Welcome and good morning. Thank you all for joining us. My name is Will Pickering. I cover U.S. biotech at Bernstein. I have the privilege of sharing the stage with Matt Gline, CEO of Roivant. The company has had a remarkable run over the past year, certainly with brepo as the standout, far from the only value driver. We'll dig into that and the other assets over the next 50 minutes. Conference would also like to spend some time on bigger picture questions, the Roivant business model, and Matt, your view as an asset hunter about the overall health of the biotech ecosystem today. For those in the audience, please submit your questions through the Pigeonhole app so that we can make this as relevant for you as possible. With that as the preamble, Matt, how would you describe the evolution of Roivant over the past few years into the company that it is today? Yeah, thanks. Thanks for having me. It's nice to be here. I appreciate the invitation. Thanks for all the work you guys have done on us. It's been a fun early run here. Look, it's always funny when I'm at a more generalist event or just asked to talk about Roivant, because I feel like there's so much complexity in our history in that we got our start as sort of a, whatever, these words are all overused, sort of a maverick outsider biotech company, doing things our own way, walking our own path. We're built in kind of a funny way that I'm sure we'll talk a little bit about with this Vant model. I think we do bring a pretty different philosophical lens to the industry in that we are a mixture of experienced industry insider drug developers, but also a lot of outsiders like myself. I was a physicist, I was an investment banker. A lot of my leadership team had been public markets biotech investors before joining Roivant, or private markets biotech investors before joining Roivant. You take all of that history and you hold it and it sort of creates opinions, attitudes, a feeling of not fitting in, as it were. The moment that we're at in the business actually is, in some ways, it's the most normal moment in biotech. It's the moment where finally we've invested for years, we've wandered through the desert, we've reached the other side. We have a portfolio of programs that I think can convert us into, for lack of a better phrase, a real business, right? We're at this precipice of launching one and then multiple drugs and one and then multiple indications that I think stand us a real chance of building one of the next large cap biopharma companies. That's just a tremendously exciting moment to be in. That's great. BD has been a huge part of your approach historically, but the current pipeline is very full. I think 10 indications across brepocitinib, mosliciguat, Immunovant, if I'm counting roughly right. I trust that you have. How much of a focus is further BD for the company today? Yes. I'll say for those who don't know the company, look, I think if you're thinking about biotech from the outside, I think people take a relatively reductionist view on what sort of quote, unquote, "science is." There's this mental image of science as a thing that happens in the lab at the bench with a white lab coat on. Bluntly, I make that maybe defensive sounding case because we've never been that good at the white lab coat version of the activity. We have been, I think, increasingly, and I'm super proud of this, very good at the kind of science that takes place in the clinic, in doctors' offices around the world, in clinical trial design and indication selection, in understanding patients and diseases, and figuring out the right way to develop a drug, ideally in a disease where the patients have high unmet need and where not a lot of novel science has been done. If you're good at that latter kind of science, but don't fancy yourself that good at the former kind of science, you're sort of stuck, right? Because it turns out every drug must be discovered in some kind of lab before it is studied in the clinic. We have, as Will has alluded to, built basically our entire pipeline via collaboration, via BD, via acquiring programs. In fact, another thing that I'm proud of that I think we're pretty good at, in addition to sort of asset hunting, spotting things in the world that are attractive, is most of our partnerships have come from big pharma companies. I think we have built a pretty good understanding of and some very good relationships with some of the largest pharma companies in the world. They all have a problem, which is that they do all kinds of science, and sometimes the first kind of science that happens in a lab, and the second kind of science that happens in the clinic, and the third kind of science that happens when you're trying to build a commercial business, don't all align in a nice train that makes you want to start on the same projects that you want to end on. Big Pharma companies often have really great things that fall by the wayside, not because they're not great, but because they don't fit with the antecedent strategic commitments the companies have made. I think what we've built a lot of our portfolio around is bringing in those programs. It is profoundly a part of our DNA to be on the hunt. Frankly, biopharma is a treading water industry. It's like I'm not sure it's actually scientifically accurate, but they say that if sharks stop swimming, they die. If Pharma companies stop replenishing their pipeline, they die because our drugs are all wasting assets. From the minute you invent a drug, it has a fixed life before the patent runs out. We are always on the hunt, and I think that skill serves us well in developing the drugs we have now. Absolutely, we continue to look for programs and we'll continue to bring more in. That said, I completely agree with the comment that you made. Our pipeline is rich and exciting, and there's plenty to do just within the context of the late-stage clinical programs that we're bringing to market. As you look at the biotech landscape today, both from an innovation perspective, but also looking at valuation, how attractive is that for an asset hunter? Look, I think the last really 25 years in biotech have been pretty remarkable in that we went from an industry in the early 2000s where 99.5% of drugs were small molecule pills of the same general sort that had been around a long time, and the big story from the previous 25 years had been the invention of modern synthetic medicinal