Good morning, everybody. Thank you for attending. This is the Fireside Chat with Matt Gline at Roivant. Maybe I'll introduce myself very quickly, Albert Wong with Morgan Stanley on the investment banking side, and Matt, if you could give a quick intro before we get started. Sure, yeah. I'm. It's good to see those of you that are here. I'm Matt Gline. I'm the CEO of Roivant. We are, well, I think most of you probably know, but we are a nine-ish billion-dollar market cap biotech company, developing a portfolio of pretty exciting programs and looking for more because we have about $6 billion in cash. We're facing a just absolutely packed next eighteen months, so I'm excited to dive into that. Okay, and well, it sounds like you know many of the people here, but for the uninitiated, can you give a quick overview of the Vants- Yeah -that exist within Roivant and, you know, just kind of some of the ownership structure? Sure, yeah. So if you're not familiar with the companies, the way that we're built is we're a therapeutic agnostic, really, drug developer. What we're really good at is finding unique programs in the world, in different places, bringing them in, and developing them in capital-efficient ways. We are structured in a sort of unusual way, where when we bring a program in, we hire a management team specific to that program and put them in, really, an independent company called a vant, that we then control. Most of them we wholly own, some of them we partially own. And at this point, the sort of most important of our late-stage vants... So we have Immunovant, which is developing a franchise in anti-FcRn antibodies. I suspect that most people in the audience who are focused on Immunovant are actually next door, listening to Amgen talk about Uplizna, but that's one of our programs. We have Priovant developing brepocitinib, which is a dual inhibitor of TYK2 and JAK1 that we got from Pfizer, that's targeted against orphan rheumatology and immunology. We have Dermavant developing Vtama, or commercializing at this point, Vtama, a topical aryl hydrocarbon modulator for psoriasis and soon-to-be atopic dermatitis, and then we have Genevant, which is developing a portfolio of lipid nanoparticle technologies, but is best known for having an active litigation around IP with Moderna and Pfizer. Okay. And in owning the different components of this, you said some of them are wholly owned, some of them are partially owned. Is there a strategy behind that? And what would you say are the synergies among the vants or the core competencies at Roivant in general that keeps it all together? Yeah, look, so, in general, we love the programs we're developing. We want to own as much of them as we can. Immunovant is a publicly traded company. We used to do that more earlier in our life before we ourselves were public, so we own about 60% of it, the rest is publicly floated. Otherwise, for us, in terms of ownership and sort of how we think about that piece, it's really just a tool for partnering, right? Like, what we are really good at, actually, is finding great programs, concocting development strategies for them, and extracting them from partners. And historically, our best partners, in many cases, have been big pharma companies that are, and this is a great moment for it, sort of in these sort of ever-shifting seas, trying to steer a big ship, and, you know, oftentimes wind up with things in their late stage pipeline that just aren't on strategy for them. And so what we're really good at is spotting those opportunities, bring them in, and we've done some pretty exciting deals in the past. We last year had a round trip of an anti-TL1A antibody from Pfizer, where we acquired it, and then we sold it to Roche for about $7 billion. That was almost a year ago, almost exactly a year ago. And anyway, the ownership piece of it for us is just a means to an end. It's one way for us to share in upside with our partners that allows us to be creative and flexible in how we bring these programs in. Okay. So, I guess starting with Immunovant, since you brought it up, if you look at the Immunovant website, 1402 is listed first. True. Can you talk about the two compounds and if it should be viewed as first generation, second generation, or first product and the follow on? Yeah. So FcRn is just an amazing target landscape. One of the things that we've been working on over the last few months, we talked a bit about an earnings call, is I think it's important for people to refocus themselves on just how big the biology that FcRn covers can be. I think we've gotten into this tendency, myasthenia gravis, is where Vyvgart has had early commercial success, sort of thinking about a small pie being sliced up in little pieces, when in fact, this is a giant buffet of patient opportunity. And so, you know, I think what we've been thinking about with the franchise of 1402 and