Ladies and gentlemen, thank you for standing by. Welcome to the Roy event fourth quarter 2025 earnings call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. And to ask a question during the session, you will need to press star 1-1 on your telephone. You will then hear an automated message advised and your hand is raised. We ask that you please limit to one question, and to withdraw your question, please press star 11 again. Please be advised that today's conference is being recorded. I would like now to turn the conference over to Stephanie Lee. Please go ahead.

Good morning, and thanks for joining today's call to review business updates from Roy Vint's fourth quarter and fiscal year ended March 31, 2026. I'm Stephanie Lee with Roy Vint. Presenting today, we have Matt Klein, CEO of Roigand, and Drew Promkin, CEO of Plomagand. For those dialing in via conference call, you can find the slides being presented today, as well as the press release announcing these updates on our IR website at www.investor.roigand.com. We'll also be providing the current slide numbers as we present to help you follow along. I'd like to remind you that we'll be making certain forward-looking statements during today's presentation.

We strongly encourage you to review the information that we have filed with the SEC for more information regarding these forward-looking statements and related risks and uncertainties and with that I'll turn it over to Matt thanks Stephanie thank you everyone for dialing in this morning I'm glad to be talking we have an unexpectedly busy agenda with a bunch of topics I'm looking forward going through all of it including obviously we announced this morning which is the preliminary open label period data from the 1402 study in DGTRA as well as a plan spotlight we've been playing for a while on Mosley getting into that data which will take us through and some smaller updates on the representative program although exciting uh so a lot to cover i want to before i get into all that use one small bit of executive privilege and wish my father jerry a happy 75th birthday today is his 75th birthday so happy birthday dad he sometimes listens in on these calls i don't know if he's listening in now if not i'll catch it on the replay okay uh into the uh important topics now uh starting on important business topics now uh starting on uh slide five Well, look, this has been a pretty wild 12 months for Roivant, and we continue to see just tremendous execution of momentum across our development portfolio. An update that will get drowned in some of the other things for today, but it's actually pretty great, is that PrEP-Sytnib was awarded breakthrough designation, break therapy designation, or retainer sarcoidosis, which just underscores indication selection and development there in terms of what that could mean for those patients. Obviously, also, in this quarter, we announced LPP as an indication for BREPO, and that study is already enrolling, and we're excited about how that's going. And then a ton of work ongoing in commercial prep for the launch in DM, which, assuming FDA goes as we expect it to, will launch by the end of September. You know, obviously, the biggest data update for today in the FCRN franchise is what I mentioned earlier, which is that 1402 showed, we think, clinically meaningful, pretty exciting ACR response rates across ACR 2050 and 70 in the GTPRA study in the open-label portion. We'll talk more about that, but that's obviously encouraging data that we're looking forward to spending some time on. We're also fully enrolled on CLE with top-line data expected in that study in the second And, you know, earlier in this quarter, we announced the failure of the Botocomab studies in TED, but also that the hyperthyroid patients showed normalization, which was supportive of our great studies which are ongoing continue to enroll well also and then finally hard to believe it was this quarter but earlier this quarter we also announced our two and a quarter billion dollar settlement with Moderna and we expect to receive the first portion of that payment the nine hundred fifty million dollar upfront in July so just an incredibly busy quarter of execution for us in an incredibly busy fiscal year for us it's really hard to believe how much has changed in a year for Roy Vint none of that though is to say on slide six that we're done and the next 12 months are also incredibly exciting obviously one of the most important things going on we will hopefully be launching brepacitinib intramatomyositis you know by the end of September the phase 3 study in cancer sarcoidosis we expect to begin this year as well and we expect the NIU phase 3 top-line data in the back half of this year so a transformative year for BREPO as all that comes around we'll spend time on this today, but the Moseley PHLB Phase 2B top line data is expected in the second That also will potentially underscore that as a really important program, and hopefully we'll be looking forward to that data and to talk more about it. Obviously D to TRA, some of the data is around today, but we're looking forward to providing a pretty significant update later this year with a little bit more data as well as detailed analysis we're doing at a patient level and hopefully with some feedback from FDA on a go-forward plan given what we've now seen. And then, obviously, we'll get to see all the POC top-line data as well. And then, you know, next year is a huge year with 1402 data in Graves and MG coming in. A ton to look forward to, and frankly, as much in the windshield in the rear view mirror. I think I've got the car analogy right there. I'm going to go in now without spending any more time on the preamble and talk a little bit about