This is a pre-cocktail hour. Yeah, that's right. All right. All right, All right, thanks everyone. Welcome to the Goldman Sachs Annual Healthcare Conference. Thrilled to be closing the second day here with Roivant CEO Matt Gline. Maybe I'll just turn it to you, Matt. There's a lot going on. How do you want to think about an overview here? Yeah, look, it's almost cocktail hour. Thank you for having me. It's great to be here. It's been a long day. Look, I feel really excited about what our next sort of run looks like here. I think it all starts with, in the second half, we have data coming in brepocitinib and a phase III challenge around myositis. I think, to dive right in, I think that sets us up for a more or less unprecedented in our history, two- to three-year period, in which we have phase three data and sort of stacking commercial launches, first in DM, then in NIU, then starting in Immunovant. When I think about kind of what the next phase looks like as an overview, it really for us is now about execution and getting these programs that we've been talking about for years over the finish line into market. Yep. I know I feel like we wait for a long time. Now we're talking about phase three data in the third quarter for brepocitinib. Maybe just talk about the VALOR study in dermatomyositis. Remind us the rationale for brepo in this patient population. Can you talk to some of the clinical evidence that exists for the mechanism? Yeah, beautiful. So look, first of all, brepocitinib is a dual inhibitor of JAK1 and TYK2. It's a great drug. It has generated positive data in a half a dozen patients. You see some of the best data ever seen in those indications in psoriasis and psoriatic arthritis and alopecia, HS. So it's a very effective sort of JAK inhibitor. And we think TYK2 also gives us a lot of great activity on the interferon side. And so it's just a really, really strong drug. DM is known to be an interferon-driven disease among other things. So the basic biology looks really good for JAK1 and TYK2 inhibitor, the cytokines involved, or the cytokines we work on. There is also a fair amount of clinical experience with JAK inhibitors and DM. There are three now investigator-initiated studies, including a pretty large one in tofacitinib, that have shown good clinical benefit, not placebo-controlled, and hundreds of case reports. Docs are pretty primed to use these. DM is treated by mostly in the U.S. at these myositis referral centers by especially rheum and dermatologists. A lot of them have a lot of experience with JAK inhibitors. Clearly, the doc community just believes that JAK inhibitors work in DM. There is a fair amount of supportive clinical evidence. The study itself is a 52-week, 241-patient placebo-controlled study. It has placebo and two different doses of brepocitinib, although it is powered for the high dose. It is 52 weeks long. The endpoint is mean total improvement score, or TIS, which is an endpoint with some puts and takes. Obviously, it is the endpoint that is sort of widely validated in DM at this point. Fifty-two weeks is what the FDA mandates for new studies in the indication. Okay, perfect. I want to talk about TIS in a second. But let's start with dosing. You mentioned there's two doses. How did you determine the doses that were appropriate to take for this patient population? Yeah, so I think dosing in the study was largely regulatory-driven in nature in terms of having a couple of doses. 30 mg has been a highly efficacious dose of brepocitinib across other indications and studies, and clearly has the level of pharmacodynamic exposure that we want. We felt good about it as a dose. Okay, so talk to me about TIS. How does it work? How's it measured? How do you think about kind of controlling that outcome? TIS is a largely artificial measure. It really exists only in the context of studies. It stands for total improvement score, which also defies all kinds of linguistic characterization because you can't say TIS score because the S already stands for score. And you can't say TIS delta because it is itself a delta. And so change in TIS is also not a meaningful thing to say because it all starts at zero. Anyway, TIS is what? Literally just TIS. Just TIS. TIS starts at zero for every patient at the beginning of the study. It's meant to cross a whole bunch of different subscores. It's the same for all myositis. It's not specific to DM. And it measures muscle activity, skin activity, muscle enzyme levels, muscle testing, a whole bunch of different measures of both muscle and skin. Yes, that's kind of how it works. Because it starts at zero and is really used in clinical trials, it's not like the way DM is managed in the community. So it's not like patients walk around saying, "My TIS this year is 27." They don't know their TIS. It's not a thing that was ever measured or described. Our view is that a statistically significant study here is the one we need, that no one is looking for a specific numerical mean TIS because it's not a sort of clinically meaningful measure. Okay, so a couple of follow-up questions on that. Maybe one, how do you think about baseline patient