with Bato, is how to take advantage of this whole area of new biology, whether you want to call it autoimmune disease, or B-cell biology, or whatever, how to take advantage of it, how to use the remarkable qualities that FcRn has, the elegance with which FcRn has cleared this relatively difficult bar, and then to take advantage of the attributes of our program. So as you may know from the history, batoclimab was the first program we carried forward into phase II studies. The thing that we have been focused on with our franchise is that we have two major advantages versus basically anybody else. One is our programs suppress IgG very deeply. They suppress IgG by, call it, 85% on repeat dosing, which we think has been shown over and over again in multiple settings, certainly in our own TED study and the Graves data that we'll put out relatively shortly, in individual patient-level data from all of our competitors' myasthenia gravis programs, in the Sjogren's data that put out earlier this year. It's been clearly shown that the deeper you can suppress autoantibodies, the more that benefits these patients. That's not actually that surprising. That, again, these diseases are driven by autoantibodies, so you would think the more you can suppress them, the better. And both batoclimab and 1402 suppress IgG as deeply as certainly any other anti-FcRn antibody we've seen, and really as well as anything currently out there. The other thing that we have going for us is that both 1402 and batoclimab, at this point, are set up to be concentrated in simple sub-Q auto-injectors, the same kind as whatever, as Dupixent or as Humira or whatever, all of the other sort of widely successful commercial auto-injector drugs, which actually, at the moment, we are the only anti-FcRn franchise that has that in any of their programs. There's others that are working towards it that have sort of less optimal sub-Q formats, but we're the only one that has that property. So batoclimab was the first one we developed because it was the easiest to concentrate in that way, and then we hit a scientific hiccup. We found that we also impacted albumin, which we knew. That meant we impacted LDL. And so basically, as soon as we found that out, we started working on 1402, which is basically batoclimab minus albumin and LDL. It is the same deep suppression of IgG, the same simple sub-Q format, but without an impact on albumin and LDLs. So we think of 1402 as the lead program because in any indication where 1402 can be at the front of or at the head of the pack, it's just gonna make sense to go with the program that has the cleaner analyte profile. But batoclimab is also a great drug, and it's in phase III studies at this point in myasthenia gravis. It's in late-stage studies in CIDP and TED, and it's gonna read out. We're gonna put out this data from our Graves phase II program very soon. Batoclimab is also an important program, but it's sort of, we think of it as a first-generation program where we would only advance it commercially in places where there was a real reason to do so, because for everything else, 1402 can clearly be a winner. Mm-hmm. Okay. And so, when you think of the various competitors out there, so J&J, I think, just filed, Yep. And they touted six-month data. Yep. Does that impact your thinking at all on batoclimab or 1402? Yeah, so we've known that nipocalimab was gonna file for a while, and I think the nipocalimab data was fine, and I think it is a big tent, as it were. There's just a lot of room for multiple agents, so I don't think anything specifically about the nipocalimab filing affects our strategy. Look, I think nipocalimab played out roughly as we would've predicted, which is to say, nipocalimab also impacts albumin. J&J structured their clinical program to limit albumin reductions at the expense of going after a lower IgG suppression. They got to a little bit less than what argenx delivers from an IgG perspective and delivered efficacy that was interesting in the overall context, but, like, not that different from what argenx shows with Vyvgart. The one thing that nipocalimab really has going for it is, you pointed it out, you know, nipocalimab studied at six-month endpoint with longer sort of chronic dosing, and I think that's, like, a useful paradigm from a payer perspective, a useful paradigm from a patient perspective, 'cause that's what these patients want, and so I think that'll be successful. Remember, Vyvgart's big success has come from Vyvgart. It's come on the IV side. Mm-hmm. So I'm not sure the fact that, that nipocalimab is an IV is gonna be a big liability for J&J. So I think that's all sort of clear. I think that still leaves open the swim lane that we see for ourselves, which is deeper IgG suppression in a simple sub-Q, and so I don't think it changes that much about our strategy. Look, the other thing that I think it's important