Cover U.S. Biotech at Bernstein. Very pleased to be joined this afternoon by Matt Gline from Roivant. Matt, thanks so much for coming, and maybe if I'll hand it over to you for some opening remarks on the company. Yeah, thanks. Thanks for having us. I'm very aware there's like a large 40-minute timer here that's counting down slowly, so I'm aware of the time to fill. We have a lot to say, though. So look, I'm CEO of Roivant. We are a biopharma company. I think most are probably at least somewhat familiar with us. We mostly focus on development stage drug development, clinical stage drug development. And today we have a portfolio of several quite late-stage clinical programs, one of which now in sort of registration with the FDA after some positive data last week. Really excited about all that. I'm sure we'll talk about all those programs. We've been around about 10 years. We've got about a $10 billion market cap, about $4.5 billion of cash after the sale of the drug to Roche a few years back. And one of our programs is a public subsidiary, Immunovant, an Anti-FcRn Antibody. I'm sure we'll talk about that one too. But that has about a $2 billion market value for our stake. So that's kind of the general profile of the company. Great. Why don't we start with the Dermatomyositis data that you had last week? Really exciting. Would you like to just share some of the highlights and also some of the feedback that you've gotten from investors over the past week? I can talk for a long time about this program. This was phase three data that we just generated last week in the Valor study in a drug called Brepocitinib, which is a dual inhibitor of JAK1 and TYK2 that we acquired from Pfizer a number of years ago. Dermatomyositis is a rare immunological inflammatory disease that's marked both by a very bad skin rash and muscle inflammation and wasting. These are very sick patients, five-year mortality of somewhere between 10%-30%, lots of disability and lifestyle issues associated with it. And frankly, just like an untreatable disease up until recently. The vast majority of patients are really only on either corticosteroids or immunosuppressants or like old immunosuppressants or some combination of the two. IVIG is used in a relatively small minority of patients. Then a bunch of stuff is used off-label. But no new therapy is successfully developed in a long time. There have been a number of failures, Rituximab, others, Stelara, et cetera, in clinical development. And this was the first study to succeed for a novel mechanism in dermatomyositis really in decades. Again, this is an IVIG got approved recently. It was a 52-week study of two doses of Brepocitinib against background meds, against steroids and Methotrexate and other things. We showed beautiful separation from placebo at week 52 on TISS, which is the endpoint total improvement score. It's one of these sort of composite immunology endpoints that measures quality of life and skin coverage and muscle enzymes and a whole bunch of other things. And just a lovely data set, really clean separation, sort of textbook quality. We had nine key secondary endpoints. We hit all of them. Dermatomyositis has us at both muscle and skin presentation. We hit on both muscle and skin. I think as we've talked to docs since the data set came out, I think just an enormous amount of positivity coming back to us. Obviously, one piece of this is there were some of these docs who were like literally tearing up. There just hadn't been a successful study in so long that to see a novel mechanism approved was quite meaningful, but just like the breadth of the data was impressive in terms of the number of things we hit on, and then the last point I'll make as a framing point is the study was run with a steroid taper, so we had a mandatory taper of background steroids starting at week 12, going out to week 36, and we sort of required patients to get below five milligrams and then encouraged patients to go even lower. We viewed that in the same way that you might for like a lupus study as a risk mitigant, really, a way to encourage separation from placebo. What I don't think we fully understood until we sort of looked at the data and lived with it is the extent to which we showed very significant clinical benefit on the primary and the secondaries. We also showed a very significant delta in the amount of steroid taper possible at high-dose Brepocitinib versus on either low dose or placebo. I think that actually has been viewed by the doc community as like another benefit of the drug. It's something the drug has delivered. These patients are eager to get off steroids. If you've ever been on high-dose oral prednisone like a Pred-Pak or something like that, it sucks. It's like not a pleasant thing. These patients are on 10 plus milligrams of Prednisone in many cases for like a significant portion of the year. The idea that you can get them down by 70% and still offer a clinical benefit above and beyond what they were seeing on steroids is a huge asset and something that docs have really responded to. And these immunology composites, as you said, they can be kind of hard to understand what that means in the real world. You brought up the steroid example. Maybe just say a little bit more about some other examples of what this drug could mean in the day-to-day lives of patients. Yeah, sure. So we measured a whole bunch of things. Again, sort of TISS is a composite of a whole bunch of things, and we measured a bunch of things specifically. One key measure of skin disease is this scale