chemistry that lets us do some version of designing those drugs intentionally, to now we have mRNA vaccines and monoclonal antibodies are used left, right, and center, and people are injecting themselves with unapproved peptides manufactured by small Chinese CDMOs. The world is crazy in terms of the kinds of things that people are working on. While our understanding of human biology remains what I'll call nascent across the industry, it's gotten better, and I think that has made for an explosion of ideas. Look, I think anyone living in the world knows that we are still far behind in terms of our fight versus disease, illness, and aging. With the explosion of ideas and a lot of territory left to cover, it's a good time to be an asset hunter. There's a lot out there that could be valuable. Then there's all kinds of more localized shifts, right? There's geopolitical things going on. There's the incredible pace and quality of antibody discovery, especially in China. There's the pace with which you can run early clinical trials in places like Australia, New Zealand, and China. There's a series of global and U.S. political factors buffeting big pharma that creates a need for shift in their portfolios, and I think all of that also benefits us. Excellent. Well, why don't we. Sure Parts of the pipeline. We'll start with brepocitinib. You're approaching your first commercial launch in dermatomyositis. Could you start by framing the opportunity and then talk through the key priorities for your commercial team to drive that launch? Yeah, perfect. I get ever so slightly defensive, although maybe it's not serving me well when people call it our first commercial launch because, in fact, we have had now six or seven FDA approvals come effectively through our business. Many of them have been commercialized externally, a number of them through Sumitomo, a company we partnered with a few years ago on a first generation of our pipeline. We did in fact launch a drug called VTAMA in psoriasis. I'm not sure it benefits me to bring it up in a setting like this because it didn't go spectacularly well, but it went fine, and then we sold it to Organon a couple of years after we launched it because it just didn't fit with the quality of the pipeline that we had in-house. We learned an enormous amount about what it takes to launch a drug and what we think will make us successful, including enormous amount that makes us more and more excited about launching brepocitinib. I think that's kind of where we're at now. What would you say are the top priorities for your commercial team to really drive- Yeah That launch? One of the cool things about the current moment is if we're at this stage, if we were about to launch a drug like brepocitinib and it were 2019, I think there'd be a lot of healthy skepticism. We'd be a sort of short launch story. You look out over the past five or six years and probably first Horizon with TEPEZZA, Horizon, argenx obviously, Insmed now, Madrigal, Verona, BridgeBio, there have been a number of very successful commercial launches from and out of biotech. In fact, I suspect that at least some of those drugs have been launched better in the hands of companies like argenx than they might have been in the hands of big pharma companies, that argenx's creativity in crafting a modern commercial strategy has been really transformative. The first thing that we're trying to do is. Look, I hope eventually people describe us in the same terms that they describe companies like argenx as a commercial innovator. Before that, I hope they simply say they learned the lessons that argenx taught us. We are trying to do everything that argenx and Horizon and others have done. That includes. Look, the world has had some structural shifts on access, for example, where rebating, at least in orphan disease, is less a part of the landscape and where patient support has been an enormously important part of access. For example, we hired this woman, Leigh Liberatore, who built TEPEZZA's patient support organization, and she is building our patient support organization. I think one of the things about launching an orphan disease that's become increasingly true is these patients, and this is true in DM, are treated at a more and more concentrated set of referral centers. A, we've built excellent relationships with those referral centers. They were the people who ran our clinical trial in many cases, and they are where we are spending a lot of our commercial time and medical education time now. B, I think you build a field force therefore that is the right people, not necessarily to call on a community dermatologist, but to call on an expert in the field who spent their entire career treating dermatomyositis patients. That means we have recruited one of our field force personnel, one of our sales reps is a career-long myositis KOL who left clinical practice because she was so excited about what dermatomyositis might do that she thought she'd take a hand at helping make it a success. I think that is, she's not really a sales rep therefore, she's sort of a medical affairs professional. She's a jack of all trades, I think that's the sort of thing that is a really high priority for us in making sure we're making the launch a success. The point that you made about short the launch not being as successful of an investment strategy today as it was maybe a few years ago. Part of that is these companies have done a good job. Part of it, I think, is also that I think expectations have been a little bit more well-grounded. How are you thinking about what that means for communication with investors about the early launch, about KPIs, what you're planning to share for brepocitinib? This is a subject of healthy debate at Roivant and other places historically. Bluntly, I think we've learned a few things from recent launches and from the investor trajectory of recently launched companies. The first is, I have a great deal of confidence in the ultimate commercial potential of brepocitinib as a drug, specifically in dermatomyositis and across indications. There's a lot of these patients. We can talk more about it. They have high unmet need. It's not a very competitively intense field right now in terms of people who are offering them options. Look, at some level, this isn't rocket science. The only other approved therapy in dermatomyositis requires on-label that you spend eight hours a day, five days a month