to realize... So we're gonna put out MG data in batoclimab early next year. Mm-hmm. That data, whether we like it or not, is really important data because it will show. We will suppress IgG in that study in our sort of 24 weeks by, call it, 80%-85%, and the hope is that we can demonstrate a clear dose response, clear higher clinical benefit at 85% IgG suppression than we or others have been able to show, I call it 60%-65% IgG suppression. And if that's true, it will open a whole bunch of doors for us, right? It'll open the door for we could conceivably file BATO and MG. It'll give us a clear running room forward on what exactly to do with 1402 and MG. But I think all of the other places where I've mentioned that the deeper is better hypothesis has played out in data- Mm-hmm. They all require some imaginative leap to compare to our peers. Once the MG data's out, I don't think any imagination is gonna be required. You're gonna be able to look at the data set and sort of see what the world sees in terms of what we can do, what Vyvgart can do, et cetera. And so I think it will open a set of doors in terms of how people see the more is better hypothesis, assuming it plays out the way that we would like it to. Mm-hmm. Mm-hmm. And if you were J&J or argenx, and people say, "Well, what is the drawback for batoclimab or 1402?" Besides being earlier, is there anything that they would point at or try to highlight? Yeah, like, obviously, earlier is a big advantage, especially for Vyvgart that got there first. Versus batoclimab, I think they would clearly talk about the LDL liabilities, and I think that's a real talking point for them, and it's one of the reasons that we are being really thoughtful about how the guidance data guides us on BATO development. Mm-hmm. argenx had an R&D day over the summer. Look, argenx is an amazing company. They've done a phenomenal job executing. Vyvgart is a great drug. I think argenx has what to worry about with 1402, to be honest. I think a deeper IgG suppression is gonna matter, and I think, you know what I think they will try and talk to is it not mattering as much as we think it's gonna matter, right? They'll try and talk about threshold effects, or they'll try and talk about other things. They'll talk about the fact that by the time we launch, they may or may not, but may have a sub-Q format that's more competitive. Mm-hmm. You know, I think that's sort of the rub. Now, the interesting thing is, you mentioned earlier, I guess one of the great things about FcRn as a space, and one of the challenging things about FcRn as a space, is IgG suppression has been an amazing biomarker for clinical benefit. Mm-hmm. What that means is, if you have a phase II study that shows either a dose response or just like what 60% IgG suppression does, you basically have the information you need to go straight to a pivotal study. Mm-hmm. And so what that means is everybody's phase II studies are effectively anybody's phase II studies, right? We're gonna put out our Graves data. The reason we've waited so long to put this data out is precisely so that we can be right in phase II- Mm-hmm ... very shortly after we do, right, right in phase III, rather, with 1402, very shortly after we put the data out, so that we can be in that pivotal registrational kind of program before our peers. Conversely, what that means is, if you look at a disease like Sjögren's, or you look at a disease like, you know, myositis, when that reads out or whatever, we can take the phase II data of our peers, and we can use that to inform a pivotal program for 1402 that will line up in terms of trial completion with our peers. What that means is, other than MG and sort of CIDP, actually, we're not really that far behind in any of these other indications, and in some sense, we're right neck and neck, where it's just gonna come down to clinical execution. I think that's another reason why we think 1402 is just a phenomenal opportunity, 'cause we think we're gonna be able to take it right into, yeah, kind of pivotal registrational programs in every indication where there is phase II data from any agent. Okay. Can you, just recap then, what are the near-term milestones, let's say, until mid-next year? Yeah. With you. And this, by the way, is like one of the reasons it's fun to be at this conference this fall is. Look, I think we are just heading into an incredibly. I mean, I think you're asking specifically on Immunovant. We're heading into an incredibly data-rich period for Roivant. So we've got coming up imminently, we have the Graves' data at Immunovant. Mm-hmm. Other things coming soon at Immunovant, we have the MG data at the beginning of next year. We have CIDP data and TED data all in the ballpark of the next 12 months, less than 12 months. On top of that, we plan to unveil our full clinical program for 14.02, or at least the first four to five