called CDASI. It's a gold standard for measuring skin disease and dermatomyositis. We saw a very significant reduction in CDASI for these patients. Improvement in CDASI for these patients. So their rash goes way down. And rash is one of the most sort of complained about quality of life symptoms of dermatomyositis. There's this thing called the HAQ-DI. It's a health assessment questionnaire. It's a disability index. It measures things like there's measures of muscle function in TISS that are things like manual muscle testing where like a doctor literally puts out his hand and says, "Push up on my hand." And they're like, "Annie, you seem like a two today." That's like a way that this is formally measured. But in some ways, these disability questionnaires are better. They ask patients things like, "Do you have trouble walking up the stairs? Do you have trouble carrying your groceries? Do you have trouble loading up your fridge? Do you have trouble cooking dinner?" And we saw a very statistically significant benefit on that disability index. I think those are actually the kinds of things that really matter to patients living with the disease on a day-to-day basis. And so we were particularly pleased about some of that data. Great. You'll have an important first mover advantage in this space, but there are some other companies that have drugs in late-stage development. Based on your own data and what you've seen from the phase II from those other companies, what do you believe are going to be the key differentiators for Brepo in a competitive market? Yeah, that's obviously a hard question to answer. We don't know what the profile of those other drugs is going to be. The first thing is basically all of the drugs in late-stage development differ from Brepo in one pretty important way, which is that Brepo is an oral medication. It's one pill once daily. So it should have a significant advantage, especially again, you think about these 75% of these patients who are only treated on background steroids and immunosuppressants. That's their regimen now is pills every day. And the idea that they can replace those pills with something that will give them better benefit and better tolerability is a huge asset. Of the other mechanisms in development, probably the two that are "furthest along," there are some anti-interferon antibodies. There's Dazukibart from Pfizer. And then not Lilly, AstraZeneca has an ongoing study of Anifrolumab. There was some phase two data for Sifalimumab that looked promising, but first of all, it was two separate very small studies, one in skin and one in muscle, and the patient population is talking about like single-digit n's, so it's just hard to know. Interferon-directed therapy should work in dermatomyositis. It's an interferonopathy. I don't know that you get as broad coverage as you do with a JAK1, TYK2, because for example, with TYK2, you also get suppression of IL-12 and IL-23, which we know is also separately active, especially in the muscle disease, so I think there is reason to believe that we have sort of broader coverage, but I think the mechanism of those anti-interferon drugs makes sense. We'll just have to see what the full data sets look like, and then the other mechanism that's in late-stage development is an Anti-FcRn Antibody, efgartigimod from Argenx. That drug put out phase two data in June in a study not specifically in dermatomyositis, but in a sort of multiple myositis population. It didn't have a steroid taper. It was a very different patient population. So I think you probably can't apples to apples compare the outcomes. It looked like it was somewhat efficacious, as you would expect. It's a disease that is also treatable with IVIG. And it should be a viable option. I do think in this disease, like DM treating physicians will gravitate towards a drug with data specifically in dermatomyositis. So I think we will have an advantage in that direction. And it's possible we'll have an efficacy benefit as well, but it'll be a little bit hard to compare because again, I think like the steroid taper dynamics and things like that make it sort of hard to directly read through. And you have your own FcRn with Immunovant. We do. You could have chosen to develop that in DM, and you chose instead to go with Brepo. So what were some of the considerations around that decision? Yeah, I'll say we still could develop 1402 in DM. I think we're happy with the portfolio of indications we're currently studying. But I do think the data is promising from FcRn antibody. And we like dermatomyositis and myositis more generally as a commercial market. So I wouldn't say we've ruled it out. Having said that, look, I think what did we like about DM for Brepocitinib? First of all, it's a disease where the biology is pretty well suited to dual inhibition of JAK1 and TYK2. So as I mentioned, there's both sort of interferon components, which are actually signaled by both JAK1 and TYK2. And then there's things like IL-12 and IL-23 contributions to the disease that are signaled specifically by TYK2. So I think there's sort of a benefit to the breadth of coverage. I think there was something nice about going after an oral medication for this disease, and then the other thing that's been a big boon to us, bluntly, is the docs who treat DM patients are rheumatologists and dermatologists. They are familiar with JAK inhibition as a pathway. They're familiar with it from all the rheumatological disorders. They're familiar with it from atopic dermatitis, from abrocitinib and other things, and