this DGTRA data, which I would call surprisingly good. We were pretty excited to see what we saw here. It has been a little bit hard to process just how exciting this data is, and so we're still doing a lot of work on it. As a reminder on slide eight of what we're talking about today, this was a unique study designed in a few ways. First of all, as I think everyone's aware, this was a study in heavily refractory patients. Every patient in this study, in addition to failing steroids and DMARs, also had to fail at least two advanced lines of therapy. So most commonly, that's two of, for example, TNS, Jax, and IL-6s. and we'll talk a little bit about that there's obviously some other things that could be in that bucket as well the study also had a pretty strict entry criteria on autoantibody positivity we had a criteria on ACPA positive above a certain level and that was also specific to the study of design and then the other way which the study was unique is it was a randomized withdrawal study with two periods first an open-label active treatment period of 16 weeks at high dose 1402 600 milligrams followed by a period to 12-week re-randomization where ACR20 responders at week 14 and 16 both are re-randomized into a 12-week randomized withdrawal period where some of them stay on 600, some go down to 300, and some go down to placebo. What we have to share today is preliminary data. We're still actually cleaning and finalizing it all, but it shouldn't move very much from here. On the top line treatment effect from period one, period two is still ongoing with more than half of patients still being dosed in the study. So we don't have any data or information about period two to share today. And then even for period one, there's a whole bunch of data like IgG, for example, that we haven't analyzed fully and are not ready to share. So nothing to say about it other than that we're going to be sharing a pretty limited subset of this data today. On slide nine, you can see baseline characteristics for the patients in the study. We're running with 165 valuable patients. I'm not going to go through all of this in detail I would say this is quite a sick patient population obviously by design it's refractory and we'll talk more about that a second but for example if you look at the DAS28 CRP score 6.1 that's quite high for a study like this there's a bunch of measures on here that suggest a quite sick population which was the goal right this is the population that we we set out to enroll and so we feel we feel good about who's in the study on prior lines of therapy specifically on 10 so you know you can see on the right hand side, we succeeded with our entry criteria. That is basically all of these patients have failed more than two advanced therapy mechanisms. And that's very different than either the Nippo study or really any of the later line RA studies that have been run. And actually one thing that we're highlighting today is I think it's pretty interesting, 65% of these patients roughly have failed specifically JAK inhibitors. And notably, and we'll highlight this elsewhere as well, basically every single one of the patients who fail a JAK inhibitor also failed a TNF. So, this is a TNF and JAK refractory patient population that we're focused on. So, look, slide 11 is the headline here, and the headline is, with all the appropriate caveats for an open-label study, these numbers are high. We saw 73% of patients roughly with ACR20 responses, and not just that, but we saw quite deep responses. We saw over half of patients with an ACR50 and over a third of patients with an ACR70. And notably, once you get out to the deeper end of that with ACR 50s and ACR 70s, you just don't see a lot of placebo response in that level of responder analysis. And so, you know, it feels to us like looking at this data. There's something going on that's meaningful and interesting with this drug and something that merits enthusiasm and a lot of further investigation. And we're certainly doing all that work now as we get ready to take the program forward. I'll highlight on slide 12 the one other bit of interesting data from the study that we're able to present today, which is we pulled out the subset of patients who are JAK-experienced. Remember, those patients, 107 of them are both JAK and TNF-experienced, all of them. Some of them have also failed something else as well. And one of the things that I think is maybe most exciting about this data is it's basically fully preserved in that subset. And so as you think about that opportunity where these patients have really failed all of the most advanced options available to them, we're able to deliver, in an open-level setting, pretty exciting response rates for those patients, which I think bodes well for the exact biological thesis with which we ran the study to begin with, that auto-antibody positivity is an orthogonal mechanism to some of the other anti-inflammatory options, and that for aqua-positive patients, this could be an effective treatment option. So, look, I think on slide 13, just to reiterate what we're showing here, look, these are six patients a difficult to treat patient population who have failed a lot or all of the available options and come in with with highly active disease we show really great response rates in the data that we're excited to see how they evolved through the rest of this study and on deeper patient level analysis and also notably this is the largest patient population dose with IMFD4-2 to date it was safe and well tolerated in the study nothing new drug related from a safety signal perspective identified, so a clean data set overall and further underscoring what we think we've got with 1402. Path forward from here, obviously, you