retires to deliberate and decide. We wait at the courthouse the entire time the jury is deliberating, just in case the jury has a question or, of course, so that we're there when they return with their verdict. The jury is going to decide, are our patents valid? Did Moderna infringe the patents? If yes, did Moderna willfully infringe the patents as opposed to doing it by mistake or out of ignorance? And what dollar amount should Moderna be required to pay Genevant and Arbutus to compensate fairly for its infringement? After that, we'll all go home, but it's not over. There will be a period for post-trial briefing to the court, which is when the parties ask the judge to fix things they think the jury got wrong. It also involves some financial decisions, like if there was a damages award, how much interest should be added? Should Moderna be required to post a bond? And if infringement was willful, should the jury's damages award be increased? It is also likely that one or both sides will appeal to the U.S. Court of Appeals for the Federal Circuit. In the international proceedings against Moderna, 2026 will also be a busy year. And a few key differences between our international proceedings and the U.S. proceeding is that because we filed the international proceedings this year, earlier in 2025, long after the COVID pandemic ended, we are seeking injunctions to stop Moderna from continuing to sell vaccines that practice our technology without permission. And in many international jurisdictions, we have the possibility to recover Moderna's profits rather than a reasonable royalty if we prevail in the infringement and validity phase of the case. Now I'll turn to the Pfizer and BioNTech case. The Pfizer and BioNTech litigation starts from a similar place in that BioNTech also had a license to Genevant's LNP technology and had been using it since well before COVID. Like Moderna, BioNTech did not have authorization to use Genevant's LNP in its COVID vaccine. We did have a question submitted earlier today, so thank you for that, about what is the status of Genevant's license with BioNTech. That license remains in effect today. BioNTech did recently provide notice of termination for the oncology portion of the collaboration, but we are still in the notice period. We filed this lawsuit in April of 2023, so a little bit more than 2.5 years ago, and so we're a little behind where we are in the Moderna case. Last December, the court heard the claim construction hearing, which was, again, where the court decides the meaning of terms in the patents that the parties dispute. That claim construction ruling issued in September. Now we're in fact discovery, which happens before you get to expert discovery, and we're waiting for future case deadlines to be set. We don't know exactly when that's going to happen. We filed the lawsuit against Pfizer and BioNTech because public disclosures indicated that they were in fact using our LNP. In addition to the pre-COVID license that BioNTech had obtained from Genevant, Pfizer and BioNTech's emergency use authorization filing with the FDA disclosed a recipe for the LNP that was covered by one or more of our particle composition patents. In addition, I mentioned that we are also asserting patents on manufacturing methods in this case. That is because a CNN feature that toured Pfizer's manufacturing facility and showed them using our patented manufacturing equipment, which is known as a T-Mixer. So in closing, I'll just reiterate that this is a very long road, but it's a very important road for us. We are fully committed to ensuring that our scientists' seminal contributions to LNP technology and the important role that our scientists' inventions played in the remarkable COVID vaccines are acknowledged and rewarded properly. Thank you. As Matt mentioned, I won't be taking any Q&A, so I think Richard, I'm handing it off to him for a financial update. Thanks. Thank you. Thank you, Lindsay. Just wanted to lay out the opportunity from a financial perspective that's in front of us. Looking at the portfolio across brepocitinib, Immunovant, and mosliciguat, we have clear untapped high-value growth drivers with $15 billion peak revenue potential. If I look at the bottom part of this graph, you can see brepocitinib, where we anticipate our first launch in 2027. Ben highlighted the phenomenal data we had in dermatomyositis across 10 very important endpoints, the high unmet need. And remember, this is a once-per-day pill for a very devastating disease, as we heard from patients. So I'm very excited to sort of, this will be the bottom part of the launch. And then about a year later, you have the non-infectious uveitis launch for brepocitinib. Moving on here, which again is supported by very strong clinical data we had seen in the phase II study. We know that the study is fully enrolled, and I'm excited to see that. And then we're waiting for the POC study for CS, which will add a third layer of potential growth to that base layer. As we look at sort of the middle part of the graph here for IMVT-1402, that's comprised of five pivotal studies that we have ongoing for 1402, and we obviously have one POC study there. The biggest opportunity is in Graves' disease, as Eric laid out. There's an incredible unmet need there, a very motivated patient population. And as I reflect on the data and also Dr. Lupo discussion, we clearly have disease-modifying benefit. We really have been pioneering the Graves' disease space, and we have disease-modifying potential. We're way in front and have the best presentation with autoinjector. So that's an incredible potential opportunity of growth. Obviously, myasthenia gravis, as Eric talked about, we have proven and shown that greater than