indications, where we're going into pivotal studies and where those regulatory discussions and preparations are well underway. And then that's just in the Immunovant franchise. We also have data from our sarcoidosis program coming later this year in phase II. We have data the back half of next year in brepocitinib, in dermatomyositis, which is a pivotal registrational program that will read out a little bit more than a year from now. And then we have a ton of progress coming on the litigations with Moderna and Pfizer. And on top of that, we've said very shortly, we're unveiling one new program that we've already got in-house, that I think will also be an exciting program for people to follow, and we're excited to talk more about it. So it's just a really rich period coming here. Okay. Yeah, I wanna come back to the new programs. Yeah. but maybe just to round out Yeah, sure. -the other programs. Vtama, how is the commercialization? You guys are in your third year? Yeah, like two, two, two and change years. Yeah, it's been fine, is the short answer to that question. Look, in psoriasis, I'd say it's been a successful launch in the sense that it's on a path to profitability. Mm-hmm. It's been a slower grind than I think our original hypothesis around psoriasis would've hoped for, but it's been a good product. Docs who use it really like it. There are some docs that use a lot. There's a lot of docs who use a little. You know, one exciting thing, the AD approval, so the PDUFA date's late this year, and so that should be coming. AD is 3x-4x times as large a market as psoriasis, so I think we're excited to see how that plays out. I think it could be quite different in terms of doc dynamics and patient dynamics, et cetera. And I think there's an outcome where AD takes off like a rocket ship, and this is a big blockbuster product, and I think there's an outcome where it is merely a mid-nine-figure, profitable derm topical. Mm-hmm. I think either of those are pretty good. But obviously, what we had hoped for was to break that topical ceiling, and so that's why you probably catch a measure of some reservation in my voice. Okay. And, the growth- It is not a subject of much investor intrigue right now. Right. Right. Is that growth a function of just getting more AD, or more indications, or is it you have to throw more sales force into it? No. Look, I think in psoriasis, what's gonna drive growth is ultimately this is a... and I say this, like, there have been a couple of new agents approved in psoriasis and a few new agents coming in AD that are topicals that are just, like, better at some level than corticosteroids, right? Mm-hmm. They're safer, they're more potent, they can be used in younger children, they can be used all over the body, et cetera. And Vtama, in our view. Look, it's our preferred among them. Mm-hmm. We think it's the best of those agents, but there's a few in that category. And I think what we are all finding, all of the companies doing this, is that docs who really sit down and focus on it, love the product, understand the profile, understand what's good about it, but corticosteroids have been generic since, I don't know, 1957 in some cases, and so these docs have just been writing steroids their whole lives, and changing that behavior is hard. And so I. You know, there's a certain amount of, like, we've done a little bit of DTC, we've played around with some of the assist to try to understand what it takes to drive demand. But I actually think a big piece of it is just anybody who's tried to change a bad habit knows it takes time, and I think one of the things we're finding with these docs is it takes more time than we had hoped. Right. and my honest prediction is, at the Morgan Stanley Healthcare Conference in 2045, when Vtama is generic, it will be used as much or more as many or most corticosteroids. And the question is: How do we pull that forward, and how do we get as much of that benefit, as we can for having developed the drug? Okay. Talking about the TYK2 JAK market, what's the name of that drug? Repasitinib. Yeah, brepocitinib. How do you think about that in the context of just, you know, very crowded market, or there's a product with just TYK2 on the market already and a few in development? Yeah. Look, our view on that drug when we brought it in was, there was this moment in JAK inhibitor development, where JAK inhibitors were not non-inferior to TNFs on some cardiovascular risk, and just everything got thrown out, the baby with the bathwater. And our view is, we took a look at brepocitinib, and we were like: Holy cow! This is a great drug. It is an incredibly powerful suppressor of cytokines that are prevalent in a wide variety of inflammatory diseases. It suppresses both JAK1 cytokines and TYK2 cytokines like interferons, and so it's good in diseases that need the sort of combination of cytokine suppression that we