look at this data and you feel pretty good about what this could be, you know, significant potential benefit, a differentiated mechanism, a difficult to treat population with not a lot of options, so we're actively working right now to get ready to talk to FDA about this data and plan a path forward. The data is encouraging. I'll make one comment about it, which is the depth of responses is exactly what's exciting about the data set. It's exactly what makes us believe there is something beyond placebo happening in the data set. But as you'll recall, the randomized withdrawal period, the primary endpoint of period two is do patients taken off drug lose their ACR20 response in 12 weeks, which was a relatively short period to begin with and almost certainly would have been fine if we had seen more marginal benefit on ACR20. But the truth is, once you're looking at ACR50 and 70 responders, I think the bar has actually gotten a fair amount higher for period two. And so paradoxically, I think we still have a good shot of success there. But in some ways, period two is less meaningful than it might otherwise have been. And I think there are plenty of scenarios where we don't see a p-value in period two and continue forward with the drug given the overall quality of this data. And diversely, depending on FDA's feedback, potentially situations where we do see a p-value in period two and just need to make sure we're comfortable with the plan forward. So I think much more interesting than the period two data at this point is more patient-level analysis, as well as the results of those FDA discussions. And we expect to share all of that in the second half of this year. We're working on it right now. And my hope, given the quality of this data, is that we'll be coming back to you with an enthusiastic update about next steps here that laid the groundwork for just a really big opportunity. Remember, we presented some data at our investor day suggesting this is at least a 70,000 patient population and some more specific revised commercial analysis that Immunivant has now done that looks like that number could be 85,000 or higher. It's a big patient population in need. And I think, you know, underscoring that the speed with which this trial was rolled, the enthusiasm that physicians have for putting patients on study is just further evidence that there's really something interesting here. And with that, I actually just want to also just give a shout-out to the Immunivant team who have continued to execute really well. Obviously, the data itself is strong, but also the speed of enrollment, the speed with which we're moving through these studies, the full enrollment on CLE. And I think that spans all of our programs. I think we're excited about what, obviously, what Privant's been able to do with RepSittin from a clinical enrollment perspective. We're excited about the speed of enrollment from Mosley. Obviously, the quality of that data, we'll find out soon. But, look, we're really excited about what we've been able to do across the portfolio on clinical execution. So much appreciation for the enormous number of people who are working toward those goals. I'm going to pivot now to Mosley-Sigawatt and do a little bit of a data preview there because, you know, the next time we get together, that data could potentially be very close in front of us. And so we wanted to get out ahead of that and give people a chance to just ground themselves in what's coming, as we did last year around this time or a little later for BREPO, the endometriosis. Look, I'll do a little bit of an introduction here, and then you all heard from Drew back yesterday in December. He's in the room with me and is going to talk through a little bit more about the program. Intense on that medical need. These patients, in the extreme significant proportion of them die. They're very sick. There's currently only one approved mechanism with two therapies and we think there's probably 200,000 patients across the US and Europe and that one mechanism is underscoring multiple really great launches at this point. So we're excited to see the commercial enthusiasm and excited to see these patients have access to something that provides real benefit already and we're hoping to add to that. Moseley has a completely differentiated mechanism of action for the disease. It's an SDC activator. It's an inhaled SDC activator. It is potentially the first non-proposanol that could be available for these patients we expect this to be a polypharmacy combination therapy market as PAH has been and we think Mosley has a chance to be first line has chance to be a major part of the treatment paradigm and we're just looking forward to getting this data moving forward there in our phase one data across healthy volunteers the pulmonary hypertension patients and drew will remind us of the state specifically we saw among the best PVR reductions to date and one thing we're going to remind people of today is that, you know, although we saw a 38% PVR reduction in some of those patients, that basically anything that has ever showed 20-plus percent PVR reductions has been able to deliver clinically meaningful benefit. I think it's true that there has not been any class of drugs showing a 20-plus percent PVR reduction that has not gone on to be a commercially successful class of drugs. And then finally, as a reminder, unsurprisingly, the top line date from that study is on track, and we expect to get it in the second half of 2026, it's 135 patients studied. So with that, I'm going to hand it over to Drew, who's going to take you through the next handful of slides here on the program, and then I'll come back for a little summary at the end and the rest of the presentation.