characteristics then given TIS is not going to be something that can establish your baseline? The TIS baseline is zero. All of our patients have a baseline TIS of zero. Exactly. The study is designed to enroll patients who have both. To take a tiny step back, DM is a severe inflammatory disease that presents both with a sort of muscle wasting, muscle non-prone wasting set of symptoms and skin symptoms. The main requirement of our study on entry is patients who have both active skin and muscle disease. There is a minimum baseline CDACI level. There is a threshold range of baseline muscle testing scores. By the way, minor plug, we have a dermatomyositis investor event next week on the 17th. Next Tuesday at 1:00 P.M., right? Yeah, next Tuesday at 1:00 P.M. where we will talk a lot about these points. Anyway, the main baseline characteristics for us is we want sick patients across both measures. That's how I'd say we've thought about baseline characteristics. Okay, so then given this is an improvement score and there's a bunch of different things that are improvements, are there things that are easier to get improvement in than others? How do you think about the impact of the different components of the TIS score on trial execution? I mean, almost certainly the answer to that question is yes, that there are just like in general, some of these things are easier to hit than others. I'll say we've talked a lot about MG-ADL and MG improvement and MG. TIS is, in this narrow and specific way, a "better" endpoint than MG-ADL. MG-ADL has this scale problem where the example I always give is one of the MG-ADL subscores is respiratory. You get zero points if you have no shortness of breath, one point if you have shortness of breath in motion, two points if you have shortness of breath at rest, and three points if you're mechanically ventilated. This is not an even score. Placebo will affect these points very differently. That is one of the problems with MG-ADL, you get these weird distortions. The nice thing about TIS is there's so many subcomponents that each individual thing is quite small. It is not like MG-ADL where there's enormous weighting on relatively small numbers of things. I think there is speculation in at least the investor community that JAK inhibitors should work particularly well on the skin symptoms, which represent maybe 20% or 30% of the total components of TIS. I think that's fair. JAKs work really well and TYK2s work really well on skin disease. Also, we have lots of evidence from the investigator-sponsored studies and other things of patients improving on muscle function as well. We feel pretty good about sort of the breadth of it. Okay, in terms of powering assumptions, what's embedded in those? How are you? Yeah, so we're going to put all of that out next week in more detail. So maybe mostly I'll ask to wait until then. But the short answer is we can detect quite small deltas in TIS with statistical significance. Okay. There is a forced taper in the steroid taper study. How do you anticipate that affects outcomes? Yeah, look, I think if you were going to spend time being nervous about this study, and it's a totally reasonable thing to do, the thing you would be nervous about probably is just variability in placebo. The steroid taper is designed as it is in every immunology setting to manage that risk. The way that our taper works is it starts at week 12 and we force patients to be below 5 mg by week 36. We'll talk more about this next week too. I think the point of that taper is to make sure that as we get into the 52-week endpoint, the patients on placebo are properly worsening so that we can measure and focus on the drug effects for patients that are getting benefit. You maybe just answered this, but what is the thing that you worry about as you think about execution? Yeah, I think the biggest thing to worry about in this study is placebo. Okay. What should we think about as next steps pending success on the VALOR trial? Yeah, if the trial is successful, I think we will be gearing up for a launch in DM. I think it's a great market for a biotech company to launch a product. As I think I said before, concentrated prescriber-based, focused on these myositis referral centers, patient population with very high unmet need. The only sort of "novel next-generation therapy" approved is an IVIG, OCTAGAM from Pfizer. Other than that, it's really steroids and ISTs. There is a huge opportunity for something that's sort of next-generation efficacious therapy to enter into the field. I think we are really excited about that being the first of a number of stacking launches for us. We think it could be a really big opportunity. Okay, great. Maybe talk a little bit more about the market opportunity, how many patients, and how should we think about which are appropriate candidates for new therapies? Yeah, perfect. We have said we think there's about 40,000 patients. There's a pretty wide range. I think Argenx, for example, that has a myasthenia program, has had 70,000. Any which way you shop it, sort of tens and tens of thousands of patients. Probably not so, so different in size from an MG or