IgG 70% suppression has a meaningful impact on efficacy. We saw the same in Graves. So we have an opportunity to differentiate there with a best-in-class efficacy profile. And then I'm excited to see the data in difficult-to-treat RA and also in CLE, which are wild cards right now, but again, where we could potentially differentiate. And then, of course, we have Sjögren's and CIDP, so that's for the middle layer. Then thinking about our latest broad analysis from Bayer for mosli, again, we had shown incredible data in PAH. This is, again, a very easy once-a-day DPI. We know that this market is just at the beginning of forming, and I'm excited to see the data in 2026 to inform the potential there. But we're, again, a third layer of growth. I think if you take all of this together, you can see $15 billion + of stacked launches in potential revenue peak sales, and that's probability unadjusted. Going to the next slide, how are we going to actually fund this? We're in a very unique position with $4.4 billion cash as of the last reported September quarter, that everything we talked about today is fully funded. That includes the programs we talked about, that includes the launches. And we're very happy to also invest in our winners, like we announced this morning, where we put $350 million into Immunovant in gross proceeds ourselves, along with $550 million in total with some great investors. And that has extended Immunovant's runway now to the Graves' disease launch. That leaves $2 billion available for new opportunities, either in the current portfolio or externally. And just to remind folks of our 10-year history here, we have a very high bar for deals. We usually will take a small upfront, run a POC study. If it doesn't work, we kill it. So we have a lot of opportunity to drive additional value and to deploy that capital very carefully. We have also, as Matt talked about, returned very meaningful capital back to shareholders, reducing our share count by 14% at roughly $10. And we have an additional $500 million left over in that share purchase authorization to deploy opportunistically. We've been moving on to sort of kind of how we're modeling the business over the next three years. Look, as Matt talked about, these are very tractable launches. So I anticipate over the next three years, we'll have modest growth in SG&A. Obviously, as we are launching brepocitinib, then NIU, and then get into the Immunovant launches, you can see that SG&A is growing to the low-mid $400 million range in 2028. The R&D programs are fully funded in the low- to mid-$600 million range. Essentially, as the phase III is completed and we have some readouts for the POC studies, that'll sort of move up and down. But again, that should be fairly stable. And look, I think we are in a very unique position here to generate data, have very meaningful launches, and have the incredible discipline to execute, as you can see, with the focus on the financial metrics. I'll pass it on to Matt. Thank you, Richard. Okay. We have some non-GAAP disclosures in here. And now, home stretch. So thank you again for listening all day today. We have a lot that we wanted to get through. We're really excited, as you can tell, about a bunch of different aspects of our portfolio and what's coming up. I just want to come a little bit back to the heart of this, which is to talk about where we are and where we're headed. Look, we think we're really well positioned for the next year, for the next several years. We think we have creative development programs with well-chosen indications. We think we're capitalized and funded through profitability, which is something that so few of our peers can say confidently. We think we have the ability to successfully commercialize launches, successfully commercialize drugs in the kinds of indications that our peers have shown a good ability to do it, and we think brepocitinib and DM is a perfect first example of exactly that sort of thing. And we think we have the ability to reinvest into a next generation of our pipeline, including indications for our existing programs that we haven't announced yet, as well as some new things that we are truly excited to get going on and to share. 2026 is another great year for us now, especially with some of the major data catalysts pulled in. We have obviously the brepo DM N DA filing kicking off the year, but also in brepo, we now have another, as you heard from earlier today, equally large indication reading out a complete pivotal program within 2026. I think this has the potential to be DM-like in scope and its data that's now coming next year. We obviously have the phase II-B data in PH-ILD, which I think has the potential to add a further leg to the stool that we feel really good about. We have the D2T RA study reading out next year, which you heard Eric talk a little bit about, but which again, interesting upside opportunity if that works out the way that we'd like it to. We have a couple of POC studies, proof-of-concept studies reading out for CLE for 1402 and for cutaneous sarcoidosis, also important programs. And then we have certainly, not least of all, the LNP jury trial that will take place in March. So a lot going on in 2026, frankly, a very busy year ahead, daunting to look at it on a page, but we'll get there. In terms of what we're focused on, look, we're obviously focused on preparing for the brepocitinib launch. We're wanting to make sure that team has everything they need, and that's an opportunity that we can't afford not to nail. We are looking to progress 1402 development across multiple pivotal studies. There's an enormous amount of work going on there. Obviously, Graves is a top priority in getting that study fully enrolled, getting that