Thanks, Amelia, Matt. And I can tell you there's a lot of excitement about Moseley-C-Guad. So Moseley is an inhaled SGC activator that's delivered directly to the lungs to activate SGC and restore impaired SGC function. SGC is a key enzyme in the NO-SGC-CGMP pathway, and in oxidative stress environments like PHILD, nitric oxide may be reduced and the SGC binding site can become impaired, leading to SGC dysfunction. Now, typically, SGC is activated when nitric oxide engages SGC in the presence of heme, and CGMP is then produced. Unlike CGMP, SGC stimulators, that requires nitric oxide and heme to activate the SGC. Inhaled moseciguat binds to the heme pocket, independent of the need for NO and heme, producing CGMP, which results in vasodilation of the pulmonary arteries and potential reduction of fibrosis and inflammation of the lung tissue. Next slide. So we know many pulmonary diseases are heterogeneous in nature, And that fact can make patient treatment complex. To start, there's disease of the pulmonary vasculature and disease of the lung parenchyma. The combination of these two disorders is embodied in pulmonary hypertension with interstitial lung disease, which is the first indication we're exploring in our Phase II focus study. We believe Mosley has the potential to address both the pulmonary vascular and the lung parenchymal diseases experienced with patients with PHILD. Mosley, next slide, I want to make sure that, what I'm going to do is call out the slide numbers if everyone's got it. Okay, okay, I'll call out, you'll call out the slide numbers, you just call mine. Okay, thank you very much, I appreciate that, I want to make sure we're family. Okay, Mosley's preclinical properties led Bayer to take Mosel-Siguat into Phase I trials in a total of 170 patients, including healthy volunteers and patients who group 1 PAH and group 4 CTAS. In the Phase I study, FHIR studied Moseciguat in 132 healthy volunteers and 38 pH patients. The healthy volunteers underwent studies with single and multiple-dose formats, and Moseley proved to be well-tolerated, active, and had an extended half-life of approximately 40 hours. And in the Phase I-B Atmos study, 38 patients with pH were dosed in a single ascending dose format, and Moseley again proved to be very active, producing deep PBR reductions, and was very well tolerated. On to slide 20. So, and with one dose of Moseley in pH patients, that's exactly what we saw. A single dose of Moseley Ciguat reduced PBR in these patients early and sustained through the three-hour observation period with a mean PBR reduction of greater than 30 percent, and a mean peak PBR reduction of approximately 38%. This places Moseley's PBR reductions amongst the highest reduction seen in single and multi-dose trials in pH treatment space. With one dose of Moseley's CGUAT, we also saw CGMP levels rise as measured in plasma with no associated clinically meaningful systemic side effects, including systemic blood pressure and heart rate. We also observed the desired impact on other hemodynamic measures, including mean reduction in MPAP of up to 20% and mean increase in cardiac output of up to 25%. Slide 21. Moza-Sequat was also well-tolerated in Phase I patients in healthy volunteers and patients with pH, with treatment-emergent adverse events being moderate in intensity across both groups. And all doses were well-tolerated, and we did not see significant cough, which is often exacerbated by inhaled treprostenils, and we did not see clinically relevant systemic side effects, which we believe in great part was due to the inhaled direct delivery of Moseley to the lungs and the limited bioavailability of Moseley in circulation. Slide 22. So with Mosley's Phase I tolerability and clinical profile, we look to take Mosley into Phase II development, an indication where there exists a major unmet medical need. And we felt that PHILD was an exciting opportunity for development. Given the primary site of PHILD, it's in the lungs, involving the pulmonary vasculature and the lung parenchyma. and the currently approved treprosanil treatments have high treatment burden, as well as tolerability challenges with highly variable efficacy. And so, Mosley lines up really nicely in this moment. Since it was delivered directly to the lungs, it has a once-daily dosing that's been very well-tolerated and produced limited incremental cough and systemic side effects in Phase I, and has the potential to address both the pulmonary vascular and lung parenchymal diseases. Slide 23. So, to go a little deeper into PHILD patient populations and the opportunity, PHILD represents a large and underserved market where new drugs are sorely needed for these patients. There are up to approximately 200,000 patients in the U.S. and Europe, likely underdiagnosed given the lack of treatment options in particular. And this is a sick population and severe subgroup of PH, less than a five-year median survival, and the combination of pH and ILD represents an increasingly poor prognosis compared to each alone. And I mentioned previously the lack of treatment, as there are currently only two approved FDA toprostenil drugs, leaving room for significant improvement. Slide 