so I think there's like a lot of enthusiasm and in fact, some off-label use of JAK inhibitors already, and I think a lot of these docs are like eager to see an on-label JAK inhibitor to add to their practice, and I think they're primed to believe that Brepocitinib may even be better than the kinds of JAK inhibitors they've been using because it is such a sort of specific gun that hits both JAK1 and TYK2. Like, where along the patient journey would the doc consider prescribing Brepo, and kind of what% of all the DM patients would that encompass? So we track, call it 35,000-40,000 dermatomyositis patients in active treatment. There's more, some of whom may come into treatment with the addition of a novel option, as you see a lot in these rare diseases. But we track about 35,000-40,000. Of those, 75% of them only use steroid and old generation immunosuppressants. And then about 25% sort of split between IVIG and a soup of other things. To be honest, I think roughly any patient with DM should be interesting as a potential Brepo patient. And certainly any patient with DM who is on, call it greater than 10 milligrams of oral prednisone should be interesting because I think that's a pretty crappy experience. And often those patients are not being well controlled. So I think the whole market is eligible. I think especially the moderate or severe population that are looking for new options is going to be interesting. I think a patient who is, first of all, like a "incident patient" that is a patient who's on steroids or Methotrexate or whatever and is looking for a change. Previously, IVIG might have been the thing. Some of the standard regimens for IVIG and DM involve like five consecutive days a month of five- to six-hour-a-day infusions. This is no joke. I think the idea of a once pill daily regimen will be an appealing alternative even against a backdrop, whatever. I think like you also could argue for differential efficacy and things like that, but like just on form factor alone. Frankly, I suspect there are patients on IVIG who would like to switch things up. Also, obviously, patients who are on off-label therapies who are struggling with coverage, whose doctors don't have support, et cetera. Like, I think there's options for those patients as well. So, I think the entire market, I think certainly we could exist in a sort of refractory third and fourth line setting against the stuff that's used. But I also think just patients who are not getting fully controlled on steroids, and there are many, I think are great patients for us. So, I think a huge percent of the market is addressable. If you listen to some of your competitor banks have done KOL calls in the wake of the data. And frankly, like the numbers that docs on those calls use to describe like whatever they say they're going to use 30% or 40% or 50% of their patients to start on Brepocitinib. Obviously, if that were true, we'd be very pleased out of the gate. Say a bit about the safety profile you observed and how you think about JAK class risk in the context of this disease? It's a great question. So first of all, Brepocitinib is a relatively bog standard JAK inhibitor from a safety perspective. It's probably on like the more benign end. We have about 1,500 patients in the safety database. Pfizer studied the drug in a whole bunch of indications. I think it looks like it's on the more benign end of a typical JAK inhibitor, but we'll have all of that stuff, and I strongly expect that there will be a class warning on the drug, although we don't know, and it's an FDA determination. It's a different patient population. There are a few truths here. One is, look, I think when we first in-licensed the drug from Pfizer in 2021, I think this was a big question. The truth is the market's kind of spoken. I think like you look in like less severe diseases or diseases with more treatment options, let's say like ulcerative colitis or whatever, where you could go through Entyvio and you could go through Humira and all these things. Those drugs are widely used in IBD. There's still many, many patients who go to Rinvoq for the level of efficacy that it provides. So I think like given that in those populations, docs are very happy to use JAK inhibitors. I don't think there's going to be that much of a debate specifically about JAK class safety. There's a couple of other things to keep in mind. One is many of the safety issues associated with steroids and immunosuppressants overlap with the ones for JAK inhibitors. And so it's a little bit of like you're helping to reduce the dose of those things. And so therefore there's at least some positive aspect to the trade-off. And in fact, many of these same issues are also just sequelae of dermatomyositis. These patients have many of these same issues, heart disease and malignancies and things like that that are sometimes associated at very low levels with JAK inhibitors. In fact, if you look at the safety data in the study itself, it looked extremely clean, actually. Placebo in general looked worse. Placebo looked worse than the drug arm. Some of that's just, it's compared to the thousands of patients that we hope to treat eventually. It's a relatively small patient population. Frankly, JAK class issues are real but infrequent. But some of it, to be honest, is you treat these patients, you make them healthier, you actually reduce the number of cardiac events related to the disease. You reduce the number of cardiac events related to high-dose steroids. And there's some like balancing act where actually some