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

We're going to get going with our next company presenter at the BofA Annual Healthcare Conference. I am pleased to be introducing Roivant and Chief Executive Officer, Matt Gline. My name is Jason Gerberry. I cover SMID-cap biotech and specialty pharma. And I'm joined by my colleague, Chi Fong, as well. Both of us collectively cover Immunovant and Roivant. And so this is a great opportunity, I think, to have a discussion around a lot of the key assets that funnel up into the Roivant umbrella.

Awesome. Thanks so much for having me. It's great to be here. Appreciate it.

Yes. So maybe we can start with just some of the recent changes as it pertains to the Immunovant and what that ultimately means from a development perspective, hyper-focus within certain assets within Immunovant, within the portfolio, and then we'll dig down a little deeper from there.

Sure. Yes. Perfect. Look, I think the things you're referring to -- we've had a portfolio of anti-FcRn antibodies in development of Immunovant for a little while, batoclimab and IMVT-1402. And we're at this pretty natural moment of transition where we read out our late-stage studies in batoclimab in MG and CIDP. And we're sort of transitioning our focus more or less fully at this point to IMVT-1402, our next-generation program. And we're really excited about the data that we put out there. We think it sets us up really well for success with the sort of main program. But we just took the opportunity -- Pete was ready to retire, and so we took the opportunity for a management change. And Eric Venker, who had been President and CEO of Roivant, is now President of Roivant and CEO of Immunovant. And he took the reins from Pete with a laser focus on what is the most important thing of the next leg of Immunovant's journey, which is clinical execution. I told Eric on his first day on the job, priorities 1 through 6 is patient enrollment in Graves' disease and 7 and beyond is everything else, that's really sort of setting up to focus on those clinical trials and make sure we're going to win where we have the natural lead and the right to do so.

Okay. And does -- it seems like at least for the indications that you publicly stated, nothing has really changed in terms of the prioritization or what you're working on. Maybe in terms of what's behind the scenes, has anything really changed in terms of the prioritization of FcRn programs?

Nothing super significant. Look, I think my view has been for a while that Graves is a really unique opportunity for us. It's a first-to-clinic indication. It's one of these wide-open spaces. It's got an enormous prevalent patient population with, we think, pretty high unmet need. And so we get to be for Graves what Argenx is in myasthenia gravis or what Horizon was in TED. And it feels really good to sort of have that space, but it also feels like a burden to win that you sort of set yourself up, and now you want to pull it through. I think that's as opposed to something like myasthenia gravis where the Immunovant team has been focused for a while on execution because it's sort of the classic FcRn indication at this point. But my view has been, look, that's more of an uphill battle in terms of commercial success in MG, precisely because Argenx has such a commanding presence there and such a popular drug that even with what I think is best-in-class data, we're sort of coming from that position. So I think we're really focused on the indications where we can be first. We're really focused on the indications where we can be very close to the front of the pack. And then in something like MG, look, I think there's sort of almost an obligation to be in MG as an FcRn. I think there's like a real opportunity to do something there, and we could talk a little bit about how I see that market evolving. But I think in some ways, that's like a little bit of a lower priority relative to making sure we win in the spaces where we're ahead.

Yes. I suppose like if you were working on TNFs back at the get-go and you were behind AbbVie, you may still develop RA, but maybe you were trying to make your hay in another setting.

We are AbbVie in this situation. We're behind Enbrel, which was the first TNF with the worst form factor. And so we're playing to win in all the indications that...

I like that. I like that. But -- so you ultimately have a mix, right, of some fast follower stuff, some areas where you're first and perhaps you're interrogating the biology. And so there's a little bit of a different clinical risk profile. And hopefully, that's going to net out with a really big swath of opportunities in front of you.

There's no one on stage, but I hope so, too.

Got it. Okay. And Graves, I mean, we've done some work on Graves, and it's an interesting category. I think investors maybe struggle a little bit to understand the market and maybe because they just haven't seen anything, right, other than methimazole, which is generic and has a nice amount of volume, right? I imagine that, that's a decent proxy for starting to think about maybe the number of patients who become -- this doesn't work for them at some point in time. And that ultimately sort of becomes the opportunity set for an FcRn. And so I guess as you think about that opportunity, do you feel like you've got a good handle on how many patients are out there and how it's going to be to enroll a trial, right? Could you say that, that's going to be the push is to enroll this trial faster? But there are also criteria that are strict to get these patients in the study.