something like that. It's a sick patient population without a lot of options. I think most patients ought to be viewed as eligible. Obviously, this will be in a sort of steroid and IST refractory population. Other than that, I think anyone's fair game. Okay. How should we think about pricing? Orphan pricing. Look, I think the two comparators, as it were, is IVIG, which is priced sort of maybe around $200,000 right now. And then we've got FcRns. Argenx is looking in the space. And that would be FcRn pricing is called $500,000-$600,000 a year. So that probably sets the bookends. And I think we'll be somewhere in that range. Okay. You're also evaluating this in NIU, non-infectious uveitis. Remind us the phase II data you reported last year. Yeah, great. NIU is an inflammatory eye disease. There are about 400,000 NIU patients, but most of those have front of the eye disease and are treated with topical steroids. About 70,000 patients have inflammation in the back of the eye and are basically treated either with steroids and ISTs or HUMIRA is approved, but does not work very, very well. We ran a non-placebo-controlled dose-ranging study in brepocitinib studying 15 and 45 milligrams in NIU, which read out last year. For context, the sort of FDA phase III endpoint for NIU is time to clinical failure or time to treatment failure, sorry, which is what it sounds like. It is like how long you were on therapy before you worsen such that the treatment's not working. The way these NIU studies work is they start out with a very high burst dose of steroids that then rapidly tapers. During that taper is when a lot of these patients fail because they're no longer on systemic steroids. In HUMIRA's case, they had a time to treatment failure of about, I think, a little bit under six months. The placebo time to treatment failure of, call it, three months or two moths- three months, I think. Our phase II study, at the end of the 12-month study, more than half the patients had not failed yet. It was greater than 12 months was the median time to treatment failure. The other thing that we measured was just the percentage of patients who had a treatment failure. In HUMIRA, which is the only other sort of real placebo-controlled recent study that succeeded, their placebo was like, I want to say, as we measured it, there are a couple of different ways of measuring these things. We measured it maybe 80% of these patients approximately. This is a little while since I looked at the data. I am not going to get the exact numbers right, but about 80% of these patients failed versus about 60% in the drug arm. Our study had at the high dose something like 20-something percent, low 20s percent treatment failure rates. Really exciting data as compared to what the field's been able to generate. I think the dosing is higher in this patient population than in DM. So talk about that. Yes. I think, first of all, obviously some time passed between the initiation of the DM study and the initiation of the NIU study. We saw just more data from our other programs and more data from really Pfizer's other studies. That reaffirmed our view that 45 is likely a pretty safe dose for this patient population. Also, NIU is an inflammatory disease where you want to hit it hard, fast. These endpoints are about time to failure. There is this rapid steroid taper. You want to deliver the anti-inflammatory benefit quite quickly, especially because NIU is actually, I think, the third leading cause of blindness in America. These patients have an acute disease and need rapid treatment. Our view was it was a patient population that would be happy to take on whatever liabilities came from 45 instead of 30 in order to get sort of maximum efficacy benefit. That is how we made that decision. Okay. Can you talk to us about the phase III trial design? There are two ongoing pivotal programs in NIU now, two ongoing pivotal studies in NIU. We've said they're going to read out in the first half of 2027. They're enrolling really nicely. That phase two data is obviously a huge boon to enrollment. They're as simple as it gets. They are 52-ish week studies that measure time to treatment failure as their primary and will measure other things like treatment failure rate and other sort of measures of eye progression across the different subcomponents of treatment failure. Yeah, it's measuring a pretty sick patient population. We're not specifically studying the HUMIRA refractory setting, but we have HUMIRA refractory patients in the trial. Our view was it should be representative of NIU patients needing treatment. Okay. You talked about the steroid burst and taper, I guess. What is the role of that in this patient population? This is actually an important point that I sort of neglected to mention earlier. First of all, you have to use the steroid tapers for a few different reasons in this study. One of them is, again, these are acutely sick patients who are coming in for treatment. Steroids work really quickly. You really do not want these patients going blind or failing immediately. You start them on this high burst dose of steroids, quite a high dose of oral prednisone, like