of these patients actually like overall get better. And that's before you even think about like the risk-benefit analysis of like the benefit of the drug on treating the direct symptoms of the disease. So I think overall, I think the risk-benefit is going to be just fine and not an issue here. Do you want to give a high-level overview of the other indications that you've got on deck for Brepo? Sure, yes. So we have two other indications that we've announced publicly and a whole host of others that we've thought about or are actively thinking about. The next major indication for us is non-infectious uveitis, which is an inflammatory disease of the eye. There's about 400,000 NIU patients in the U.S., of which about 70,000 have the sort of problematic back of eye version of the disease where if you have front of eye inflammation, you can usually treat it with a topical steroid of some kind. But if you have back of eye disease, you really have to do something systemic generally. And eye inflammation is considered a very high priority by ophthalmologists. If you don't treat it quickly, it can lead to blindness. NIU is one of the leading causes of blindness in the U.S. So it's a serious disease. And again, it's marked by a few options. Really, the only novel approved medicine is Humira, which doesn't work great in this population. On their primary endpoint or on their major endpoints, more than half of patients fail treatment compared with less than a third for our therapy. In fact, if you do the apples-to-apples comparison, theirs is more like two-thirds and ours is less than a third. And so that was based on our phase two study that we ran that gave us a lot of conviction in the indication. That's in a pair of pivotal studies that we'll read out on current guidance in the first half of 2027. And those are enrolling very nicely. Then the other indication that we're studying is cutaneous sarcoidosis, which is a really bad skin inflammatory disease that again has basically no approved therapies and where JAK inhibition has been shown effective in some small open-label studies and where we are running a phase 2 study that we'll read out next year. How do you think about the level of clinical development risk for those indications versus, I mean, you know for DM now it worked, right? It's like your ingoing view. My going in view was that DM was a riskier proposition than NIU because we had our own phase 2 data in NIU while we didn't have any kind of phase 2 data in dermatomyositis, and so I feel pretty good about that study. There's still risks. There are some failed studies out there in NIU in different mechanisms, including a study that failed last year from Acelyrin for an IL-17A or something, and so there's a variety of difficulties there, but I feel pretty good based on the quality of the data we generate in phase 2. Look, cutaneous sarcoidosis is riskier in that all of the data sets that exist today are not placebo-controlled and pretty small. We'll know a lot more after we generate the data set. If I had to guess biologically, Brepocitinib almost certainly will improve the sort of pathophysiology of cutaneous sarcoidosis patients. I think there's a real question about like how easy or hard that's going to be to show in a clinical trial setting, and we'll find out based on this phase 2. For that patient population, what's, like, how many of these patients are there and what portion would be addressable for sarcoid? Yeah, it's broadly similar in size, what I'd say. Tens of thousands of patients with cutaneous sarcoidosis with no good options right now. So these patients are really sick. So I think it's sort of not so dissimilar an opportunity from a dermatomyositis. What are the right pricing comps to keep in mind? Yeah, it's premature to talk about pricing until we have an approved product, and some of that's in FDA's hands. You know, look, I think DM is a rare disease. I think access is going to matter. But I think there's a pretty good blueprint these days for how companies handle rare disease launches in terms of a lot of patient support and a lot of work by the doctors and the patients and the sponsors to try and help each patient make their way through the payer process. You know, dermatomyositis, as far as comps are concerned or whatever, I mean, Octagam, which is the approved IVIG, is $250,000 a year-ish, maybe a little more. And if Efgartigimod gets approved, you know, the range of pricing for Efgartigimod is, call it $250,000-$300,000 in MG up to $500,000 or $600,000 a year in other indications. So all of which to say sort of rare disease pricing is what seems appropriate for Dermatomyositis according to what our peers think, and look, our view is these are patients that have a lot of other options, and it'll be important to us to make sure that whatever price point we choose, that all the patients who need the drug have good access to it. Great. Can we shift over towards Immunovant? Would you like to give an overview of IMVT-1402 and batoclimab and what you've done so far? Yeah, sure. So Immunovant is a subsidiary of ours developing a portfolio of anti-FcRn antibodies. This is a class of drug that's pretty widely followed. Obviously, Argenx is the class leader and has Efgartigimod that's doing on an annualized basis probably $4 billion now in MG and CIDP. We have two anti-FcRn antibodies. Our lead at this point is a drug called IMVT-1402. And the thing about our portfolio of antibodies is they suppress IgG, we believe, more deeply than Argenx or Efgartigimod is able to suppress