Roivant Sciences Ltd. (ROIV) Earnings Call Transcript & Summary

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. And maybe I'll just turn it to you, Matt. There's a lot going on. So how do you want to think about an overview here?

Yes. Look, I -- 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. And I think it all starts with -- in the second half, we have data coming in brepocitinib in a Phase III trial in dermatomyositis. And I think to dive right in, I think that sets us up for a more or less unprecedented in our history, 2- to 3-year period in which we have Phase III data and sort of stacking commercial launches first in DM, then in NIU, then starting in Immunovant. And so when I think about kind of what the next phase looks like it is 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.

Yes. I know I feel like we waited for a long time. And now we're talking about Phase III data in the third quarter for brepocitinib.

So maybe just talk about the VALOR study in dermatomyositis. Remind us the rationale for brepo in this patient population? And can you talk to some of the clinical evidence that exists for the mechanism?

Yes, 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 half a dozen patients. You see Crohn's, 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 are the cytokines we work on. There is also a fair amount of clinical experience with JAK inhibitors in DM. There are 3 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 prime to use the remember, DM is treated by -- mostly in the U.S. at these myositis referral centers by specialty room and dermatologists and a lot of them have a lot of experience with JAK inhibitors. And clearly, the doc community just believes that JAK inhibitors work in DM. So there's a fair amount of support of clinical evidence. The study itself is a 52-week 241-patient placebo-controlled study. It's got placebo and 2 different doses of brepocitinib, although it's powered for the high dose. It's 52 weeks long. The endpoint is mean Total Improvement Score, or TIS, which is an endpoint with some puts and takes. But obviously, it's the endpoint that is sort of widely validated in DM at this point, and 52 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 2 doses. How did you determine the doses that were appropriate to take for this patient population?

Yes. So I think dosing in the study was largely regulatory-driven in nature in terms of having a couple of doses. And then 30 milligrams has been a highly efficacious dose of brepo across other indications and studies and clearly has the level of pharmacodynamic exposure that we want. And so we felt good about it as a dose.

Okay. So talk to me about TIS. How does it work? How is 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 is a -- 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 anyway. TIS starts at 0 for every patient at the beginning of the study, it's meant across 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. It's not a -- because it starts at 0 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 like my TIS this year is 27. They don't know their TIS. It's not a thing that was ever measured or described. And so our view is that a statistically significant study here is the when we need that no one is looking for a specific numerical mean 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 0. All of our patients have a baseline TIS of 0. So we have -- the study is designed to enroll patients who have both. So DM to take a tiny step back, DM is a severe inflammatory disease that presents both with the sort of muscle wasting set of symptoms and skin symptoms. And the main requirement of our study on entry is patients who have both active skin and muscle disease. So there's a minimum baseline CDASI level. There's sort of a threshold range of baseline muscle testing scores. By the way, minor plug. We have a dermatomyositis Investor event next week on 17.

Next Tuesday, 1:00 p.m., right?

Yes, next Tuesday, 1:00 p.m. where we will talk a lot about these points. But anyway, the main baseline characteristics for us, we want sick patients across both measures. And 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 like easier to get improvement in than others? And how do you think about like 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 like we've talked a lot about MG-ADL and MG improvement in MG. TIS is in this narrow and specific way, a "better endpoint than MG-ADL". And that MG-ADL has this like scale problem where the example I always give is one of the MG-ADL subscores is respiratory. And you get 0 points if you have no shortness of breath, 1 point if you have shortness of breath in motion, 2 points if you have shortness of breath at rest and 3 points if you're mechanically ventilated. So this is not an even score and placebo will affect these points very differently. And that's one of the problems of MG-ADL is like you get these weird distortions. The nice thing about TIS is there's so many subcomponents each individual thing is quite small. And so it's not like MG-ADL where there's like enormous weighting on like 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. But also, we have lots of evidence from the investigator-sponsored studies and other things of patients improving on muscle function as well. So we feel pretty good about sort of the breadth of it.

Okay. In terms of powering assumptions, what's embedded in those higher yield?