a miserably high dose of oral prednisone. Then you take them off pretty quickly over about six weeks- eight weeks. We actually had in our phase II, we did not have a placebo arm, but our steroid taper was actually quite a bit more aggressive than the HUMIRA phase III steroid taper. Because the data was good, we're sort of pulling that aggressive steroid taper into our own phase III study, which among other things should be helpful for separation from placebo because with an aggressive taper, you would expect more placebo patients to worsen quickly. Okay. What do you think the market's missing with respect to the NIU opportunity? Everything. I mean, are we getting any credit for NIU at all? No, that's what I'm asking. Look, I mean. I don't know. I'm on maternity leave. Fair. Welcome back. Thank you. Congratulations. Look, I think the people that have spent time on NIU have gotten increasingly excited about it. I think people look at our phase II data and think it's a pretty clean shot on goal from a probability of success perspective. I think mostly what it takes at this point is spending time talking to docs about our data. HUMIRA, there's about 40,000 patients on biologics generally, most of which are on HUMIRA. HUMIRA, as we said before, fails in 50%-60% of patients depending on how you count it. The HUMIRA refractory population is probably 20,000 patients. At the kind of price points that we're talking about, if we got 25% of that population, it would be a large blockbuster drug. I think the answer is people are just not engaging with it in part because the data's still 2027. Yeah, we said that once. It's a little ways away. It's on the back end of DM and other things. I think once people spend time in the market opportunity, I'm not getting a lot of pushback from people who have done that work. I think the biggest knock against it is just it's not a very big indication for HUMIRA. Part of that is it doesn't work that well. Part of that is the 30,000 patients on HUMIRA at a HUMIRA price point is very different than 10,000 patients on something at an orphan price point. I see. Okay. You've also disclosed phase II study in cutaneous sarcoidosis. Maybe you can share the mechanistic clinical data rationale for this program. Yes. Cutaneous sarcoid is another one of these orphan inflammatory diseases. We know sarcoid pretty well because we had a failed phase II program in sarcoid late last year. Cutaneous sarcoid is a bad disease. If you look it up online, you'll get a sense for it. It's like a very bad skin disease. Very painful, very uncomfortable, and really no good options for these patients. Mechanistically, it's an inflammatory disease driven by some of the very same cytokines as some of these others. It's clearly got interferon involvement. It's clearly got involvement from a number of these other sort of classic JAK and TYK2 cytokines. Like DM, there's a little bit of clinical evidence pointing in favor of the indication. In this case, there was an open label study of tofacitinib in which I forget how many patients it was. It was like very small, 6 or 8 or 10 or something. But 100% of the patients in the study had clinically meaningful improvement. Again, that's an open label study. JAKs clearly have some benefit. Obviously, we don't need to show a 100% response rate to have a promising drug in here. We're running a dose-ranging phase II designed to show that we can deliver benefits to cutaneous sarcoid patients. If we're successful, I think it'll set us up for a nice pivotal program. Okay. So what does that look like in terms of a nice clinical profile to set us up for registration? Yeah. Look, I think it depends a lot on what placebo does. In general, I think you're looking for a meaningful separation, decent response rate across a number of endpoints. Okay. What are the most relevant endpoints in this? Yeah. These are similar to other derm indications. There's overall sort of investigator assessments of disease involvement. Okay. How do you think about further indication expansion? We just talked about three. There are different places JAKs could work. The more time we spend thinking about brepo, the more excited we get about it. There are other indications that we are actively working up right now, some of which we could be prepared to initiate late-stage trials shortly. It just depends on how the final work comes through for us. I think there are a number of other indications that we think could really matter here. Frankly, it feels like the kind of drug that could stack, that if you get a couple of indications approved, you could sort of start building on it a little bit like HUMIRA or Enbrel or something like that, where as you get these indications, they kind of add and build on each other. Some of them have overlapping prescribers as well. Okay. I guess where does brepo indication expansion sit on your priority list? This will hopefully be a good segue to the rest of our conversation. How do you think about allocating resources behind this program versus some of the other things you could be doing? I mean, we judge that indication by indication and opportunity by