IgG. There's various reasons why we believe that to be true. And we think they in practice suppress IgG as deeply as anybody in late-stage clinical development or deeper. And we just think, so the way these antibodies work to take a super quick step back is they regulate FcRn, which in itself regulates the recycling of IgG in the body. And so when you affect, when you block FcRn in this way, you deplete IgG in our case by close to 80%, which as it turns out has relatively few safety sequelae, but is very efficacious for treating diseases marked by pathogenic IgG autoantibodies. And so that's the areas in which this is studied, MG, CIDP, we're studying Graves' disease, et cetera. And our hope is that by depleting those antibodies more deeply, we will see greater clinical benefit. Also, in most of the indications we're very excited about, we are sort of first in those indications for, in some cases, any mechanism and certainly for an FcRn. And think that will give us a real opportunity to do something interesting. You've been looking to settle this debate around deeper is better. Would you like to summarize what you've shown so far and kind of what the feedback from investors has been around that? No. I will though. Look, the honest answer is these debates start to feel silly at some point in that we're ultimately going to generate data for our drug in the indications in which we commercialize it, and the debate will be what patients choose and what doctors choose and what the data look like. We believe we have consistently over and over again demonstrated that individual patients with deeper IgG reduction get better treatment benefit in MG and CIDP and Graves' disease in TED. We believe we have shown in MG where we have large placebo-controlled phase three studies that we're able to provide better sort of absolute MG ADL improvements than other drugs with lesser IgG suppression have been able to provide. There are other people who quibble with those opinions, especially in MG where market dynamics have changed and placebo rates are different than they used to be. And so it's just like hard to do good apples-to-apples comparisons. Ultimately, when 1402 is developed in MG, it will have a label and we will focus on things like effectively disease remission, our ability to drive minimal symptom expression in patients. And I believe we will be able to do that better than other agents. And I think that will matter to those patients. But to be honest, like MG where that debate is most acute is a knife fight anyway at this point. There's a million different drugs being developed in MG and many of them work well. And I believe that we should be able to take reasonable share in what looks like a very big market and that we will have a really compelling option. But I'm much more excited, frankly, about indications like Graves' disease where we are out in front. We have paved the way on this biology. We have demonstrated pretty conclusively in phase two studies that this biology works really well in these patients and does some interesting things. And we will be the first in that indication. And I think that will set us up really nicely for telling our own story and not getting mired down in the bog of a point here and a point there kind of debates. Although again, I think we'll do better than a point here and a point there when push comes to shove. That looks to me like hands down your largest opportunity in terms of addressable patients for that drug. The beautiful thing about Graves' disease is it's almost not a rare disease. It's got like 300-350,000 sort of prevalent patients. There's millions of patients with Graves' disease. Many of them are treated well on existing options from the 1950s, but about 330,000 of them are just not. They can never get controlled on methimazole or other anti-thyroid drugs, and so they just live uncomfortably. There's actually no other good option for them, well, there's no other good therapeutic option for them, so their choices are either live uncomfortably while cycling on and off methimazole, a drug with lots of side effects, or have their thyroid surgically removed or irradiated and then live the rest of their life on synthetic thyroid hormones, which has its own issues associated with it, including that you have to be on synthetic thyroid hormones for the rest of your life. These patients have no good options. We're studying only that sort of most refractory patient population. I just think there's a huge opportunity to change what standard of care looks like for those patients. Why do you think other biotech companies, some of your FcRn competitors have not gone after that indication before? First of all, I think that is changing rapidly. Like for example, Biohaven with an IgG degrader has a program. There's a number of TSH receptor programs now out there, KinetX, a couple of others. I do think like, look, I want to pat ourselves on the back. I think we've like paved the way in Graves' and people now see it as an interesting opportunity. In terms of like specifically FcRn competitors, I don't know, and you have to ask them. The obviously self-serving answer to that question is that we have shown that deeper IgG suppression yields better treatment benefit in these patients and we suppress IgG more deeply, and so it seems to me that we would be a tough act to follow, and others like Argenx, for example, is going after TED, which is a sort of downstream of Graves' kind of an indication. So there are like different approaches to this. That said, would it surprise