Yes. 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 force taper in the steroid taper study. How do you anticipate that affects outcomes?

Yes. 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. And 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 force patients to be below 5 milligrams by week 36. We'll talk more about this next week, too. But 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 effect for the patients that are getting benefit.

You maybe just answered this, but what is the thing that you worry about as you think about execution?

Yes. I think the biggest thing to worry about in this study is placebo

Okay. What should we think about as the next steps pending success on the VALOR trial?

Yes. 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 base. 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. And so there's a huge opportunity for something that's sort of next-generation efficacious therapy to enter into the field. And I think we are really excited about that being the first of a number of stacking launches for us, and we think it could be a really big opportunity.

Okay. Great. So maybe talk a little bit more about the market opportunity, how many patients? And how should we think about which are like appropriate candidates for new therapies?

Yes, perfect. So we have said we think there's about 40,000 patients. There's a pretty wide range. So I think argenx, for example, that has a myositis program has said 70,000. But any which way you shop at sort of tens and tens of thousands of patients, probably not like so, so different in size from an MG or something like that. And it's a sick patient population without a lot of options. So I think like most patients ought to be viewed as like eligible. Obviously, this will be in a sort of steroid and IST refractory population. But other than that, I think anyone's fair game.

Okay. How should we think about pricing?

Orphan pricing. Look, I think the 2 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 call it $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, noninfectious uveitis. Remind us the Phase II data you reported last year.

Yes, great. So 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 topic 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. So 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's like how long you were on therapy for before you worsen such that the treatment is not working. And the way these NIU studies work is they start out with a very high burst dose of steroids that then rapidly tapers. And during that tapers when a lot of these patients fail because they're no longer on systemic steroids. So in HUMIRA's case, they had a time to treatment failure of about, I think, a little bit under 6 months and the placebo time to treatment failure of, call it, 3 months or 2 to 3 months, I think. Our Phase II study at the end of the 12-month study, more than half of the patients had not failed yet. So it was greater than 12 months median time to treatment failure. The other thing that we measured was just the percentage of patients who had a treatment failure. And so again, 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's a couple of different ways of measuring these things, but as we measured it maybe 80% of these patients approximately, this is a little wild since I looked at this data, so I'm -- not 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. So really exciting data as compared to what the field has been able to generate.

I think the dosing is higher in this patient population than DM. So talk about that.

Yes. So I think, first of all, obviously, some time passed between the initiation of the DM study and initiation of the NIU study. And so we saw just like more data from other programs, and that -- more data from really Pfizer's other studies, and 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's this rapid steroid taper. So you want to deliver the anti-inflammatory benefit quite quickly, especially because -- so NIU is actually like, I think, the third leading cause of blindness in America, like these patients have an acute disease and need rapid treatment. And so our view was it was a patient population that would be happy to take on whatever liabilities came from 45 to 30 in order to get sort of maximum efficacy benefit, and that's how we made that decision.

Okay. Can you talk to us about the Phase III trial design?

So there are 2 ongoing pivotal programs in NIU now, 2 ongoing pivotal studies in NIU. We said they're going to read out in the first half of '27. They're enrolling really nicely. That Phase II data is obviously a huge boon to enrollment. And they're as simple as it gets. They are 52-ish week studies that measure time to treatment failure as their primary, and we'll measure other things like treatment failure rate and other sort of measures of eye progression across the different subcomponents of treatment failure. And yes, 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. And our view is it should be representative of NIU patients needing treatment.

Okay. What is -- you talked about the steroid burst and taper. I guess, like what is the role of that in this patient population?

It's actually an important point that I sort of neglected to mention earlier. So 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 and steroids work really quickly, and you really don't want these patients going blind or failing immediately. So you start them on this high dose of steroids. It's quite a high dose of oral prednisone, like a miserably high dose of oral prednisone. And then you take them off pretty quickly over about 6 to 8 weeks. And we actually had in our Phase II, we didn't have a placebo arm, but our steroid taper was actually quite a bit more aggressive than the HUMIRA Phase III steroid taper. And 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 is missing with respect to the NIU opportunity?