can deliver. And also, that we're not particularly well-equipped to compete with either, call it Bristol, in the sort of- Mm-hmm ... allosteric TYK2 space, nor, and look, I think there were all kinds of predictions on what the black box label were gonna do to Rinvoq, and they were all wrong. Fundamentally, Rinvoq has sold incredibly well since then, but we are also not the kind of company that's gonna compete particularly effectively with AbbVie. And so we said: Okay, what is the place where we can take brepocitinib, where we can have white space? And it became clear is that fundamentally no one was pursuing an orphan rheum, orphan immunology strategy with JAK inhibitors. And so there are indications like the ones we're going after, like dermatomyositis, like non-infectious uveitis, like a couple of others that we're working on now, where they're not actually crowded and where we have what we think is among the most powerful anti-inflammatory agents ever developed. And so we think there's a ton of unmet patient need, and we think it's a huge sleeper opportunity with just an amazing, amazing drug. Brepocitinib has shown great. It's, I think it's shown, like, some of the best Crohn's data ever shown, some of the best UC data ever shown. It's shown great data in alopecia and hidradenitis suppurativa, and psoriasis, and alopecia. It, it's just like amazing data over and over again, mostly in indications where we won't take it forward because we don't think we have the, again, the muscle to be that big. Right. Right. Okay, sarcoid, namilumab? Namilumab, yep, anti-GM-CSF antibody. Data is when? Late this year. Okay. Can you talk a little bit about that and how that works? Yeah. So that's a program, it's an anti-GM-CSF antibody. Mm-hmm. GM-CSF is a target that's involved in the formation of macrophages, which are directly in the line of pathophysiology for sarcoidosis. Those macrophages go on to cause granuloma formation, which are what causes the symptomology of sarcoid, the pathophysiology. And so sarcoid's a bad disease, couple hundred thousand patients, not a lot of options, not that much promising in late-stage development. A tough disease, right? People have studied it before. It's got a lot of the inflammatory disease challenges. These patients are on, you know, corticosteroid background therapy that gets moved around a lot. You have all kinds of difficult things. The endpoints are hard. It's just a tough, i t's a tough space in which to develop. GM-CSF, to be honest, is a target with a little bit of a checkered history of its own, right? It's sort of a target that's been in search of an indication. Mm-hmm. We think we found the right cross here. We think the biology is good. We think the disease is an important disease. It's a 120 -ish patient study, it's fully enrolled. Obviously, it's reading out later this year. If the study is successful, we've got a huge opportunity, but we've described it publicly as effectively a flyer, right? There's like real risk in that study. Mm-hmm. Because it's novel, untested biology in a difficult-to-study disease. But if it hits, I think it's worth a lot of value at that point. And what's the edge that you have? I mean, is this gonna be history repeating itself, but you've designed the trial better, or is the- The edge in sarcoid or the... I think the- The edge in your The edge that we have here is that no one has ever studied a GM-CSF in sarcoidosis before. In sarcoidosis. And so, if we are right, and if we get some combination of lucky and do a good job running the study, we will have a unique proposition, and we think sarcoid is a really good indication in which to try GM-CSF biology. Okay. Got it. Okay, moving on to your $6 billion cash position. Yeah. BE is clearly a important component of your growth. Yeah. How do you think about areas you're looking for? You know, are you looking for things that are larger trials- Yeah. others can't afford? So I've been saying this for months, and it's just still true, so I'll say it again. This is an incredibly exciting moment to have our business model and capital because. And there's a lot of things we're excited about. We're excited about some biotech companies, we're not companies, but programs out of biotech companies. We're excited about some programs in off-the-run geographies. Again, we're going to announce a deal that we did a little while ago with a big pharma company next week in a pretty interesting space that we can talk more about. I said next week, soon. We're going to announce it soon. But we, we're working through all these different opportunities, but the thing that we've been best at in our history is working with big pharma companies on partnerships, and big pharma is in an unbelievably transformational moment right now, where there's this wall of patent cliffs coming for many, many different big pharma companies, right from Keytruda