consecutively in an infusion center receiving an IV infusion, and we are a once daily oral that provides probably better clinical benefit. This is not the most uphill battle in terms of convincing people that it's an attractive alternative. I think all of that pulls together to a high set of expectations. That said, no one has launched a novel targeted therapy in dermatomyositis ever. The pace of the launch, how quickly we'll be able to get doctors changing clinical practice, how quickly we'll be able to work with payers in this specific population and do the education work, I just think it's basically impossible to know. We've certainly seen launches rocket out of the gate, and we've seen more slow and steady ramps. My general view is, I expect, I think everyone should expect slow and steady. Also there is zero benefit to providing guidance. Just standing up there and giving people a sense of what I think is we're going to have to wait and see, and we're going to do our level best to make it a long-term success. Along the way, I'm sure we'll have fits and starts, but I'm excited for where it heads. Frankly, I think the companies that have attempted to provide guidance have not been rewarded for providing that guidance anyway. I'm not sure. That's also a lesson learned from a Darwinian process. Yep. Other indicators like new start forms, have you thought about whether you'll be sharing that information? Yes, the answer is most of our decisions on that basis are going to be rooted in commercial and competitive dynamics. We will be, as all orphan launches do now, using tailored, quite narrow, focused, limited distribution. And in general, for a variety of commercial reasons, when you do that, you pretty rarely wind up sharing scripts. Our scripts will probably not be widely available on a regular basis just because of our commercial distribution plans. That's just how that's going to play out. Got it. What are you hearing from docs on the likely mix of patients in terms of prior therapy? One of the questions that we get a lot is the pace of JAK switching. Look, taking a tiny step back. In claims data sets today, there are about 40,000 patients actively treated for dermatomyositis. That is a portion of the total dermatomyositis population. I think epidemiology suggests maybe that number is 70+. It's also relatively difficult to diagnose condition, there's probably more patients out there who have either not received the diagnosis at all or have received a lupus diagnosis or whatever, who may very well have dermatomyositis and show up later once we arrive. Of those 40,000 patients, about 75% of them are on steroids and immunosuppressants, prednisone, methotrexate, and many of those patients are poorly controlled. The way we know they're poorly controlled is they're on quite high doses of steroids, in many cases more than six months a year on greater than 10 or even greater than 20 mg of prednisone. If you've ever had an allergic reaction, you've spent time on 20+ mg of prednisone, it's a miserable existence for three days. I cannot imagine doing it for six months. You know those patients are poorly controlled because they're making that choice. That is absolutely one of the early groups of patients that we are most enthusiastic about. Those patients are not on other therapies for a variety of reasons. They can't spend five days a month in an infusion center. They don't want to take an unapproved B-cell depleting drug like rituximab or whatever that has failed clinical trials in dermatomyositis. They're sort of stuck with steroids and DMARDs and dealing with the unsuccessful treatment that comes with it. You can imagine an IVIG patient spending all this time in an IVIG infusion center thinking that maybe a one-pill regimen sounds good. That's another place where I think we will get early patients. About 25% of the patient population is on something other than steroids and DMARDs. That's like about half of those patients are on IVIG, and the other half are on a collection of off-label stuff. The vast majority of the off-label stuff are literally drugs that have failed dermatomyositis trials, but that probably provide some benefit in inflammatory diseases, or docs are trying it because they don't have anything else to do. Some small, low to mid-single-digit% of those patients are on off-label JAK inhibitors. The truth of the off-label JAK inhibitor population, when you actually do the math, low single-digit% of a 40,000-patient number, it's hundreds of patients, basically. Maybe a couple of thousand patients in total. It's actually a pretty concentrated group. For example, I think at another bank's KOL call, Julie Paik at Johns Hopkins said she had 70 patients on off-label tofacitinib. That's a relatively significant percentage of the total patients on off-label JAK inhibitors. What she said she would do is switch those patients as soon as she could, basically. I think what will wind up happening is prescriber by prescriber. Some docs will be eager to switch. Some docs will say, "Look, at least the off-label JAK patients are kind of on something that works for them. I'm going to go with my high-dose steroid patients." I think some of that will come down to access and how easy we make it to get patients on drug. I think some of it will come down to how the docs that were on our trial and have a lot of familiarity with brepocitinib may be faster to use it. The docs that were not on our trial and are still coming to speed with it may do a little more experimentation. I think it'll be a mixture. Yeah. In terms of competition, VYVGART, they've got the phase III IM later this year. Assuming that works, how much of a swing factor are the actual results really in terms of brepocitinib's future market share, do you think? Yeah, look, they're 18 months behind us probably, and so we're not that far. Right now, we do have to outrun the bear, as it were. That is, it's not about the competitors, it's just about the disease. Later, we only have to outrun them or something. Look, first of all, I think DM is one of these diseases where the unmet need is so large and there are so many patients that more share of voice by the industry, more new therapies, more options for doctors is mostly going to be a rising tide. And I think VYVGART, in MG, has benefited from the existence of the complement pathway programs. I think I will benefit from the existence of VYVGART. And I think