me terribly if some of our FcRn competitors ultimately show up in Graves' disease? It would not. Because I think it's a really big opportunity with a lot of unmet need. And frankly, with a patient population of this size, there's 330,000 untreated patients. We're not even really competing with anybody else. We're just competing with ourselves and our ability to get out and tell the value proposition story and put good data in front of those docs and patients. How would you compare and contrast 1402 with the Biohaven degrader? That's a hard question to answer because 1402 is an FcRn antibody, which is a class that has many thousands of patients' worth of data at this point. So like we understand how anti-FcRn antibodies work in the body. We understand their sequelae, their toxic, their all kinds of things, tissue penetration issues, everything. Whereas IgG degradation is much more experimental at this stage. And I think there are approximately zero patients' worth of data on IgG degradation. There's subjects in healthy volunteer studies that show they can degrade IgG generally. There's like, you can talk to around Biohaven's lead IgG degrader. You can talk to like it spares IgG3, which may be a good or a bad thing depending on the specific indication that you're going after. But they will, they have engineered other degraders that don't do that or do different things and they will engineer others. To me, it looks from the outside like IgG degradation is a comparable mechanism in terms of what you can do with it versus anti-FcRn antibodies, and with a bunch of unknown unknowns about how that sort of acts once you get into larger patient populations, it's behind, but other than that, it seems reasonable as a thing to try. The one thing I'd say is, I know Biohaven is doing this. Like if I were in that space, I would be focusing on a thing that they can do that we can't, which is to attempt to engineer specificity to specific IgG autoantibodies, in which case instead of suppressing them by 80%, you could suppress them by 99% because there's going to be no sort of safety issue associated with just eliminating the autoantibody. That's a different molecule. It's a different approach. Some diseases have great homogeneity of autoantibody. You should be able to do that. Some diseases don't. I think like those are things they'll be able to do that we can't. One of your other indications is difficult to treat RA. Could you compare and contrast what Nipocalimab showed in RA versus what you expect to show and why you expect your results to be different? Yeah. So Nipocalimab is the J&J Anti-FcRn Antibody. They got it from acquiring Momenta a number of years ago. So in effectively a first-line RA study or a sort of all-comers RA study a couple of years ago, they showed clear activity. That is, they showed that there was a dose-dependent improvement in RA patients from treating with FcRn. It wasn't like extraordinary activity, but it was clear it was dose-dependent and maybe most encouraging to us. It was correlated to the level of autoantibodies in the patient, which seems constructive. The rub is a few-fold. One is the way that J&J is developing it, we haven't talked at all about albumin and LDL and that's just fine. But like the way that J&J is developing Nipocalimab, clearly underdoses the drug in order to sort of optimize for safety and tolerability. And so they typically suppress IgG in their studies by maybe a little under 60% or thereabouts, which is just a different profile than our drug from an IgG suppression perspective. And then they ran a quite different study than the one we've chosen to run. The study that you're referring to they ran was sort of as adjunctive therapy alongside a TNF, which led to Cimzia because it doesn't have Fc binding regions like the whole thing. Look, I think part of this is TNFs work quite well in RA. And so you're adding that as a therapy. It's going to be like difficult to sort of piece apart the benefit of the FcRn versus the TNF. They studied an earlier line patient population. What we've chosen to do is to go after the most recalcitrant patients, the sort of fourth line D2T patients, to go after them with the deepest IgG suppression that we believe can be delivered now and to try and sort of generate a different result that way. So it's a different study. I believe FcRns are active based on the data that J&J showed last year. It would have been nice if they had shown a little bit more numerical separation together with the TNF. But overall, I think we've got a real shot at helping. And obviously, it's a very different patient population if we succeed in terms of like we will not be in the competitive scrum with all of the other RA stuff. We will play sort of after it. And I think if we're successful, that'll be a great place to be as an FcRn. But it's a high bar. And frankly, you know I think we are not given a ton of credit for it right now. And that's just fine. We'll see what the data looks like next year. How would you rank order the different indications you're going after for 1402 in terms of your overall level of excitement? Yeah. I mean, so I'm incredibly excited about Graves'. It's just this huge white space opportunity. I'm excited for some of the other more white spacey opportunities we're going after like CLE. But that's phase two study. It's early. We'll have to see. The competitive bar is high. So it really depends a lot what that phase two data looks like. I'm excited about indications like Sjogren's because we will not be meaningfully