to everything at Bristol, to the bunch of things at Pfizer, et cetera, and they're at various times. But that plus some development reprioritization, that may not be as big a deal, but clearly, IRA has, like, affected the way that pharma's doing development. There was, as of last year, a giant pile of M&A activity that reshaped a number of late-stage pipelines. There's all these programs that are in this transitional moment, gonna fall off eventually, and that is what we are good at. We are good at finding those programs ahead of time, spotting that they're gonna become available, and then you think about what those programs are. You're a big pharma company, you're very earnings-focused, you're trying to figure out how to manage P&L. You don't have a cash problem, right? These guys can borrow for nothing, but you need to manage P&L risk. There's not a lot you can do cutting early-stage R&D. Mm-hmm. It just takes a lot, a lot of cuts to make a difference. You can't cut sort of post-approval spend, you can't cut marketing spend. Those are all the in-line programs that are delivering the earnings. So it really, ultimately, in the end, it always comes back to finding expensive late-stage R&D- Mm-hmm. That can save those kind of dollars. When you think about it, who out there is looking for those programs, can spend hundreds of millions of dollars on a phase III program, and has a strong track record for developing late-stage drugs? That, like, is a series of narrowings that results in just, like, a very small circle of companies or institutions, and so we get to be pretty unique at most of those tables. And the downside to this is always bet the over on how long it takes big pharma to realize what they need to do, always bet the over on how long it takes them to actually transact on something. But the upside is, I'm telling you, when we do it, you will not believe the quality of the programs that will be available to us, that are available to us, that in time, we will extract. And it's really just a question of getting there and getting those programs across the line. But the moment is incredible, and the quality of programs that are either on the table or that we think are, like, just at the edge of the table, and with some pushing and prodding will make it onto the table, is really exciting. Mm-hmm. Do you have a particular structure that you try to abide by when you're partnering with pharma? Or is it flexible, depending on how you can get the product out or the asset? I like to say no pharma company has a Roivant-shaped hole in their business, and they don't walk around thinking about us. Mm-hmm. And so the thing that we have realized over time is that the way to win these deals is just to be flexible on structure. In general, another nice thing about partnering with big pharma companies, I mentioned this before, they're not very cash sensitive, right? They have unbelievable access to capital, and so they're generally not hunting for big upfront payments. What they're hunting for is they, as institutions, or at least they as R&D teams, et cetera, really believe in the program, it made it to phase III because they were focused on it. And so what they want is participation in the success, and that works great for us. That means we can spend comparatively few dollars upfront, which is good because we're pretty stingy, and then we can spend more dollars on actually running a clinical program. So basically, all of our deals, including frankly, with biotech companies, et cetera, have in common that, like, we're just not much to the chagrin of M&A bankers who call us from time to time, we're not great buyers of, like, public biotech companies at big premiums. Mm-hmm. But what we are really good at is creative partnering that can try and solve for, certainly the needs of a big pharma company in a way that gives us just, just unbelievable access. And do you have a limitation on therapeutic areas or say, "We're not touching- Yeah - indication X, Y, Z? If you think about our business model at some level, it's. Other companies have strategies you sort of visualize as a cookie cutter, and our strategy is to look at the dough that forms outside of everybody else's cookie cutters. That means if we said, "We're only an, we're only an oncology company, we're only an immunology company," well, the shape of the cookie dough left over is not a clean portfolio in one of those areas. We sort of have to, by nature, be flexible. There are certain things that are easier or harder to do with that strategy. For starters, like, capital O, oncology, has always been a tough space for us because, first of all, it's very competitive. Everybody thinks of themselves as an oncology company. The spaces between the cookie cutters are pretty small to begin with. And second of all, so much of that field has gone in the way of combination therapy development. And