24. Now, the core field of drugs in development for the treatment of pH ILD is rather sparse. There are three companies, all with toprostenil treatments in different formulations, and all of these troposinol treatments continue to have a range of challenges. Cerolutinib, with its different mechanism, has also run into recent challenges as Gossamer's Phase III Proceratrial in PAH did not meet its primary endpoints, coming off challenges in Phase II as well. And the result of the recent Proceratrial outcome, Gossamer has paused its planned studies in PHILD. So, Mosley, on the other hand, with its first-in-class opportunity as an inhaled SCC activator, as one fairly dosing, positive tolerability, and positive activity in its profile from Phase I studies, and this really positions Mosley to be a leader in the treatment of patients with PHILD upon its approval. I also wanted to share about, and this is slide 25, I also wanted to share our thoughts about how we see PHILD and the market and how it's going to develop. We actually think the PAH market provides a likely roadmap for that development. In the early days, supportive care was the only option for patients with PAH, and this is what we currently see, and that's the reality of PHILD patients in most regions outside of the U.S. where there are limited treatment options. Over time, drugs with newer mechanisms were approved, a combination therapy involving multiple mechanisms of action became more common. As a median survival of these pH patients has also steadily increased as time went on from two and a half years to where they are today at 12 to 15 years, and treatment guidelines evolved alongside the data, which reinforced the evolution of the treatment paradigm. Today, revenue in the PAH market has really reached a stellar level at $100 billion in aggregate sales and a robust $7 billion per year, with 15 drugs approved, and there remains a good pricing environment and commercial opportunity for these newer therapies because this is driven by the complex nature of PAH. And finally, a key takeaway is that today, over 40% of patients with PAH initiate their treatment with dual therapy, 15% of these patients will add a third therapy by the end of the year. The combo therapy, as Matt said, is really the norm. And so we are currently deep into our phase two study exploring most of CWAT in our blinded phase two placebo-controlled and randomized study in adults in PHILD. The study is a multi-center study across the globe. We're targeting 120 We ended enrollment with 135 patients. During the screening period, the investigators look hard to find patients to confirm ILD, elevated baseline PVR, indicative of pH, and limits on the level of fibrosis and emphysema as determined by CAT scan. If eligible for the study, the patients then randomized two-to-one placebo, drug to placebo, and then they go through a rapid up titration. And that moves from one milligram to two milligrams. to four milligrams, and Matt may have spoken about it, but seen really great progress there with the vast majority, over 95% of our patients achieving that four milligram dose and sustaining on well through the week 16 period. So that's been very attractive and positive. And at week 16, the primary endpoint is change from baseline PVR, and that's determined at 16 weeks, alongside the secondary endpoint of change from baseline six-minute walk and change from baseline NT pro BMP and then the patient moved on to week 24 secondary and exploratory endpoints and then they all go on drug if they weren't on drug into the long-term extension slide 27 so very importantly and as we get closer to data in the second half of this year we've focused very heavily in designing our phase 2 study and defining our patient population, and we carefully designed around the Seventh World Symposium on Pulmonary Hypertension, and these guidelines are crucial for PH-ILD patient selection. We targeted patients with worsening symptoms of PH, mild to moderate impaired lung function based on pulmonary functional testing, elevated PVR and mean pulmonary arterial pressures were crucial, and also we excluded severe emphysema to ensure a cleaner ILD population. The result is that the study population closely mirrors the recommended guidelines and more severe patients. And on slide 28, as you can see, this effort is reflected in our baseline data in focus. Our mean PVR came in at 7.1 Woods units, so very elevated. Mean pulmonary arterial pressures of 39.3, consistent with our desired thresholds and confirming we enrolled patients with significant hemodynamic involvement. The lung disease mix also looks well-balanced, and we protected for emphysema, both in number of patients and level of severity as determined by the CAT scan, and this was very important from all of those learnings. And we also explored background therapy, including exploring PDE5s on background, and this is also consistent with real-world practice. So this careful patient selection and enrichment gives us confidence we've enrolled the right population to detect meaningful treatment effect. We're very much looking forward to our Phase 2 data in the second half of this year. Matt, back to you.