Yes. Perfect. Yes. Look, so Graves, for those who are not super familiar with it, is an autoantibody-mediated disease where you develop antibodies to various parts of your thyroid function. And so these patients untreated have out-of-whack thyroid hormone levels, and there's millions of Graves patients in the U.S., but as a disease, it's mostly treated with any thyroid drugs, principally methimazole approved, I think, in the 1950s or something. It's been around a really long time. And basically, what doctors have said for many decades at this point is either you can get controlled on methimazole or you're kind of screwed, we can take the thyroid out and treat it with Synthroid. But those are kind of the options basically. And so I think the sort of system around Graves patients has grown up around that idea. Methimazole, as you pointed out, is very widely used. Again, there's millions of patients on methimazole. We think there's about 350 -- a combination of like talking to docs looking at claims data and sort of surveys -- literature surveys, we think it's probably about 350,000 Graves patients in the U.S. who are effectively refractory to all available treatment options. That is they cannot get properly controlled on methimazole. Either they've explored high doses and don't tolerate them. They've been on high-dose methimazole for a long time and still have out-of-whack thyroid hormone levels, or they've been on and off methimazole, but the disease just keeps coming back. They can't lick it. And that's an astronomically large number of patients actually for a "Rare disease." So it's a big population. I think there's a little bit of heterogeneity in the in doc base here. There are docs who -- a lot of Graves patients are treated at roughly community endocrinologists, right? They're treated sort of in their local communities by regular-treating physicians. I think some of those docs, 90% of their patients are well controlled on methimazole. When you call them, they shrugged, and they're like, methimazole is okay. But then once you start talking to like the specialty centers, the people that treat the harder cases, I think they see a need in this like large refractory patient population. I think we feel really good about the size of that population, what we need to do to access it. The problem from a clinical trial perspective is many, many -- there hasn't been a novel drug in Graves' disease in, again, 70 years. Most of these docs' offices have not been involved in a trial in a long time. And so it's not like onc or even like rheumatology or whatever where the big practices all have site coordinators and they've all got a study like study people on staff. These are like you're going in there and you are paving the way for execution, and you're like the first in there, which is a huge opportunity like it was for Argenx in MG, but I think it like clouds the enrollment picture a little bit because I think the docs, on the one hand, in the study are super enthusiastic about patient flow. And we've got docs like Kahaly who ran the Phase II who, I think, has tens of patients, in theory, eligible for the study. In Kahaly's case, he's obviously got the infrastructure. But for a lot of these practices, even though they have a lot of patient demand, they don't yet have the tools as a practice to get the patients on to the study and to monitor them. And so I think that's the operational challenge that we're working on.

I see. I see. Yes. So I guess like when we think about -- obviously, there's a little bit of heavy lifting that goes into that in terms of getting good quality trial sites that can have a high volume up and operationalized. Maybe just the value proposition of the therapy in Graves, we hear surgery, radiation, not great, maybe even trending down, that might even be why we're seeing an uptick in methimazole. We hear, anecdotally, people stay on methimazole way beyond like when it's going to help them anymore.

Yes. I totally agree with all of that. And I think there -- in 2020, I was just looking at this data, there were like 93,000 thyroidectomies or something. Those numbers have actually come down a lot post COVID. What I think that really means is if those numbers are 20,000 or 30,000 now, there's 70,000 patients who should be treated in some way, but have decided that -- and if you talk to patients who had thyroidectomies, it's not that great, right? They're on lifelong Synthroid. They're still managing to fluctuations in hormone levels via Synthroid and other things. And so there's just like all of these patients who like just have this pent-up demand. I think roughly speaking, there are 3 important value -- 3 to 4 important value props in Graves. One is just these patients feel crappy all the time. They're sick. They're not controlled on methimazole. They can't control their weight. They can't control their energy level. It's just pretty unpleasant. The second is being on lifelong methimazole, and these are patients who are refractory, you can't get into remission, is its own trouble. And methimazole at high doses is pretty unpleasant, and it contributes to weight gain and other things that patients don't like. And so I think the -- in addition to just like getting patients feeling better, getting patients off methimazole is actually, I think, like a real value prop. And we had over 50% of patients on our high dose get off methimazole in 12 weeks, which is pretty great. Then I think the third value prop for us is if we can show -- and we have some remission data coming out midyear this year. If we can show off-drug remission, I think that's like another level of benefit. If we can say to patients, hey, for some decent percentage of patients who get controlled on our drug, you don't even have to be on our drug for life. You can get off our drug, and you can remain clear of any medication potentially. So I think that's like a potential value proposition that we're going to be able to talk more about later this year. And then the last piece, which is really the focus of the second Graves study, it's now getting up and running, is as many of you will know from Tepezza, TED is a big market that is effectively a presentation of late-stage or refractory Graves' disease. And we think we're going to be able to show that in hyperthyroid patients with proptosis that we can reduce the onset of TED, that we can improve proptosis in those patients. We see a little bit of that evidence in our existing Phase II data. And so we're running the second Phase III for Graves in a way that's designed to like include a bunch of proptosis patients and show that we can benefit there, too. And I think that will also be an important part of the value proposition.