opportunity. But so far, the things we are looking at for indication expansion opportunities for brepo look very good as things to do. That is, like, the incremental cost of running these studies compared with the potential benefit is big. Some of that is contingent on continuing to find what I would call white space indications where we can be first and have a meaningful swim lane. But we have a good number of those that we're excited about. Is any of this contingent on whether it works in DM? Mostly no. I mean, it depends a little bit on how it fails in DM, if it fails in DM. Mostly no in the narrow sense that Brevo has been an active agent in so many indications. It's not like the DM failure is going to convince us it's not active. Frankly, we have a quite large portfolio, a quite large sort of collection of safety data at this point. We know what we've got. Look, I think the Pfizer-designed SLE study obviously didn't work. If we continue to get beaten up by placebo in these studies, I think we'll be thinking about indications where we can manage that risk a little more aggressively. It might affect a little bit just like our own antecedent estimate of how likely we are to be able to win these studies. That would probably translate to other mechanisms, not only brepo. I think brepo is going to be about as good as it gets in a bunch of these areas. Okay. Maybe we can spend a little time on Immunovant. You obviously took a greater role in the strategic direction and execution there. I guess what compelled you to take that step on Immunovant? It was a natural moment of transition for the business. Batoclimab had kind of rolled off its studies. We were really launching into the 1402 program at scale. I think it is just a moment where Pete had done a beautiful job with the regulatory dance of last year. We had gotten all of these studies started. We had gotten the regulators lined up on paths to pivotal and everything else. We are sort of moving to a phase of acute aggressive clinical execution and enrollment. Pete was ready to retire. Our view was like, this is a good moment for us to put somebody in charge of the company who we know is going to run these trials exactly as we like to run trials, having learned from our experience at brepocitinib, for example, about how we wanted to do that. Eric is somebody who's been on the leadership team at Roivant for a very long time and has seen those things firsthand. I think he's going to do an awesome job there. Okay. One of the changes was just kind of streamlining the clinical programs you're executing. Talk to us about why that was the right decision. Yeah. I'd say a couple of things about that. One of them is, and I take some responsibility for this. Our older messaging on FcRn 1402 was we're going to do 10 indications by whatever, a little bit earlier than this time next year. It turns out if you tell the world you're going to run 10 indications, but do not tell them what the indications are, what they do is they model a lot of burn and no benefit. It was basically useless messaging. We were getting no credit for the indications. We were just getting penalized for the spend. The first thing is just that does not make sense. If we ever want to initiate new indications, we'll present the cost of those studies as well as the opportunity associated with them at the same time. Second of all, it did not make a ton of sense to us in hindsight to have an antecedent commitment to that breadth versus a laser focus on just executing. We feel like Graves', for example, is such a big market, such a big opportunity that if we can win there, it will set us up for the long future in a really sort of powerful way. Obviously, if we have to choose between rapid enrollment of Graves' and slowing that down so that we can study something in a proof of concept, it just obviously made sense to make sure we were able to prioritize Graves'. By doing away with the sort of overall commitment, we can still add new indications if they are great indications, but we can focus on execution and make sure we are prioritizing winning where we are. Okay. You did obviously make some personnel changes with the positioning of Eric there. Any other personnel changes that need to happen for Immunovant from here? Do they need any roles? Look, I think with any fast-growing company, obviously, and with a change in leadership at the top, I'm sure there will be more sort of people making decisions in various directions. Mostly, I think the answer is we're really happy with the team Pete built. We're really happy with the overall setup there. I think we expect that team to be able to execute really well. Okay. You had MG data, CIDP data earlier this year. Just what are the key take homes you want people to take from this? We believe, and it's clear that maybe not everybody else believes, but we believe that those data sets, especially the MG data set, mostly answered the question. Deeper IgG suppression can yield better clinical benefit. We were happy with the way that we showed that against a backdrop of changes in the overall environment and higher placebo rates than historical on MG- ADL, overall