Awesome. Thank you. Thanks, Drew. So look, a lot to be excited about on the program here. I just want to, a couple quick reminders and a summary on slide 22 and 23 here. On slide 22, so Drew talked about this in detail, but just as a reminder, the primary endpoint of this study is PVR. That is the same as the primary endpoint for the Phase II programs across a variety of other PHLG studies or mechanisms or drugs, and we're doing the same thing following a well-trodden path there. We will then, in Phase III, move to a six-minute walk and other clinically relevant endpoints as the way that the trial is measured I want to remind everybody this study is not powered to achieve a p-value on six minute walk we may or may not achieve a p-value what we're really looking for is affirmation of dosing affirmation of safety affirmation of PVR in this patient population and we will obviously look for interesting trends and patient level data on six minute walk but I want to make sure we've been clear ahead of time this is not a study designed to achieve a p-value on six minute walk and that's not what we're looking for is our own criteria to go from here that's the point I wanted to highlight um I want to highlight it now while having not seen any of that data so that I can't possibly be telegraphing anything about the study other than how it was designed on slide 23 yeah just just to recap what what drew we said here first of all again with appreciation of home event team this study enrolled very quickly with with all the patients enrolled within 12 months of the first patient being dosed early discontinuation rates compare favorably to what we've seen in previous PHLV studies look with with with this and 20 bucks you can buy two pizzas at Domino but our investors our investigators are enthusiastic about the program they're excited the feedback's good I think we're feeling great about about how the study is being run and then and this is a great thing for for safety it's a great thing for the opportunity as Drew said 95% of the participants reach the maximum dose during their titration and all of the blinded safety reviews in the ongoing assessments by the DMC have continued to affirm the safety of the program and allow people to run the study. Obviously, there's lots of things that don't get revealed until the data is unblinded, but it certainly gives us comfort that the patients are achieving high dose and that things are moving as they should basis. So again, thank you to Drew. Happy to provide this update now ahead of that data. I'm really looking forward to seeing the outcome from this program in just a few short months at this point, so looking forward to it. Lastly, in terms of the pipeline updates today, I'm going to give a brief recap of where we are on BREPO. BREPO has been the focus of so much of our conversation for the past 10 months. It's less of the focus today as we're in execution mode there, but just as a reminder on slide 25 here, um, sorry, that's, uh, I'm looking at the wrong slide numbers. As a reminder on the next slide, on the first slide of the BREPO section, um, it's slide 32, sorry. Uh, look, this is a huge opportunity for us. There's, uh, possibly close to 300,000 patients addressable by the existing indications, and just a ton of data coming over the next 12 to 24 months between the potential approval, obviously, in dermatomyositis, but also the NIU data, the potential for the NIU launch, the ongoing program that will start enrolling soon, the currently enrolling study at LPP, and potentially more indications to come, so just a lot of great stuff coming for BREPO and a really exciting moment from here. You know, on slide 33, we've put this up a few times, but just to remind people, first of all, these are sick patients and there are really very few options for them in dermatomyositis. As a reminder, you know, 75% of these patients are on principally steroids and in many cases on very high doses of steroids, over 10 milligrams a day for a good portion of the year. And beyond that, it's a combination of IVIG, which as a reminder, the sort of established treatment paradigm for IVIG and dermatomyositis is somewhere between four and five days a month uh consecutive in an infusion center uh so so a really arduous path and then other than that it's off-label stuff much of what has not been successful in studies but is used because there's no other options so we feel really great looking forward here to our ability to bring a new option to these patients um and and on slide 34 further underscoring again this is not new we presented this before, further underscoring the need here. These patients are treated as with PH, for that matter, with polypharmacy on multiple lines of therapy. They're bouncing around. They have accumulated organ damage with high systemic steroid exposures. It's just a tough experience for these patients, and we think a new option is going to go far. We're not saying a lot on slide 35 about our commercial progress. First of all, it is and will become a more competitive field, And second of all, we're mostly just head down in execution mode. But I'll just say, suffice to say, we're doing all the things that you would expect us to be doing at this stage. We're in the thick of payer engagement. We're working with the physician community. We're partnering with specialty pharmacies to make sure distribution is effective for these patients. We've built a strong commercial team that we're really excited about. And we continue to do unbranded patient engagement. We talked about dermatomyositis.com when we got together in December. And I'm super pleased with the work that team is doing. I think they are executing on the commercial side with the same vigor that they executed on the clinical side, and I'm excited to see what we're able to do there later this year and beyond. We have also been moving along on the scientific and medical side. As we look at slide 36, this is a small subset of the presentations that have been made of this data, but this data has been presented all over at this point and continues to be presented all over, both at the major medical meetings as well as at a whole host of regional myositis meetings and rheumatology meetings. And notably, in March, the phase three data was published in NEJM, which is a testament to how exciting the data is, a testament to the importance of the study, the quality of the study. And, you know, we couldn't be more excited for that publication as well. Finally, just a super quick recap on LPP, which we announced just about a month and a half ago. A fourth indication for repositinib, it's a highly morbid disorder with no FDA-approved therapy. These patients are miserable. They are in a ton of pain. It's a really tough disease that, in addition to pain, causes itch, burning, redness, scaling, generally irreversible hair loss. There's probably 100,000 or so such patients in the U.S. that's been growing in prevalence over time, and there's nothing to prove, so we have an opportunity to do something really interesting for these patients. Our trial design on slide 38 we talked about when we first unveiled the program is a sort of continuous enrolling Phase 2b3 Pivotal that's designed to give us an endpoint validation and is that is going to get us into hopefully registration there so we're really forward to that and there's just a ton of reasons to be excited about the program on slide 39 the high end that need in LPP the the mechanistic rationale for for BREPO is strong it's a th1 dominant disease where dual JAK-1, JAK-2 innovation should work specifically well. We think we've got the right trial design, and there's obviously some overlapping prescriber base and KOL community with our existing indications, so it all sort of fits together, and we're excited to see how that program continues from here. I'm going to wrap up quickly with the financial update, and then we'll get to Q&A, so I'm not going to spend a ton of time on this. Financial quarter was relatively straightforward. we continue to be in a strong position from a cash perspective 4.3 billion in cash cash equivalents as of 331 before the Moderna settlement no debt we continue to retire shares repurchased a fair amount in this quarter and you need to have an active program and you know spend continues to be sort of as it has been over time R&D has grown a bit at the scope of the programs have increased but that's all for the good and looking forward to the future there is a couple of slides in here that I'm not going to talk to now but we've gotten a few questions on accounting treatment as the launch gets closer and so there's some good reference material in here on slides 44 and 45 if you're trying to build models or understand our financial statements in the future and look I've talked about this a fair amount already but on slide 46 and 47 we just have a great run ahead of us here we got a lot to do obviously we've been fortunate and have had high quality execution so far with the quality of our data sets a high bar for the stuff coming next which I couldn't be I couldn't be more excited for us so a lot of really great data coming in our existing programs and new programs and looking forward to sharing all of it in the period to come as well as obviously getting back on the commercial arena and watching all of that play through so with that I'm going to say thank you again I'm gonna say thank you to obviously all of you for listening thank you to all of our teams pull map private new event for doing to run high quality studies executing well generating quality data, couldn't ask more of these drugs, couldn't ask more of these And obviously a great thank you to the investigators and the patients who work with us and make this happen. So thank you to everybody who makes this work. And I'm going to pass it over to the operator for Q&A so that we can get to it.