How is the trial -- it seems like there's a question that has to be answered as to how long -- how much therapy do I need to drive a remission, right? Do I need 6 months? Do I need a year? Do I need 18 months? If I listen to the Biohaven view of the world, they think it's a chronic therapy for Graves, and I know they want to fast follow you in the setting. So as you think about the trial and how clinicians will get answers to the question of how long do I need to incorporate FcRn therapy to get the patient to remission, or do I just keep it on board indefinitely, how do you think the trial answers those questions?

Yes. I mean, the main -- for the first Graves study, the main answer to that question is we put a line in the sand, and we said we're going to treat for 6 months and then we randomize. And so the hope is that we can get a reasonable number of patients after 24 weeks of therapy into remission. We'll find out. We will titrate that a little bit based on what we see in the midyear remission data this year, but I think our hope is that we will see a reasonable rate of remission. I do think...

[indiscernible] is like you go 6 months post treatment?

Six months post treatment without drug and still have clear thyroid hormone levels and are euthyroid. I think in practice, it will vary a lot by patient. And I think there will be patients who are not -- who are either not in remission, that is like they're euthyroid at 6 months, but their disease recurs if they go off therapy. But if they were on therapy for 8 or 10 or 12 months, they might go into remission. And I also think there are likely to be some patients who just like aren't yet euthyroid by 6 months, but on continued therapy, get there 8 months or 10 months or 12 months. I think it's going to be a little bit about disease severity, about levels of autoantibodies. And also I think TSH, in particular, is kind of a complicated piece of this puzzle. What seems to happen in general with methimazole as well is you dose these patients, and T3 and T4 get controlled pretty quickly. But TSH is something that the body sort of regulates as a secondary phenomenon over time. And literature suggests that 6 months is about enough time to do that, but no one really knows. And so I think like we're going to learn a little bit about that in the study. And I think for patients who take 10 months for their TSH to get normal, I think what you might find is if you pull them off drug -- we wouldn't, in this study, pull them off drug if their TSH was abnormal. When the TSH is abnormal, T3 and T4 start to climb back up. And I think you can get these sort of negative -- we believe you can get these sort of negative feedback cycles in these patients where the TRAb levels come back up, the antibody levels come back up and they sort of are sick again. Whereas if you can get everything normal and sitting pretty for a few months, you've had a sort of homeostatic benefit where, all of a sudden, you don't have to worry as much about continued therapy.

Okay. And so just to round out the Graves discussion, so you had some of the Phase II data. I think it was either 50% or 70% of patients got to kind of T3, T4 normalization.

Yes. Yes, 70%. But on high dose, it was like, I think, 76% or something of patients got to T3 and T4 normalization, and then about 56% got off ATDs.

Okay. And so then is more of the purpose of this upcoming update just to see how well they do and kind of they're off therapy?

That's exactly right. Yes. It's -- for the patients who were clear at the end of that 24 weeks of treatment to follow them for 6 months off therapy and to see how many of them stayed clear off drug for 6 months. We think it's a pretty interesting dataset because, again, these were all refractory patients. And I think what doctors say if you talk to them is like, these are not patients who spontaneously remit. That is like these were not patients who absent our intervention were likely to go into remission. So it'll be a pretty interesting outcome.

Yes. Okay. And then just -- it is novel territory here. So just, I guess, I'd ask the obligatory question around FDA interaction and kind of alignment on the right pathway forward for Phase III design.