change from baseline. I think in that sense, those studies did what we wanted them to. They did the best that we frankly thought they could do. We were happy with the way that looked. Look, I think it reminded us or highlighted for us the extent to which the bar to, sorry, excuse me, commercially unseat VYVGART is high. VYVGART's a well-loved drug. It's very popular in MG. The docs like it. The patients like it. It works pretty well. I think the goal for us in MG has to be, one, to generate the most compelling possible data set to continue to leverage the form factor and other things. Two, to help patients and docs understand the switching dynamics and the benefits of trying out multiple among these agents. Three, to move the market toward the places where we will unambiguously win, which are places like driving clinical remission, driving durable clinical remissions, the kinds of things where deeper IgG suppression will absolutely win even on a placebo-adjusted basis, and to focus the entire patient and doc community on those possibilities. I think that's all important. Those are all lessons from the MG data set. We were really happy with what the drug delivered in MG. In CIDP, we reported a more limited subset of data. Looking at the deeper versus less deep IgG suppression cuts, it looks to us like we have a potentially truly best-in-class drug with quite differentiated efficacy if the 1402 program delivers in a similar way. There, I think we have an opportunity to win a market that Argenx is doing a really lovely job with, but where I think efgart's data looks IVIG-like in quality. I think if we can deliver something that is a step function better, which I think our data suggests we may be able to do, I think that'll set us up in a different way. Okay. Myasthenia gravis is relatively crowded. But as you think about where the puck is moving for this indication, you talked a little bit about this. But maybe you could help us understand how you think this market is going to break down in the next 5 years-1 0 years. Yeah. Perfect. First of all, I'll say I'm excited about MG. I think it's a good market. It's definitely not the indication I'm most excited about because it's crowded. Most excited about Graves', some of these other markets. MG is a little lower on that list because these dynamics are hard to unseat. In terms of where I think the puck is moving, first of all, and I said this a minute ago, but I think focusing patients and docs on, I think in some ways, this is the same as has happened in every other immunology area, moving from IgA to PASI 25 to PASI 50 to PASI 75 to PASI 90 to PASI 100, moving from ACR 20 to ACR 50 to ACR 70, moving from clinical response in UC to clinical remission in UC, moving to these deeper response endpoints and to these durability of response endpoints is something that as drugs improve in literally every category, we have seen progress. I think the same thing is going to happen in MG. I think it is incumbent on us to drive the market in that direction, to try and partner with the other companies entering the space that have the same incentive. If you're developing a T-cell engager in MG, you're also looking to prove to the world that you can drive deeper, more durable response than an FcRn even. You have to because the T-cell engagers are going to have different safety liabilities. I think the whole field is going to move in that direction. We can be at the forefront. We can be the next generation FcRn that has generated that data that uses deeper IgG suppression to deliver that benefit. I think that's a big and important piece of it. I think there's others. You see Argenx looking at ocular MG. You see people talking about earlier lines of therapy. I think all of those things are also ways in which the FcRn market can grow. We will be very focused on how nipocalimab does in its early launch because I think one of the things out of our hands and out of our control, the two biggest drivers of the size of the market opportunity for us in MG are going to be how large the overall market turns out to be. If MG as an overall category is a $5 billion market, that's going to be very different than if it's a $10 billion, $11 billion, or $12 billion market. I just don't think we know yet. The other piece of that is how high a switch market it is. If it turns out that with nipo on the market, docs who have, whatever, patients are on a couple of cycles of VYVGART, they're happy but not happy enough. Docs are like, "Why don't you try six months of continuous therapy on nipo?" If that is the way this works and patients kind of switch back and forth and split in and out of different entries in the class, the market opportunity for us is much bigger than if brand loyalty winds up keeping docs more or less exclusively using VYVGART for their patients or something like that. are tons of other things to talk about, but I'd love to let you on Graves' disease. A lot of people are following you now into this market. Maybe you could talk about why you're so excited about that one. Fast following is the finest form of flattery, right? Look, I think Graves' is like the