Everything. I mean, are we getting any credit for NIU at all?

No, that's why I'm asking. I don't know, I'm on maternity leaves.

Welcome back. Congratulations. Look, I think the people that have spent time on NIU have gotten increasingly excited about it. And I think people look at our Phase II data and I 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% to 60% of patients depending on how you count it. And so the HUMIRA refractory population is probably 20,000 patients. And at the kind of price points that we're talking about, if we got 25% of that population would be a large blockbuster drug. And so I think the answer is like people are just not engaging with it in part because it's, the data is still 2027. That's a little ways away, and it's on the back end of DM and other things. But I think -- I don't -- once people spend time in the market opportunity, I'm not getting like 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. But part of that is it doesn't work that well. And 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 like rationale for this program.

Yes. So cutaneous sarcoid is another one of these orphan inflammatory diseases. It's -- so 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, 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 TYK cytokines. And 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 meaningful -- clinically meaningful improvement. Again, that's an open-label study. JAKs clearly have some benefit. And obviously, we don't need to show 100% response rate to have a promising drug in here. So we're running a dose-ranging Phase II designed to like show that we can deliver benefits to sarcoid patients. And if we're successful, I think it will 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?

Yes. Look, I think it depends a lot on what placebo does. But in general, I think you're looking for like a meaningful separation, decent response rate across a number of endpoints.

Okay. What are the most relevant endpoints in this?

Yes. These are similar to other derm indications. There's like overall sort of investigator assessments of disease.

Okay. How do you think about further indication expansion? We just talked about 3. There's JAKs could work.

The more time we spend thinking about brepo, the more excited we get about it. So there's other indications that we are actively working up right now, some of which we could be prepared to initiate late-stage trials shortly. And it just depends on how the final work comes through for us. But I think there's a number of other indications that we think could really matter here. And 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 Rinvoq or something like that, where sort of as you get these indications, they kind of add and build on each other and some of them have overlapping prescribers as well.

Okay. I guess where does like brepo indication expansion sit on your priority list, and this will hopefully be a good segue to the rest of our conversation. But like 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 like 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 as compared to the potential benefit is big. Some of that's contingent on continuing to find what I would call white space indications where we can be first and have like 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, but mostly no in the narrow sense that brepo 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. And frankly, we have a quite large portfolio of -- quite large sort of collection of safety data at this point. So 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. So it might affect a little bit just like our own anti estimate of how likely we are to be able to win these studies. But 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 Imunovant?

Yes, it was a natural moment of transition for the business. Batoclimab kind of rolled off its studies. We were really launching into the 1402 program at scale. And I think it's a moment where Pete had done a beautiful job with the regulat/ory dance of last year. We had gotten all these studies started. We've gotten the regulators lined up on paths to pivotal and everything else. But we're sort of moving to a phase of acute aggressive clinical execution and enrollment. Pete was ready to retire. And 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. And 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 like streamlining the strategic -- the clinical programs you're executing. Talk to us about why that was the right decision.

Yes. So I'd say a couple of things about that. But one of them is -- and I take some responsibility for this. Our older messaging on FcRn and 1402 was we're going to do 10 indications by whatever, a little bit earlier than this time next year. And it turns out if you tell the world you're going to run 10 indications, but don't tell them what the indications are, what they do is they model a lot of burn and no benefit. And so it was basically useless messaging. Like we were getting no credit for the indications. We were just getting penalized for the spend. So the first thing is just that doesn't 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 didn't make a ton of sense to us in hindsight to like have an indent 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. And 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. And so by doing away with the sort of overall commitment, we can still add new indications of the great indications, but we can focus on execution and make sure we're 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? Any new Roles?

Look, I think with any fast-growing company, obviously, like -- and with the change in leadership at the top, I'm sure there will be more sort of people making decisions in various directions. But mostly, I think the answer is like we're really happy with the team people built. We're really happy with the overall setup there. And I think we expect that team to be able to execute really well.