I would much rather be VYVGART and MG than a complement company. I would much rather be brepocitinib and DM than VYVGART because we're first. I think, look, we're getting a lot of inbound calls now from investors, and the path they're taking to get to us is they are argenx shareholders and they're focused on DM. For the first time, they're doing KOL calls in DM, and they pick up the phone and they call DM docs and they're like, "What do you think of VYVGART?" The docs are like, "Hey, have you heard of brepocitinib?" They're calling us because they're sort of coming at this from the side, and that's an enormously rewarding thing in the sense that it helps bring people to our story. I think it just underscores the lead that we've got. Practically speaking, I think there are reasons to believe that dermatomyositis is not going to be the strongest setting for VYVGART among the myositis. The trial that VYVGART's running is across multiple different myositis. It's running in IMNM and in DM and in polymyositis. I think IMNM is more biologically on point for an FcRn, and I think their efficacy will probably be better in IMNM than it is in DM. I think that based on biological rationale. I think that because argenx's public statements to me suggest that they generally believe that too. I think if you compare our phase III data to the phase II data generated across the myositis, they didn't break it out by subtype in their phase II study. We were faster to achieve a moderate TIS response and achieved our responses against the backdrop of an aggressive steroid taper and still did comparably or better than VYVGART did. I think we will have a competitive profile. The truth is, ultimately, you're only as good as your label. If VYVGART gets lucky and blows it out of the park in this study, it'll be more of a competitive factor than if they don't. We'll just have to see what their data looks like when it comes. All right. NIU, next most mature indication. You've got the phase III later this year. Phase II, highly compelling, small cohort. Frankly, I've not heard a real strong bear case for this trial. I'm not going to sit here and ask you to articulate one. I can if you want. Maybe what were some of the risks that you sought to mitigate when you designed the phase III? Yeah. Look, NIU, non-infectious uveitis, is a basket diagnosis for inflammations of the eye that are not caused by an infection. It's a heterogeneous patient population. It has not been an area of very active clinical development. It has stymied a lot of others who have tried to develop there. It's a bad disease. An ophthalmologist's tolerance for eye inflammation is very low because NIU is the third leading cause of blindness in the U.S. right now. It's like a bad disease, patients really don't want to go blind, they're willing to get treatment. Against that backdrop, the only other sort of approved modern, quote-unquote, therapy for NIU is HUMIRA, which bluntly doesn't work that well. Somewhere between 50%-80% of patients, or 50%-75% of patients fail HUMIRA, depending on how you count it, et cetera. They fail it pretty quickly, right? The time to treatment failure in the HUMIRA study was like six months median. It's a disease with a lot of unmet need. We ran a study, it was a phase II study. It was blinded and dose ranging, but it did not have a placebo, and I said HUMIRA's time to treatment failure in their phase III was a little under six months. We went over 12 months as a median time to treatment failure. With a lot of cushion versus the field, but no placebo. The blunt level truth in immunology is that placebo response rates have crept up in every indication in history, and we didn't have placebo in our phase II. You asked me what the risks in the trial are. The biggest risk in the trial is whatever. The bear in this clinical trial is placebo, and we have to outrun it. I think that's a challenge that we're cognizant of. How do you do that? First of all, the heterogeneity of the patient population is always an obstacle. I think we've done a very good job with some creative and aggressive strategies to make sure we have the patients we need in the trial, that they are sick in the right way, that they are sick NIU patients. We have specific, what's the word I'm looking for? Adjudication criteria for making sure the right patients get into the trial. We have a very aggressive steroid taper. One of the things we did in the phase II, the way these trials all work, because tolerance for eye inflammation is poor, is you can't just bring a patient in and put them on your drug. You have to bring them in, put them on a very high dose of systemic steroids so that you get the inflammation under control, and then taper the steroids and see if you can maintain a response on your drug. The HUMIRA studies used a 12 - 16 week taper, I think. We used a much more aggressive taper than that, and we used it in the phase II in part because there was no placebo, and we wanted to give ourselves a hard test, but it worked. So we're using a similarly aggressive taper in the phase III. I think that will help control placebo response as well. How much of a headwind do you think the availability of biosimilar HUMIRA is in this market? Two things. One is, there's about 40,000 patients on TNFs with NIU, and as I said, the treatment failure rate is 50+%, and they tend to fail within six months in the clinical trials. Even if at the price points that we have in mind for brepocitinib you live entirely in a HUMIRA-refractory population, it's a blockbuster indication for us, and because ophthalmologist tolerance for eye inflammation is low, if our data are good, I think there will be a strong desire to use us aggressively in early-line settings. That'll be a question of label, it'll be a question of payer dynamics, but mostly I think there will be a lot of people fighting for early access if our data supports it. I think we will work with those people to get these patients on drug so they don't go blind. I had intended to spend a little bit more time on CS and LPP, but maybe let me just ask a broader question of what is your indication selection strategy for treprostinil. Yeah CS and LPP. I could launch into an, I think, interesting thematic history of JAK inhibitors here. In the interest of parsimony, I won't. Look, I think in 2019, if you had said, "By 2026, there will be a large, successful, important JAK inhibitor franchise