other FcRn or brepocitinib indications in that it is an area of very high unmet need. There has not been a lot of novel therapeutic development lately because there cannot be because the biology has only recently caught up with the indication. It has the other property that we are first, which is something we could not have said about MG, for example. The other thing about Graves' that is truly astonishing, actually, is the size of the market. If you talk about these other indications with tens or maybe 100,000 patients eligible for therapy, in Graves', there are probably 330,000 patients who are refractory to all therapeutic options and whose only answer is either to live sick or to get a thyroidectomy or radiation and then live on SYNTHEROID and still be sick. Our view is with that size patient population, we do not need 25% share. We do not need 10% share. 3% or 4% of that patient population is a blockbuster indication at FcRn pricing. It is just such a large patient population with so much unmet need that it feels great to be first there, to be able to paint that market the way that our competitors have painted some of the other markets, to build those first-related KOLs, and to really get to patients who are suffering with the disease and help them understand what better could look like. It is interesting. My weird tip to investors who are trying to understand Graves' has been on Reddit, the Graves' Disease subreddit. It is a very useful place to go because you just see these patients on there talking about how miserable they are on methimazole, talking about their inability to get control, talking about their apprehensions about having thyroidectomies, talking about their difficulties in recovering from thyroidectomies, but how they are happier anyway because it was such a tough disease. You read these patient stories, and you're like, "Yeah, wow, this is an underserved patient population. Yeah. Okay. Speaking of things that we've been waiting for a long time, kind of going back to the beginning, Moderna litigation is coming. Can you just give us a timeline and the key decisions we're waiting for? Yes. The day after tomorrow, there's a hearing about timelines. Right now, the timelines are a little bit uncertain until that hearing. Right now, there is no set trial date. Hopefully, maybe we'll get one at that hearing, but it's up to the judge. We will definitely have a large conversation about timelines for summary judgment. Look, I think we feel good about how that case is progressing. We feel good about the information we've presented to the court so far. Summary judgment will be an important part of this process where we and Moderna get to argue for things that we think the judge can decide. That should take place over the summer and maybe early fall. The trial should follow thereafter. Okay. Capital allocation from here. Remind us kind of the pillars that you guys are looking at. Yeah. The buckets that we've been focused on are, one, sort of making sure that our existing pipeline is funded to profitability, and we're well situated for that. We sort of set aside $2 billion-ish for deployment into new opportunities, upfront payments, but also clinical development for things not yet in our pipeline. Excited to keep prosecuting that over time as those opportunities present themselves. It's been exciting to see what we might get our hands on and a little bit slower than we would have liked in terms of pulling the trigger on things. We have bought back close to $1.5 billion in stock already and continue to look at the market as an attractive place to put capital, return cash to shareholders, and reduce the share count. Okay. We have about a minute left. I've asked you about a number of things, but there's so much going on. I haven't gotten to everything. Anything you want to make sure is highlighted or that you don't think people quite understand? Look, I think the only compound we did not talk about is mosliciguat, which normally I would say that is fine. The data is coming in the second half of next year. Today is a fun day to talk about pulmonary hypertension. One of our competitors put out some really great data. Look, we think that market is huge. We think PH-ILD looks like PAH did a few years ago. We still have, we think, the highest PVR reduction even after today ever observed in a Group 1 PAH study. The more developed that market is and the better the treprostinils do, especially in PH-ILD, the more PH-ILD patients we will diagnose and get into care, and the more of an opportunity I think we have got. That data is coming in the second half of next year. This is not an immediate near-term catalyst. It's not the thing that I think people miss most of our story, but it is something that I think in this moment, as the pulmonary hypertension patient clearly comes back into relief in people's minds, I'd say don't sleep on mosliciguat. We think it's going to be a really great drug. Beautiful. Great having you. Thanks, everyone, for joining us here and online. Thank you so much, Matt. Great. Thank you. We couldn't have timed that any better. Sorry? We couldn't have timed that one any.