Okay. You had MG data, CIDP data earlier this year. Just like 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. And we were happy with the way that we showed that against the backdrop of changes in the overall environment and higher placebo rates than historical on MG-ADL overall change from baseline. So I think in that sense, those studies did what we wanted them to. They did the best that we frankly thought they could do, and we were happy with the way that looked. Look, I think it reminded us or highlighted it for us the extent to which the bar to me -- commercially unseat VYVGART is high. VYVGART is a well-loved drug. It's very popular in MG. The docs like it, the patients like it, and it works pretty well. And so 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; and 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 we're deeper IgG expression will absolutely win even on a placebo-adjusted basis and to focus the entire patient and doc community on those possibilities. And I think that's all important. Those are all lessons from the MG data set. That's -- we were really happy with what the drug delivered in MG. In CIDP, we reported a more limited subset of data, but looking at the deeper versus less deep IgG suppression cuts, it looks to us like we have a potentially like truly best-in-class drug with quite differentiated efficacy if the 1402 program delivers in a similar way. And 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. And so 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 will 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 to 10 years.

Yes, perfect. And first of all, I'll say, like I'm excited about MG. I think it's a good market. It's definitely not like 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 like hard to unseat. In terms of like where I think the puck is moving, first of all, and I said this a minute ago, but I think like focusing patients and docs on -- I think in some ways, this is the same as has happened in every other immunology area, right, moving from IGA to PASI25 to PASI50 to PASI75 to PASI90 to PASI100, moving from ACR20 to ACR50 to ACR70, moving from clinical response in UC to clinical remission in UC, moving to these deeper response endpoints into 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, right, 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. And you have to because the T cell engagers are going to have different safety liabilities. So 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 expression to deliver that benefit. I think that's a big and important piece of it. And then 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 2 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, right? 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 or $11 billion or $12 billion market. I just don't think we know yet. And then 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. Doctors are like, why don't you try 6 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.

There's 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. So 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 a very -- an area of very high unmet need. There has not been a lot of novel therapeutic development lately because there can't be because the biology has only recently caught up with the indication. And it has the other property that we are first, which is something we couldn't have said about MG, for example. But then the other thing about Graves that's truly astonishing actually is the size of the market, right? 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 thyroctomy or radiation and then live on synthroid and still be sick. And our view is with that size patient population, we don't need 25% share. We don't need 10% share, like 3% or 4% of that patient population is a blockbuster indication at FcRn pricing and 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 KOLs and to really get to patients who are suffering with the disease and help them understand what better could look like. It's interesting. Like my weird tip to investors who are trying to understand Graves has been on Reddit, the Graves disease sub Reddit. It's actually like it's a very useful place to go because you just like see these patients on there, like talking about how miserable they are on methimazole, talking about their inability to get control, talking about their apprehensions about having thyroctomies, talking about their difficulties in recovering thyroctomies, but how they're happier anyway because it was such tough to like you read these patient stories, you're like, yes, wow, this is an underserved patient population.

Yes. I mean 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 time line and the key decisions we're waiting for?

Yes. So the day after tomorrow, there's a hearing about timelines. And 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, and then the trial should follow thereafter.

Okay. Capital allocation from here, remind us kind of like the pillars that you guys are looking at?

Yes. 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 like 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 like in terms of pulling the trigger on things. And then we've bought back close to $1.5 billion in stock already and continue to look at the market as an attractive place to put capital to 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 everything. Anything you want to make sure is highlighted or that you don't think people quite understand.

Look, I think the only other -- the only compound we didn't talk about is [indiscernible], which normally, I would say that's fine. The dates 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 -- excuse PAH did a few years ago. We still have, we think, the highest PVR reduction even after today, ever observed in a in a Group 1 PAH study. And the more developed that market is and the better the treprostinils do, especially in PH-ILD, the more PH-ILD patients will diagnose and get into care and the more of an opportunity, I think we've got. So that data is come in the second half of next year. This is not like 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 people -- as pulmonary hypertension patients clearly comes back into relief in people's mind, I'd say like don't sleep on [indiscernible]. 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.