targeting orphan disease," everyone around you would've said, "Duh." It's obvious, right? In 2019 JAK inhibitors were everywhere. They were going to be the future. The black box warning thing happened. Everyone kind of backed away. If in 2019 you said, "Oh, who is going to own that large franchise of JAK inhibitors in orphan disease?" Everyone would've just looked at you and said, "Obviously, it's going to be Eli Lilly, it's going to be Sanofi, it's going to be AbbVie. It's going to be any of the companies that had a place in JAK inhibitors and a place in orphan disease and a right to win there. The fact that an approximately random mid-cap biotech company owns that franchise is a combination of cleverness on our part that I'm proud of and random accidents of history that I'm glad to have benefited from. As a consequence, we own right now the category of JAK inhibitors in orphan inflammation, and there are many orphan inflammatory diseases. Literally almost any inflammatory disease with, call it 30 to 130,000 patients, is a good swim lane for us. Obviously, we're focusing on the diseases where we know the physicians. We're focusing on Th1-mediated disease, the places where JAK1 and TYK2 add benefit for a variety of reasons. We're looking across that space, and there are quite a lot of indications to go after. I think even more than DM being an exciting indication, though it is, or NIU being an exciting indication, though it is, the breadth of what brepocitinib could do is actually pretty staggering in terms of the number of diseases we could help. Switching over to mosliciguat, maybe would you like to start with just an overview of the drug and why you're excited about PH-ILD, and then we can shift over into expectations? Sure For the trial. It's fine. I talked at the beginning of this, you asked about BD around how we bring our drugs in. I didn't mention, we paid $14 million upfront to Pfizer for brepocitinib. We also paid $14 million upfront to Bayer for mosliciguat. Mosliciguat is a drug, it's an inhaled vasodilator. Mechanism is this thing called sGC activation. We got it from Bayer a few years ago. Basically what happened here was Bayer had a history in this chemistry. They, in fact, sort of originated the development of drugs in sGC. They were partnered with Merck on respiratory disease around a drug called Adempas that was a commercially successful drug, took $2 billion-$3 billion in peak sales, a big drug. Then Bayer and Merck had kind of a messy divorce at the end of that process, or at least they split ways and each went on down their separate path of developing a successor drug to Adempas. Both of them developed inhaled sGC drugs. Bayer's, in our view, was the better drug. Then Bayer went and did some M&A in the agrochemical space that was complicated. They had to make difficult choices around their pharma portfolio because Roundup allegedly causes cancer. So they got out of respiratory disease. This was a while ago, and they no longer had a real footprint there, and they weren't sort of doing active research in respiratory disease. Meanwhile, United Therapeutics, one of the forefathers of pulmonary hypertension development and a phenomenal company, sort of whatever, struck gold for a second time. They found pulmonary hypertension from lung disease, PH-ILD, as an indication. They got TYVASO approved there. They launched it commercially, and it has been an enormous commercial success that has engendered an entire field of literal follow-on molecules of other treprostinils similar to TYVASO from Liquidia, from Insmed, that I think are also really exciting drugs. We went to Bayer at that moment in time realizing that mosliciguat, which had been developed principally in the more competitive Group 1 pulmonary arterial hypertension, should also, in theory, work as an inhaled vasodilator in PH-ILD. Bayer was not at all really paying attention to the field and certainly wasn't going to run a novel development strategy in lung disease. We in-licensed it from them and set on retraining the program towards PH-ILD. Now we are reading out a phase II-B study later this year, the first, basically, in a non-treprostinil mechanism of a late-stage study for PH-ILD. What does a successful phase II look like for you? Yeah. In PH-ILD, as with all pulmonary hypertension, the approvable phase III endpoints are things like six-minute walk, which again, because it's a generalist conference, six-minute walk, first of all, is a widely hated endpoint in biotech. The reason is because roughly speaking, what happens is you're standing in a doctor's office, picture your doctor's office, and the doctor says, "How far can you walk in six minutes? I'm going to set a stopwatch and get out a tape measure, and you're going to go." It turns out conditions vary widely. Are you walking in a hallway? Are you walking in a waiting room? Are you walking in circles on a tile floor? Are you walking on a carpeted floor? This leads also like, did you eat your Wheaties when you woke up in the morning? Did you drink a cup of coffee? There's just a lot of things that make this a variable endpoint. It turns out that it is a relatively well-behaved endpoint in pulmonary hypertension, it's quite variable. In phase II studies in pulmonary hypertension, including in PH-ILD, the primary endpoint tends to be something called PVR, which is right-hearted blood pressure. It is a literal measure of disease activity in that you are measuring the flow of blood through the right ventricle. The way you measure it is under general anesthesia on an operating table with a catheter, it's not something that you can do regularly in very large studies, it is the primary endpoint of our study. Again, a measure of how sick these patients are is they subject themselves to a clinical trial that requires regular general anesthesia and catheterization. That's the primary endpoint. There has not been across pulmonary hypertension, a mechanism that delivers 20+% reductions in PVR and has not gone on, not just to be clinically successful on six-minute walk, but to be a multibillion-dollar class. Our view is if we can deliver 20+ benefit on PVR, nothing else really matters. That is almost certainly a good enough indicator that we will be able to deliver clinical benefit in a subsequent phase III study, that we will run the subsequent phase III study. That said, we are measuring six-minute walk in the trial. We are measuring