study set up for registration, or those studies set up for registration is high on our list. We want to convert a few different proof of concept studies into later stage programs. Obviously, for PH-ILD, that would be ideal. And then for some of the other earlier studies, CS, CLE, if the data supports it, looking forward to moving forward there. We'd like to execute on the LNP litigation. And finally, we'd like to add to the existing pipeline. So a lot for us to focus on in the next 12 months-18 months. You know, Richard put this slide up. It's schematic. We had extensive debates on how much revenue guidance to provide at this stage. The truth is we're doing our best, and we think these are really great programs. I think the point is, as a portfolio, I think there aren't very many other biotech companies with a portfolio with this breadth and this magnitude of overall opportunity. And we are really privileged to have each of these programs playing nicely together with each other and adding up to something that we think is synergistically pretty awesome. So we're looking forward to executing across all of this into building something really large and hopefully entering that graduating class we talked about earlier. I am not going to go through all of these catalysts. It's a really rich period for us in the next 36 months. This is only the stuff we've already disclosed. We've already gotten the portfolio. Sorry, mic's still on. Okay. So look, I think we've got a very busy stretch ahead. We are enormously grateful, obviously, to our patients, to our investigators, to the team at Roivant who works on these things. Sorry, I can't tell if my mic is still on. Am I good? Good. We're enormously grateful to the patients, the investigators, the team at Roivant who is working tirelessly on this. We're grateful to the investor community who has supported us along the way here, and hopefully you're all going to be with us on the journey from here. So that concludes the prepared portion of today. We have an opportunity for a little bit more Q&A. I just want to say thank you again. There was a lot of content here. Thank you to the team that put this together. Thanks to all of you for listening. It's a real privilege to be able to get in front of all of you. And I'm looking forward to a little bit of Q&A and then some lunch. Thanks, guys. Great. We are going to go first to Brian Cheng. Brian's over there. Brian Cheng from JP Morgan. I think one question that I have has always been on the BD front. There's a lot going on now across the Vant portfolio. How do you think about that? Richard, you mentioned your messaging around your potential spend on BD is very consistent. You want a small upfront. You're going to acquire something that has really strong upside potential. Where are you on that now, given Priovant is working out, and there are multiple Vants that are really slowly moving your company into commercial stage? So are you still actively looking for the next BD assets, and do you still have capacity to bring in newer assets in your story today? Thanks. Yeah, thanks, Brian. It's a great question. I'm not surprised to get it. Look, I think first of all, Roivant's DNA has been built around opportunism and careful asset hunting since the very beginning, and there is definitely no change there. We have a phenomenal team of people. I wish he could be here today. He was under the weather, but we have a phenomenal team of people working across both BD and R&D on identifying those opportunities. We are active. We are out in the world hunting. I think it's important for us to acknowledge that the profile of the company has changed in the past year, that we are cruising for commercialization across a handful of large important programs, and that we need to make sure we nail those launches, that we need to build a business that matters not at the scale we were at two, three years ago, but at the scale we're hoping to be at in two or three years, and so I think, look, we're looking at late-stage programs. We're looking at things that move the needle. We're looking at opportunities that can truly add another leg to the stool that we talked about today, but I think there are a lot of things that meet that description, and we are always in late-stage discussion on multiple of them. It's hard to know what's going to convert when. When it happens, we'll be happy to talk about it. The truth of the matter is, in the meantime, we've got so much going on in the existing portfolio and so much opportunity with what's in hand that we're mostly focused on that without waiting. Thanks, Matt. We're going to go to Sam next. Brian, if you want to. Perfect. Hi, Sam Semenkow. Thanks for taking the question, and thanks for this great presentation today. I'll just add another big picture one. Brepocitinib, you have three indications, Immunovant six, but there's a lot of opportunities beyond those. What is your capacity to maybe take on additional indications, maybe some more that are riskier or some more that we know that FcRns might work in? Just curious any thoughts there. Frank is the Chairman of the Vant Boards and also runs our R&D organization and is responsible for that capacity. So I'll hand it to him. Thanks, Matt. That's a tough setup. Okay. So look, the answer is we have more capacity and we have more ambition. There are both some late-stage programs or later-stage development programs we have in more than concept and pretty well defined right now that we may well roll out depending kind of on the last few weeks to those programs across first brepocitinib probably, and then secondly the FcRn franchise. And look, the FcRn franchise and brepocitinib share some similarities. There's kind of boundless opportunity