As a reminder to ask a question, please press star 1-1 on your telephone and wait for your name to be announced and to withdraw your question, please press star 1-1 again. and we do ask that you please limit to one question and our first question is going to come from Corinne Johnson with Goldman Sachs. Your line is open.

Good morning and happy birthday to Papa Klein as well. Maybe you could just contextualize the ACR responses you saw here at 16 weeks first. I think more kind of typical in later stage studies is a 24-week reporting timeline? And how would you expect those responses to trend with more time on therapy with kind of implications then towards the randomized withdrawal phase? Thank you.

Yeah, perfect. I appreciate it. Look, I think the first answer to that question is we don't know. This is the first time patients have been treated with this drug and the first time this patient population has been studied this way in detail. Sicker people tend to need more time to get better in general. And that's why I made the comments I made about the face use for randomized withdrawal period but in terms of week 16 versus week 24 I don't know I'll say I don't think there was anything specific about the data leading into week 16 that suggested we were done I think there's certainly a possibility for continued improvement with therapy over time but you know we'll find out as we look at that part of the patient population thanks for I appreciate the question thank you and the next question is going to come from Yasmine Rahimi with Piper Sandler.

Your line's open.

Congrats team and congrats to Papa Clean for also achieving a major milestone of 75 years so happy birthday to him as well. Quick question on mostly congrats. We're very much looking forward to the data. You've been very granular on sort of the baseline as well as what you're seeing of up titration and safety. Have you been able to look at whether your assumptions for standard deviation in PVR and six-minute are sort of tracking in alignment with what you're seeing. And I'll jump back in the queue.

Yeah, thanks. I appreciate it. So, look, I think the short answer to that question is we are largely blinded to all of that data and don't have a lot of information about it, so it's hard to say. But I think given the patient population we enrolled, we feel pretty good about where the study's headed. And, you know, we think we've got an efficacious drug, but we don't have a lot of information about sort of ongoing distributions because the latest study has been blinded. Thank you.

Thank you. And the next question will come from Andy Chin with Wolf Research. Your line's open.