other clinical endpoints, and while the study is not powered to deliver P-value statistical significance on those endpoints, it would certainly be helpful to understand magnitude of effect in those endpoints as well. With TYVASO, I think that they had a pretty big gap between peak and trough six-minute walk, which I think kind of underscores that your daily dosing could be a clinical advantage and not just a convenience advantage. Are you collecting six-minute walk at different time points post inhalation, either in this or in a future phase III? Yeah, we are measuring a bunch of different time points. One of the great things about our drug is it is quite stable in the lung, and, in fact, in phase I studies, we have like elevated cardiac output, cGMP production out 48 hours after a single dose. I think we do actually get quite a lot of benefit from the time course. Because it's 48 hours, we will get meaningful stacking over multiple days, over multiple dosing, and I think all of those things should contribute to better clinical benefit, and I think we will measure at different time points so that we can begin to sort of dimension out that effect. How do you envision the commercial opportunity for mosliciguat, either as monotherapy or combination, and what kind of evidence would you need to generate to? Yeah Support that? This is another thing where we can learn from history. In PAH, pulmonary arterial hypertension, which is a, I think, $10 billion+ category now, it's the sort of first of the pulmonary hypertensions, as it were, to be treated. What happened was, actually, treprostinil were the first modern drugs approved, epoprostenol. A series of successive classes, including systemic sGC stimulators, were approved, and each time a new class entered, two things happened. One is actually life expectancy for these patients increased by, in some cases, as much as two to three years, and the other is patients just went on multiple categories of drugs. This is a polypharmacy market. Pulmonary hypertension ultimately often kills you. It's a very bad disease. These patients go on everything they can get. They cycle drugs. They add them on top of each other. I think that is exactly what will happen in PH-ILD as well. It will be a polypharmacy market. We will be used before TYVASO, after TYVASO, on top of TYVASO, in every combination, and with other mechanisms, hopefully, as well. Practically, that means from a clinical benefit perspective, worse than TYVASO, better than TYVASO, similar to TYVASO. It doesn't matter that much in the end because most patients will wind up on most drugs. The better we are than TYVASO, the earlier we'll potentially be used. We have some other advantages. We're one inhalation once a day versus more for the others. One puff from a dry powder inhaler once a day. We don't likely cause cough as a non-target effect, which the prostacyclins do. There's a variety of reasons why we could be used in an earlier line setting, but mostly the answer is this is going to be a polypharmacy market, and everyone's going to be on top of everything. To answer your question about evidence generation, in our phase II-B study, we do not allow concurrent TYVASO use. TYVASO's only approved in the U.S. It's a global study, so it's slightly complicated. In the phase III study, we will allow some patients on concurrent TYVASO precisely because it's important that the label allow for concurrent use. However, it's important therefore to know a little bit about what we do together with TYVASO, especially from a safety perspective, but also to get some sense of efficacy. We are currently, in addition to the main phase IIb, running an open label combo study with TYVASO that has just started, so we don't have any data from it right now, but that will help inform things like stratification in the phase III. A question on the iPad, what other indications in PH could you look at, and when would you consider starting those? Yeah. Perfect. Look, I think the history of this is helpful, too. Look, locally administered vasodilators are effective in pulmonary hypertension. We'd probably work in PAH. We have good phase I data there. It's competitive, but we could go there eventually. I think PH-COPD is an interesting indication, although local vasodilation in lung disease patients with emphysema is a more complicated proposition, and there's more emphysema in the PH-COPD population, so for that reason, requires some more careful thought. Recently, though, we've also seen the prostacyclins, treprostinil, TYVASO specifically, be successful, for example, in IPF, and that is absolutely high on our list of things that we are excited to think about. Ultimately, we're going to learn a fair amount about all of that from this phase IIb later this year. We're measuring FVC in IPF patients. We'll have a sense for how we did there, albeit in a small subset. I think all of that will inform next steps. PH-ILD's a huge indication, and we wanted to make sure we nailed it, but I think we will be initiating new indications if the phase IIb data supports it pretty quickly after we get this data. Switching to Immunovant. Could you start with how IMVT-1402 is differentiated from the other FcRns in terms of either product profile or the indications that you're pursuing? Yeah, perfect. Again, I'm sure many people in this room are familiar with FcRns as a mechanism because argenx has been so enormously successful in creating that category. This is sort of, it's like a big moment in immunology in that this is sort of the HUMIRA moment for a new kind of immunology. It's the first time we've had a drug approved that can treat what I'll call B-cell disease, autoantibody-driven disease, much of which isn't even inflammatory. Graves' disease isn't really an inflammatory disease at some level. It opens up an entire set of new indications, and argenx has done a phenomenal job in MG and in CIDP and other places, creating those markets and showing real benefit for those patients. VYVGART has some limits. nipocalimab, the J&J drug, has some limits. Among them, as each of them is currently studied practically, and in VYVGART's case, probably just due to biological limitations, they don't suppress IgG more than, call it, 60% or 70%. Whereas I believe we will suppress IgG by 80+% with 1402. I think we can get better efficacy. We are formulated as a simple, standard Dupixent-style auto-injector, which is