FDA has been super constructive around the indication. I think they're eager to see a new therapy approved. Again, there's been nothing for a long time. So there's a lot of enthusiasm for the indication. And the thing that's really nice for a pharma company in Graves' disease is the disease is managed through thyroid hormone levels. That is how these patients are treated. And so FDA was pretty clear that as long as we were including sort of the conventional components of euthyroid in our study, that it was going to be what they needed.

Okay. All right. Maybe shifting gears to just MG and CIDP as you've had more time to reflect. You mentioned just the sort of the challenge, right, of a late mover, I guess, going up against Argenx and the popularity. And it seems like -- is part of the maybe tone shift a little bit the fact that like they're making progress on their subcu deliveries? I know that like simple subcu was always kind of an angle with 1401 and 1402. I just wonder if maybe kind of Argenx has been able to kind of negate that aspect of the advantage and...

I don't -- that, to me, is not a big piece of it. Look, I think we are going to have a better form factor than efgart. And I think one thing to remember is 300 of 1402 is, in our view, a pretty equivalent drug to the standard dose of efgart. And so like, for example, a study that I think is interesting is like we could potentially run -- let's just say in healthy volunteers, like a study where you put patients on, whatever, 4 weeks of efgart and then transition them to steady state 300 of 1402 and show that IgG stays flattish so that you can continue to manage these patients. I think most patients will prefer our 2cc auto-injector with 300 of 1402 over the current PFS or over a Halozyme auto-injector or whatever Argenx gets. I think it is not yet clear to us exactly what patient experience with the PFS will be, and I think that will be informative. But the short answer to your question is that's not really what's driving my view. What's driving my view, honestly, is, on the one hand, I think we have a potentially better drug. That is, I think, in my opinion, our data shows the deeper IgG suppression yields better clinical benefit. But on the other hand, Argenx is a very good drug. Efgart is a good drug. It's safe. It's well-tolerated. Docs are familiar with it. And I think they've done a pretty good job already getting into the prevalent patient population. And I think like 5 years late, which is what we will be in MG, it's like that is a tough hill to overcome. And none of that's to say that I don't think we can be a big drug in MG. I just -- especially in forms like this, I just like want to come out and say that I think we are eyes wide open about that challenge, and therefore, are more excited about some of the indications where we don't face those headwinds. I do think, though, having said that, I think there is an interesting opportunity in MG, which is I think the MG market, by rights, should go the way of many other autoimmune markets, which is to say people should stop talking about remission -- sorry, stop talking about response and start talking about remission, about MSC, about sort of deeper responses, the equivalent of a PASI75 or a PASI90, a sort of 7-point MG-ADL response or something like that. They start talking about durability of remission. I think if they do those things...

You mean about the super responder type of...

Super responders and -- yes, like, again, patients going into effectively clinical remission. I think if the field moves from a treatment guidelines and expectations perspective in that direction, we will have 2 advantages. One is -- actually, those are endpoints on which our deeper IgG suppression will just make it easier to win on a placebo-adjusted basis where placebo is not going to deliver a lot of like true clinical remission. And also bluntly, Argenx didn't generate most of that data, right? They were treated in 4-week courses. They don't have durable remission data to show. And I think one thing that helps us is many of the other therapies in development for MG are focused on things -- whatever. So it's things like T cell engagers and like bigger guns that are designed to produce deeper effects with corresponding safety liabilities. And so I think we will have the support of the community in moving towards these deeper remission endpoints because those are the kinds of settings in which these other companies are also going to want to deliver benefit.

Okay. And then I guess, lastly, just when do we think we can get a more fulsome update on the broader R&D strategy, the opportunities beyond what we already kind of know? And we've talked about it because there are a few kind of opportunities that you guys are keeping...

Yes. Look, the thing we did before, and I take some responsibility for this in indicating that we were going to pursue TED indications and we were going to tell people what they were later, was we just like basically got the Street out there modeling a bunch of burden and no benefit for a lot of indications. And so I think our current view is like we're going to evaluate opportunities as they come. And when we decide we want to invest in something, we'll talk about it concurrent with the beginning of it, and people can evaluate both the sort of capital burden of it as well as the potential benefit of it. We are right now very focused on execution of the indications we've already talked about, but it wouldn't surprise me if we announce another indication at some point along the way. We've got certainly ideas on which we're doing work, including some of these studies that we've been running overseas and things like that. So we'll see.

For example, when you drop the lupus update, right?

Exactly.

Things like that where you're kind of covertly evaluating, these aren't things that we'll see on CT.gov.