behind. And so I think if we can sort of catch up there and establish pride of place with deeper IgG suppression, that may feel different. And then like I think sort of necessarily at the bottom of that stack have to be things like MG and CIDP where I like MG and CIDP. And the truth is, if MG turns out to be a $10-plus billion-dollar market, we will be a big drug in MG. But how big will depend a lot on what that phase 3 data looks like. And to be honest, Argenx has just done a really nice job establishing themselves as the agent of choice for MG-treating physicians. And so I think unseating them in that bar is a challenge. Do you want to share an overview of the Mosliciguat and the PH-ILD program? Sure. So this is our third program. It's definitely the pick your phrase for the sort of abandoned cast aside part of our story for the moment. Mosliciguat is an sGC activator. It was originally developed by Bayer. For those who are familiar with the history of this whole area, there's a drug called Adempas that was an sGC stimulator that was jointly developed by Bayer and Merck. Bayer is really the like father or mother or grandparent of sGC chemistry. And they still have sGC directed agents for other indications. But they got out of respiratory disease a couple of years ago. And this was kind of their main bet in respiratory disease. And so we licensed it from them. It is differentiated in mechanism from Adempas. sGC activators do something slightly different than sGC stimulators. But most importantly for us, it has been formulated successfully as an inhaled therapy in a simple DPI, one puff once a day, which is incredibly important, especially for PH-ILD patients for a number of reasons I can talk about in a second. Bayer generated phase one data in many, many studies, principally in healthies and then also in pulmonary arterial hypertension group one patients, which looked really good. The sort of surrogate measure that people look at is PVR, right heart pressure. And we showed, I think basically the largest reductions in PVR seen across therapies. We are translating that over to PH-ILD, pulmonary hypertension patients sort of secondary to lung disease. Because our view is that's a wide open market. Tyvaso has launched extremely well in that market. It's just more in need. It's less of a competitive area. We think the inhaled format there is going to matter a lot because systemic vasodilation actually does not work very well in PH-ILD. You get this issue with like a VQ mismatch. Basically what happens is you dilate the disease lung tissue and you bleed out all the oxygenation benefits that you get from dilating the healthy tissue. If you can just hit the healthy tissue, which is what inhaled therapies do, you get a better effect. We think it will matter a lot. That study is ongoing now. It's a phase 2B study that we'll read out in the second half of next year. We've seen recently in some other companies that good data in pulmonary hypertension can attribute a lot of market value. My hope is that next year people will start paying more attention to this program. What do we know about how PVR translates to six-minute walk? In general, it translates quite well, is the short answer to that question. Actually, it's funny. I think six-minute walk gets a bad rap as an endpoint from things like amyloidosis where it's been a really tough endpoint, to be honest. In pulmonary hypertension in general, six-minute walk is actually pretty well behaved. Like most therapies that show a meaningful PVR reduction have been able repeatedly to show good six-minute walk performance in PAH certainly and more recently in PH-ILD. And so I think it should correlate. I think the translational question of group one PAH to group three PH-ILD is a real translational question. I think there are good reasons to believe the inhaled format will work. But until we see that data, I think that's probably the biggest risk in the study. Yeah. Do you want to talk about the status of your LNP litigation? You've had some positive news flow in the past few weeks there. Yeah. So the history here without going into all of it is we have a team of scientists who have been involved in lipid nanoparticle development for 20 years and were some of the original inventors of LNP for the delivery of oligonucleotides. And it seems to us that Pfizer and Moderna both are using our LNP in delivery of their COVID-19 vaccines. And so we've filed patent infringement lawsuits against both companies. They are progressing. Ultimately, it's mostly hard to comment on an ongoing court case. In the case of the Moderna trial, the jury trial is currently set for March of 2026. And we are in the summary judgment phase of the trial right now, going back and forth with briefs with them. It's ultimately up to the judge to decide these summary judgment issues. Don't know exactly when that will happen. The briefing is mostly done now. So it could be as soon as next month. It could be as late as early next year. It's clear that the original judge on the case seemed to intend to do that this fall. But with a new judge, it's hard to say. And again, it's up to the judge. These are, sorry, I just described the phase. These are important issues that get to the scope of the case that goes in front of a jury. But that's "all they are." There's no possibility of the judge determining the outcome. Ultimately, a jury will decide on infringement, on damages, and on whether the infringement was willful. And that will all happen in March. But there's been a lot of interesting information