something that VYVGART is not. VYVGART is a high volume long push with higher injection site reactions and things like that, or a HALO, sorry, or an IV drug. I think those are all advantages that we have. I think. Although not as important as being a better molecule, almost as important as being a better molecule. I think we've just carved out some really great white space indications for ourselves. We have pioneered modern drug development in Graves' disease, where we have an ongoing pair of registrational studies that we hope will be successful, will create the first approved novel therapy in Graves' disease since the 1950s. That's an indication with millions of total patients, hundreds of thousands of poorly controlled patients. Imitation is the finest form of flattery. We have created a cottage industry of other companies now developing Graves' disease, they're all years behind us, I think we have really built out some expertise and positioning there that's exciting. Just last week, we showed some data in a subsetting of rheumatoid arthritis that was frankly more compelling data than we expected it to be. Showed a potential role for FcRns in late-line multi-mechanism failure rheumatoid arthritis that I am excited to explore from here. Those are both indications where we're way out in front and kind of alone right now, and there's many others that we're pursuing, some of them like MG, more competitive, and some of them, like CLE, less competitive. That's where I was going to go next, was RA, if you want to share some of the highlights of that data and why you think you're able to achieve such higher ACR responses versus nipocalimab? Yes. RA, obviously not an orphan disease. Many patients with RA. It is a disease that is more complicated than Graves' disease, in that it is not just an autoantibody disease. It's an inflammatory disease, it's an autoantibody disease in some patients. There's different etiologies. It comes from different places. It's a complicated disease. The idea that FcRns could work in RA is not an idea of our own invention. We know that some of the disease is autoantibody driven. In fact, one of the exciting things about FcRns there is, unlike all of the other drugs, basically, in RA, it's not an anti-inflammatory, and so it might work differently on a different axis, and therefore work in combo or in later line settings where anti-inflammatories failed. This was the idea with which they had been studied historically. J&J has run two studies in RA. One was effectively a monotherapy study across a variety of lines of therapy, across a variety of different patients. They showed fine responses. They showed clear benefit, but nothing that was getting people out of bed. The two exciting sort of indicators in the data that were interesting, one, almost all of their responses came from the subset of patients that tested positive for autoantibodies, that was a clear way to enrich on a biomarker. Two, their efficacy appeared to be preserved irrespective of line of therapy, you look at that and you're like, "Okay, maybe there's something here in late line." In fact, even though their efficacy was kind of middling in late-line multi-mechanism failure patients, it was potentially good enough to have a commercial plan. We and J&J, after seeing that monotherapy data, each then plowed on with different strategies. J&J said, "Okay, we're going to run a combo study in early line patients comboed with a TNF." That was a study they ran. We were like, "We're going to focus on the late line multi-mechanism failure population and run the study that we ran," which was in patients who effectively failed everything they can. They failed at least two of TNFs, IL-6 and JAKs. A majority of them, as we now said, have failed TNFs and JAKs. These are late line patients without other options. The confusing thing is J&J's combo therapy pretty spectacularly didn't work. They basically didn't separate from the TNF. That was always a hard study to run. You're putting patients on a TNF for the first time. They're going to benefit significantly from the TNF, and so you have to kind of demonstrate benefit on top of something that's already helping them. But still, the level of separation was disconcertingly poor, and so I think that confused us when we saw it. Our study read out, and it showed something sort of surprising in the opposite direction, meaningfully better responses than either of the other two studies. The data that we've produced so far is data from an open label run-in period to a randomized withdrawal trial. It is nuanced data across multiple axes, and certainly one of the reasons it looks as good as it did, we showed ACR 70s in the high 30s, which is as good as anyone ever shows, basically. It's close to JAK-like in its efficacy, which in a JAK failure population is extraordinary. Especially for a mechanism that's pretty safe, like an FcRn. Part of the quality of that data has to be due to the fact that it's an open label setting. There's some rising tide effect here, you just don't spontaneously have an ACR 70 response. Those are pretty big improvements in sick patients who have failed a lot of other drugs. I think our belief is there's clearly something real happening. The other two things I think that are relevant, one is we did a pretty good job selecting for an autoantibody positive population. The J&J combo study with Cimzia was autoantibody selected, they allowed rheumatoid factor patients, for example. It's not as rigorously specifically focused on ACPA as ours. I think we generated some benefit there. Then I sort of have to believe, although I don't yet have the evidence to back this up, that the other thing that happened for us is it turns out that when you filter out patients who have failed, remember failed is an important word here, JAK inhibitors and TNFs, that those patients have tried anti-inflammatory mechanisms that are very effective for treating their RA and have not succeeded, that it must at some level be that we are enriching for a population whose disease is causally driven by autoantibodies in a way that even we didn't totally anticipate. Ultimately, we'll find out. Period two of this study is going to be harder now because we have to generate meaningful reversion in patients that have benefited a lot clinically from being on drug, we might not even hit a P value in period two. We're going to really study the patient-level data here