That's right.

But will just appear when you have signal.

When we've got something that we want to talk about, exactly.

Understood. Chi?

Yes. Sure. Matt, nice to see you here. Welcome to Vegas to our conference. I want to switch gears to brepocitinib. I know FcRn is very important, but Roivant has a broader pipeline as well, and I want to hone in on some of the other assets that you guys have at -- to late-stage in development. So first, I guess I want to focus on brepo Phase III trial in dermatomyositis. It's called the VALOR study. You guys have a Phase III readout later this year. And I'm curious your thoughts about what your expectation is for the Phase III and curious also about what do you see as the bar of success in terms of regulatory approval? And then separately, what do you see as the bar of success in the context of competitive landscape, including approved therapies such as IVIG and also pipeline development such as FcRn?

Yes. Perfect. So dermatomyositis, rare disease, we think about 40,000 patients in the U.S. I think Argenx has 70,000 patients in the U.S., sort of a perfect size market for this kind of therapy. JAK inhibition on its own, there's some evidence to suggest efficacy in DM. There was an open-label study of tofa. There's a lot of off-label case report data of docs using JAK inhibitors. It's an interferonopathy. So TYK2 should also contribute meaningfully from a biologic perspective. So I think there's like a lot of good reasons to believe in the drug. I think the only -- to be honest, I think the drug likely works in dermatomyositis. I think the sort of concern, if you were to articulate one, is that the endpoint in DM is not a great endpoint. It's the thing called TIS, which is the total improvement -- it's called total improvement score. It starts at 0 for every patient, and it can only go up. It measures improvement from baseline over the course of the study, which means placebo, on average, will be positive because it can't be negative, sort of up against the normal rare disease, immunology, placebo dynamics. We are managing this with steroid taper, which I think we're the first dermatomyositis study ever to have a mandatory steroid taper in it. But I think that would be the concern. Docs are very familiar with JAK inhibition in the space. Again, it's treated by specialty myositis referral centers, but rheumatologists generally at those centers, they use JAKs a lot in their practice. They are super enthusiastic about the possibility of an on-label JAK. I think it's something they've been looking for, for a long time, and I think they believe in TYK2 as a part of the mechanism. So I don't think the bar for either -- I think the bar for regulatory approval is a positive study from a stat sig perspective. I think the bar for commercial success is a positive study from a stat sig perspective. I don't think the treating physicians are going to be super keen in on any specific TIS, delta, placebo or whatever. And in fact, I think the IVIG approvals were largely done on a responder analysis anyway. So I think docs will be pretty happy with just any stat sig improvement. The other point that I'd make about this is TIS is actually not a DM-specific endpoint. It is across all myositis. And so I think one of the things that docs will look to is some of the other endpoints like there's a score called CDASI. That's a -- it's purely a measure of topical activity or skin activity. There's a score called -- a relatively newer scale called DMOMS, that is a subset of TIS data specific to DM patients that docs will also look at. So I think there's a couple of other places docs will look to for signal, but I think the bar here is stat sig.

Okay. Great. I wanted to ask about dosing. If I remember correctly, the VALOR trial evaluated 2 doses, 30 milligram and 15 milligram. But with your other programs such as uveitis, you guys have pushed to the 45 milligram, which is some interesting data for uveitis. Just curious why pick 30 milligram, not 45? And are you worried about leaving efficacy on the table? Or you think the 30 milligram is good to go?

I think 30 is a good dose. Look, I think, 15 is an efficacious dose of brepo in many other indications, and 30 is a very efficacious dose of brepo in a bunch of other indications in which it's been studied. So I feel good about 30. The study is powered for 30. 15 is there, I'd say, largely for regulatory reasons to show a minimally efficacious dose. But I feel good about what we're going to be able to do with 30. I think it is nice for us that NIU is at 45 and DM is at 30 because, bluntly, I think NIU can probably sustain or at least potentially sustain a slightly higher price point than DM. IVIG has a price point attached to it, et cetera. The entry of FcRns into myositis probably elevates a little bit the supportable pricing bands. But anyway, I think it's nice for us that we'll be able to price by milligram and sort of set slightly differential pricing for DM and for NIU.

Okay. Interesting. So assuming Phase III success for VALOR, can you remind us sort of what your expectation for timing for regulatory submission? Do you expect a relatively quick turnaround time? Or do you still have to approach certain safety exposure before you can submit regulatory filings?