as a part of these summary judgment briefings, including we've alleged that Moderna fraudulently misrepresented their infringement to the government. We have some evidence to point to there. Also, it looks like Moderna conducted testing similar to the testing that we've conducted and also found infringement in their own testing. And in fact, the scientist who performed that testing asked to do more of it and was told that he shouldn't do more of it because it posed uncomfortable questions, which is a nice email for a jury. So that's the sort of thing that's now become public in the last couple of months. But again, this will all play out both with the judge and with the jury. And it's sort of up to those groups to decide the outcome. Once this eventually reaches a conclusion, like what's the range of outcomes and what could it potentially mean financially for the company? It's very hard to comment on an ongoing litigation. The two COVID vaccines together have sold $150 billion worldwide. Other COVID licensing deals that we have done in other settings have between mid-single digit and mid-teens royalties attached to them. And anywhere in that range is very significant on the total denominator. But again, it's really up to a jury. Great. So at the company level, do you have a different framework in 2025 for thinking about whether to independently commercialize an asset versus how you've thought about it in the past? We have learned a lot over time about that. We did it once before with a dermatology product of Vtama that we commercialized ourselves for a while and then sold to Organon. So we've learned a lot about what we think we're good at and what we think biotech companies generally are good at. And as a spoiler, it rhymes a lot more with dermatomyositis than with psoriasis in terms of where people are succeeding who look and smell like us these days. In terms of like whether to commercialize a drug, first of all, I really like DM as a commercial opportunity for us. I think it has a lot of nice features, among them a concentrated prescriber base, about 200 centers treat a majority of the patients in the U.S., a doc population that is inclined to be excited about our drug, who we know well from running the trial, like I think it's like good features, and then just a patient population with very high unmet need is the bottom line, and so I think that sort of thing makes me excited about the commercial opportunity, and frankly, that then stacks with NIU and stacks with cutaneous sarcoid and other indications to come, and so I feel really good about the sort of go it on our own opportunity in front of us. We have demonstrated historically that we are pretty economic and sort of whatever, economically thoughtful about these decisions. And I think the answer is like, is there a partnership construct or acquisition offer that would unseat that view? Sure. I just think the bar is very high because we think these therapies are really exciting. And to be honest, I think this is truly the beginning of a new chapter for Roivant as a company, right? I think if you look forward, you think about a DM approval and launch and then an NIU approval and launch. And then you start to see things like Graves getting approved in the 2027, 2028 timeframe. It's just like these things really stack on top of each other. And I think it's like not very difficult to convince yourself that these two drugs combined, even before you get to Mosliciguat and other things, are five-plus billion-dollar commercial opportunities and then with room to run. So I just feel like we have an opportunity to sort of grow into the big leagues at this point. And I think that's a pretty exciting opportunity. Talk a bit about capital allocation. You've got a very large cash balance. How do you think about what to do with that? Yeah. So we exited the TL1A sale with about $6 billion in allocable cash. And what we said at the time was it fit roughly into thirds. Sort of $2 billion set aside for funding the existing pipeline roughly to profitability, $2 billion set aside for clinical development associated with new BD, which is all still dry powder. We haven't done a lot of that yet. And then about $2 billion we thought was sort of excess returnable to shareholders. And we've bought back $1.5 billion of stock. We've authorized another $500 million to buy back. And other than that, we're sort of plugging along on those other channels and continue to feel good about those broad buckets. On the dry powder BD angle, like what's your framework for what you think is interesting for Roivant? What we are best at is aggressive creative clinical development of late stage drugs, and so a lot of what we look at falls in that bucket, but we have indication ideas for drugs of a variety of mechanisms. We have targets that we like, and we're pretty opportunistic, so we don't do a lot of sort of true preclinical discovery work. I wouldn't expect that to change. Maybe you're on the margins, but not sort of down the fairway. There are certain indications in therapeutic areas that have been just less, whatever. We mostly in-license our programs, a lot of that from Big Pharma. For example, like Big Pharma is not often out-licensing often awesome oncology drugs, and also those things often need to be developed in combo, and so that's been like less of a focus for us than some other therapeutic areas. But in general, we're open. Great. I think that's all the time we have. Thanks so much, Matt, for joining us. Thank you. It turned out to be no problem for us.