and try and understand what's happening, and then work with FDA on a trial design for a subsequent study that I hope will be tractable and lead to a lot of benefit for these patients. Getting some more questions on the iPad, and this is more of a big picture thing, but the cash balance, you've got $4 billion. You'll be getting more from Moderna. What are your plans for that, considering that you have not spent a lot of money on transactions historically? Yeah. Look, I think one of the things about Roivant is we are sort of culturally built to be good stewards of capital. It's just sort of part of who we were to begin with, and it's led to some puzzling decisions over time. Look, I think biotech companies historically haven't bought back stock. That's changed a little bit. Like, we bought back a billion and a half dollars of stock at $10 a share because we had too much cash. That turned out to be a good investment over time. We continue to buy back stock now as we bring in more money from Moderna. What we said, lost in history at this point, is that we bought a drug from Pfizer a while ago and then sold it to Roche for a lot of money. We had a lot of cash on our balance sheet. That plus the Sumitomo deal is how we wound up sort of highly capitalized. I think what we said all along is, if we can't do it with $4 billion, we probably can't do it with $6 billion. That is like, there's an amount of money beyond which it just isn't required to build the kind of business we're building. Frankly, the kind of BD that we've done historically has been pretty capital efficient on the upfront, expensive clinical development, pretty capital efficient on the upfront. Look, I think as cash comes in above and beyond current levels, we will continue to be pretty aggressive about returning it to shareholders, just because I think balance sheet leanness is something we believe in. We have still a lot of cash, even absent that, and we'll spend a fair amount of it on breadth of development for the existing pipeline. We will add indications for Brepo, we will add indications for FcRn, we will add indications for mosliciguat, and we'll be active on the BD side. I really hope we bring programs in with expensive phase III trials. Those tend to be big indications. They tend to be exciting. They tend to be the kinds of things we can make a difference at. I hope we spend a fair amount of our money on that. AI has been a big theme for this conference. What are your expectations for how that impacts drug development and over time? What is Roivant doing today? At the current moment, at a generalist conference, I think what I'm supposed to say here is we're an AI native, AI first company building data centers in space. We're not building data centers in space. I don't know how, but I think that's what we're supposed to say. Look, there is a lot of talk about AI in biopharma, a lot of that talk centers on novel uses of AI in drug discovery, on medicinal chemistry, on biology. I think that stuff is super interesting. We have invested in it. We have built a company that is successfully using AI to model protein-protein interactions that we have a big stake in. Look, I think it could be a company that invents designed molecular glues in a way that wasn't possible for AI. There's like cool things are going to happen here. Those are the apples at the very top of the tree. Those are the hardest of the hard problems to improve with AI in biopharma. While we and others will work on them, I don't know how quickly we're going to revolutionize drug discovery. If quickly, that'll be great for us. There will be many more drugs to put into clinical development, and we are very good clinical developers. If slowly, that's okay too. In clinical development, what is clinical development really, in addition to a science problem? It is a massive logistical coordination exercise where you're reading hundreds or thousands of patients' medical charts, combing through them, literally as human beings, trying to figure out which of these patients are good for your trial. You're trying to turn around legal documents like site agreements and IRBs and IRB agreements and protocols quickly. They're all similar to each other, but different in little ways. These are all things that the AI of today, the Claude that is on all of our desks, is really good at. Our ability to prosecute large trials at scale is dramatically better than it was a year ago, and we are coming to terms with that. I'll say, look, I think we made a concerted effort to get these tools out and available to everybody, and we are building tools every day to make ourselves better at this. Again, if I were to try and defend ourselves as an AI first company, those are the things I would talk about. It's just been this incredible Darwinian process. You put Claude on the desk of a smart person running a clinical trial, and they're like, "Oh, my life is easier now. Here are the seven ways my life is easier now." I think a lot of what we're doing is just putting the right people in the right seats with the right tools, and it turns out that's making us better. One more question to close us out. If we fast-forward two to three years, what has to be true for Roivant to be a $50 billion market cap company? Yeah, look, I think some of our launches have to go well. I think that's true. I don't think DM has to be an $8 billion indication. I think DM has to be a billion and a half dollar indication in people's minds. Look, if DM is a billion or a billion and a half dollar indication, NIU is a billion and a half dollar indication, and CS and LPP are a billion or a billion and a half dollar indications, and FcRn in total is $3 or $4 billion, we're there easily, right? We're on our path to being. I don't mean that literally in three or four years. People have to believe those things in three or four years, or two or three years, for us to achieve that kind of scale. I think we have to do reasonably well commercially somewhere, and we have to keep stacking indications. To be honest, I think that's about it there. I think if you're asking me how we become a $150 billion company, there's a lot we have to do between here and there. I think the path to 40 or 50 or 60 is good execution on what we've got now. Great. Let's leave it there. Thank you, Matt. If you take nothing away from this conference, just remember we are an AI first company building data centers in space.