We have basically everything we need from a data perspective. So it's just as fast as we can file. It still takes some time. I think the -- probably the most likely thing is like looking for an approval in very early '27, so like, call it, 5 or 6 months to file in the year review. I think it's possible that can be pulled in a variety of ways. It's possible we could file faster. It's possible FDA gives us acceleration on their own. It's possible we find ways to ask for it. So -- but I think probably the base case is a very early '27 approval.

Great. Great. Next, I want to talk about your PH-ILD program that you've licensed from Bayer. Interesting program.

Thank you.

Curious, you guys are in Phase II development, some interesting Phase I data, can you give us some color on the enrollment progress? And do you have a line of sight when we might be able to see the data from the Phase II study?

Yes. Perfect. So this is an inhaled sGC activator that we licensed from Bayer. It's in a Phase IIb study looking at PH-ILD patients for the first time. We have Phase I data in group 1 pulmonary arterial hypertension patients, but this is the first time we looked at PH-ILD patients. And we've guided to second half of next year for data from that study. So that's when I think we'll have it.

Great. Great. Great. And last but not least, I want to touch upon on LMP litigation. I'll keep the question open-ended and high level. To the extent you can, can you maybe walk us through the setup and expectation ahead of some of the update that you expect? I think you have a summary judgment phase in second to third quarter and a jury trial scheduled for September for the case against Moderna.

Yes. Look, so this -- and again, there's a lot of history here and too much to talk about in 3.5 minutes. But we have a team of scientists who've been working on lipid nanoparticle since the very beginning of that field in British Columbia. And we have IP associated with the work that those scientists have conducted, and we believe that Moderna and Pfizer both are using that IP in their COVID vaccines to a suit for infringement. Where we are right now after years of preamble is the trial will be in 2025. It's currently scheduled to start September 29. This will be a jury trial, in a courtroom, 12 people in a box, they will hear evidence from experts, they will go into a room and they will come back and they will say, does it infringe? What are the damages? And was the infringement lawful? Like we will know all of that within weeks of the start of the trial. This is not like a protracted process anymore in that sense. That trial again will start in the fall. Prior to that trial, there's a series of what are called summary judgment motions where legal issues get dealt with before they ever make it to the jury. And some of those are important. One of them that's up for -- that will be up for discussion is that Moderna has claimed that they can take advantage of a World War I era part of the patent code that allows for companies to offload some liability to the U.S. government in the event that they were sort of manufacturing something for the government, which I think is an open question legally in this instance, but that's one issue that will be decided this summer in summary judgment. There are a few others, and then we'll go to trial.

Have you sized if that goes your way versus doesn't go your way and what potential damages could be if at all? Has that been like outlined in any of the documents?

There are places to see it. Look, I think the short answer is there are $150 billion worth of global COVID vaccine sales between Pfizer and Moderna. And what we said is that our other COVID collaborations, which are not necessarily precedential from a legal perspective, range from mid-single-digit to mid-teens royalty rates. And so even at the bottom end of that split between Pfizer and Moderna, this is our market cap. So the possible outcomes are obviously large. In the U.S., Moderna case, Moderna is a little bit less than half of the global COVID vaccine sales. And then the U.S. is, I think, a little bit less than half of Moderna's sales. And so you're talking about like 1/4 of the total pie or a little bit less than 1/4 of the total pie being adjudicated in this case. In terms of the range of outcomes on 1498, I think it's, at maximum, probably 60-ish percent of the U.S. case could conceivably be covered by U.S. government contractors under 1498, and at minimum, none could. And so I think the case range is sort of...

Pretty massive expand.

A pretty wide range, yes.

And so I guess the core issue is, is there public disclosure of their -- what they have in their vaccine, which they have not like disclosed, but there's some arguments that maybe it was disclosed in certain venues?

There is not public disclosure in the U.S. of the molar ratios of their vaccines. What the case will ultimately come down to in part is testing that is we were given samples of their vaccines, and we have run tests, and we will show the results of that testing to a jury. We haven't published them yet. And Moderna will -- if one presumes that we will show infringement in those results, Moderna will then talk about why they believe our testing is inappropriate and so on, and that will be the back and forth with the jury. But obviously, we feel good about our case.

All right. Well, I guess we're up against our time. Thanks so much, Matt, for joining us today.

Thanks for having me. This is really fun.

Thank you.

Thank you.

Thanks, everybody.