there in a way that's very unique, actually, mechanistically. And so I think you have to pick your spot and say, where do we think we can have a unique scientific advantage? Where do we think we can have a unique commercial advantage? I think we've been good at finding things that are unique, like Graves, bringing them to the fore. We have some ideas for brepo that I think will continue to expand that franchise. We have ideas in the FcRn franchise where there's a lot more development, frankly. I think you're looking at 2023 -20 25 current indications in development in that field. And so we have both the opportunity to kind of pioneer our own indications. And frankly, part of the reason we don't talk about them so much is because people have the opportunity to follow us when we do. And so we try to get them a little bit more advanced, especially in FcRn, before we talk about them publicly. But I think there is absolutely both active work and intuition to bring these to try to these are going to be, if we're fortunate that they are what we think they are, that they're going to be giant commercial franchises. And I think the ability to add on indications that can layer on not hundreds of millions, but billions of incremental sales is really where we're focused. Thanks, Sam. We're going to go to the center over here, please. Hi, this is Iris Gao from Guggenheim here for Yatin Suneja. Thanks a lot for taking my question. It's going to be a quick one on brepo. So is there a schedule for registration and launch in Japan? And if so, how's the market like there? Thank you. All right, I'll let Frank take that one as well. We have spent less time thinking about the Japanese market than the U.S. market. The honest truth is our focus, initial focus has been the U.S. market, just given the kind of tangible opportunity that's there and then the unmet need. That's really where we've spent the bulk of our time to date. That's a good question. There are Japanese patients in our clinical program, and I do think we will get the program registered in Japan. It's just second in priority behind making sure everything goes the way we want it to in the U.S. Yeah. We're going to Corinne next. Thanks, Corinne Jenkins, Goldman Sachs. Maybe another big picture one in terms of commercial infrastructures, you think building a thing about building that out for multiple products across multiple launches. What are some of the aspects of the commercial program that you can leverage across these different products, and what do you have to build out distinctly? And as you think about timing and team of bringing that on board? Yeah, perfect. And look, I think we've learned an enormous amount from the field on how to commercialize drugs that look like these. And I think we're standing on the shoulders of giants truly. There's some people who have done a phenomenal job with this that have a lot to teach us. I think there's a few things that are generally common among successful commercial launches in these general categories these days. I think among those things are a lot of medical affairs and patient connectivity. And I think that's underway now with all of our important programs. I think a lot of patient support post-launch in terms of helping with coverage, helping with sort of managing the complicated U.S. healthcare system. I think some of that is probably shareable between programs, and I think we're focused on thinking that through. That said, most importantly, we're building something that we think is going to work for the brepo launch in DM, and then if it works, I think there will be a lot of opportunity and interest in extending it to some of the other programs, practically speaking. Obviously, there's some other things that are obviously shared. Some of these things we either built during the Vant era and have managed to maintain some expertise or have learned about enough to know what we need. Obviously, there's a layer of market access where it's important we be able to approach the payer community with a portfolio. I think we're thinking through exactly what we need to do there. Then there's actually just like, for lack of a better word, just like some boring nuts and bolts stuff, distribution and 3PL agreements and pharmacy agreements and things like that, where if you set them up right at the beginning, you can make sure that you benefit from volume across the portfolio. That's the kind of infrastructure that I would say we are focused on generalizing now. Notably, and I think this is important, there's a kind of commercial infrastructure that I think we won't generalize, which is the laser focus on the patient and the prescriber for each of these indications, the field force, the medical affairs organizations. You just need to be in those communities to be successful. And I think that belongs at the tip of the spear as close to each program as we can possibly put it. And that's where it's being built for brepo and DM right now. These are places where we've really invested in kind of understanding to the individual clinic level, where are the patients, where is the need, where are the doctors, who do they treat, what health plans serve those patients in those clinics at that physician level. And I think that kind of preparation will serve us well. And these are also reasonably tractable indications. They don't require enormous sales force build, but we will invest in them aggressively because we think they're remarkable opportunities. Thank you. Well, it looks like, Matt, we've exhausted all the questios. So with that. Fantastic. Awesome. Well, thank you again, everybody. I really appreciate your being here. Lunch is out there. I'll catch up with as many of you as I can. Have a great day.