to be blunt, if you're picking up one thing from this company and one thing from this company and one thing from this company, the likelihood that they are together, the thing that makes the snowman-shaped cookie cutter, the thing to fit together, is not that high. And so, you know, in general, that's not been an area of focus for us. If we see things we like, we'll still do them, it's just a little harder. Mm-hmm. I'd say the same thing is true. There's certain modalities that require a nexus of expertise, and we've learned these lessons the hard way. But things like gene therapy and cell therapy, you know, they're really hard to manufacture, where you can be right on the biology, right on the target, right on the program being better, and then you can just get, like, run over by a CDMO steamroller or something like that. Like, that has been pretty challenging for us historically. And so I think, you know, again, never say never. Our only dogma is that we don't have any dogma, but those are probably the sorts of things that are less likely, but everything else is on the table. Mm-hmm. This program that we're gonna announce sometime in the near future, this month, is, for example, potentially in a new to us therapeutic area. Okay, great. Going back to your cash position, and, you know, BD is one component, but you did do a share repurchase in April, pretty sizable one. We did, yeah. Like four, We announced $1.5 billion. We've done about... Well, we've done $650 million as of the last quarter. Okay. And is that something you plan on continuing? Is it because you couldn't find BD and therefore you're doing share purchase? Yeah. Couldn't find is probably not the word that I'd use. Look, the way that I think about it is, what I said in a bunch of forums, is we can't do it with $4 billion, we probably can't do it with $6 billion. Mm-hmm. And so we're just looking to be efficient on, Mm-hmm. And frankly, we're looking to bet on ourselves, right? I think, like, our share count being lower when we do the things that are really gonna win, will win bigger for us and for the folks that own the stocks. Mm-hmm. You know, I think it's just a matter of making the right, ruthless decision with capital we've got. Okay. Okay, and, last question, and then I'll turn it to the audience here. Do you have good support from your existing shareholders? You know, some of the share repurchase was, you know, from existing shareholders. Yeah, we cleaned up Sumitomo with that specific repurchase. Uh-huh. Yeah, look, this was a bigger issue for us, when we were competing with the secondary market for primary capital need. We don't have that anymore. Mm-hmm. We have a mix of shareholders, as anyone does. Some of those shareholders are fixed life funds that are rolling off and will eventually need to sell their position. I'd say in general, my attitude has gone from wishing they would hold off to wishing they would sell sooner, which is a nice place to be. Mm-hmm. But that's a small minority of our cap table at this point, and I think what we're really hoping to do with the current moment where bluntly I think we're cheap relative to any obvious measure of fair value is to bring in shareholders who love us for who we are now. Mm-hmm. So that when we win, as we will, we deliver for those people. Okay, makes sense. Well, not too bad. With five minutes left, do we have any questions from the audience? Okay. Matt, maybe you can just recap, because milestones are very important here, and you have a lot. Maybe you can recap just what can we expect over the next couple of quarters. We can also... Just Just anyone who wants to run next door and, like, let me know what Amgen says- Do that now. Yes, so for the next few quarters, so, imminently, we have the Immunovant Graves' data and this new program that we're going to announce. Later this fall, we have the Markman hearing and the Pfizer case, which has now been scheduled for December. And we have the data from namilumab and sarcoidosis, and we also have the PDUFA date for Vtama and atopic dermatitis, which will begin the process of getting data from that launch. At the beginning of next year, we have data coming in myasthenia gravis at Immunovant and CIDP at Immunovant, and then in TED at Immunovant. We have the sort of summary judgment phase of our Moderna trial- Mm-hmm ... next spring. And then we have the actual sort of jury trial phase of the Moderna trial will be in September. And we have pivotal registrational data coming from brepocitinib and dermatomyositis next fall. Mm-hmm. So that's most of the next eighteen months, and then on top of that, I expect we will continue to announce some exciting new programs, hopefully earlier in that window. Okay, great. Well, Matt, thank you for joining us and for that overview. Awesome. Very helpful. Thanks for hosting us. Thanks for having me. Great. Thank you, everybody.