Hey, thank you for taking the question. So, Matt, I'm aware that you said with Immunivant you haven't analyzed IgG reduction, but that's still my biggest question. So, other FCRN drugs, they don't seem to be able to achieve this level of efficacy in RA, and people blame it on FAB glycosylation. Do you somehow have ACPA antibody reduction data, or will we see that data before you unblind the period 2 data, and do you expect ACPA reduction to be less than IgG reduction? Thank you.

Look, I don't have that data now, as I said, so I can't answer the question. We know from our Phase I studies that IMDb 14.02 suppresses IgG quite deeply relative to other drugs, and given the quality of the clinical data we've seen on ACR, I think it's certainly a thing to speculate on that the overall profile of 14.02 is part of what's contributing to our ability to deliver this data. Obviously, it's also a different patient population that has been studied, and it could also be partially patient selection and I think that could certainly be playing a role here so I think those are both important look I think we will continue to analyze this data I don't know at this stage exactly when we're going to present what data so I don't have a good answer to like what you're going to see before or after the period two was unblinded I think we will provide more information about what we've seen about what our analysis looks like when we're prepared to talk about the full future of the program I'll say I think mostly this has been a blessing, but also it's a curse. We've been a leader. We've wondered if this data is going to also establish a leadership role for us along the lines of which others may follow. So I do think we're going to be a little bit conservative on what exactly we say from a competitive perspective. But overall, I think the data are starting to speak for themselves here in terms of the quality of what we're able to do. And I hope we are able to see that as the data mature. Thanks, Andy.

Thank you. And our next question will come from David Reisinger with Larynx Partners. Your line is open.

Yes, thanks very much. So, congrats on the phenomenal data this morning. My question is on Moseley. So, if the phase two focus study surprisingly shows a statistically significant benefit on six-minute walk, could it represent a pivotal study? and what would the requirements be in that scenario for a future NDA filing? And then just one other on Moseley. Is the company considering development of Moseley in any additional indications? Thanks so much.

Thanks, Dave. I'm Statsig at Six Minute Walk.

I think it's impossible to say exactly what we would do until we saw the data. And so if the data looked good enough to support a productive conversation with FDA, I think we would have a conversation with FDA and the FDA has been aggressive lately on conversations about single pivotal designs. So never say never is the answer. I want to clear it's not the base case expectation and the study is not powered to show a benefit on six minute walk. So we'll see what we see. But look, I think given where we're at, we'll certainly take that as we go. And other indications, I'll say every sign around Mosley is pointing to an effective, exciting agent with a lot of things we could do with it. As we watch the field around us, Others are showing us good ideas all the time in terms of how these mechanisms might work. And we have some, our own, that others haven't shown us yet. And so I think there are absolutely opportunities for indication expansion. Although I remember we got this question about 40 times when we first unveiled Moseley, and our comment then, which is still our comment now, is manned PHILD is an area with a lot of unmet need. And even if it were the only thing we ever did with Moseley, it's a big opportunity with a lot of value to deliver to patients. So I think there's a lot of different ways to go there.

And our next question will come from Yaron Werber with TD Co. And your line's open.

Great. Thanks so much. And also congrats on the difficult-to-treat study.

So a question actually about that. Is there any chance you can amend that protocol and essentially run period one and then sort of get new patients completely into period two?

So you're not going to have that step-down issue.

And then secondly, based on our analysis, we think that about 75% of patients are ACPA positive. Is that still kind of what you think the data shows?

Yeah, thanks, Yaron. Look, I think on your first question, there's a lot of things you could imagine doing. I think the truth is between this data and detailed patient-level analysis of this data plus the period two data, we're going to have a pretty good sense for what we've got and a pretty good sense for what we need to do going forward. And so I don't know that we would gain that much from dragging this study out given the quality of the data we're seeing here. So I think we're going to do that analysis in detail. I think we're going to have the conversation with FDA. I think we're going to plot a course forward, but I think we'll have a pretty clear sense. And then look, we've done some commercial analysis of the market in various settings. There's an updated version that analysis actually in Immunovance 10K that was filed today, I think your number is within the range of what we have seen in the literature for ACPA positive patients generally.

Thank you. Thank you. And our next question comes from Brian Chang with J.P. Morgan. Your line's open.

Hey, guys. Thanks for taking our question. In this RA-Explore trial, since there's no washout period between period 1 and 2, I'm curious if you have some thought around the the tail of the efficacy from those going from drug to placebo. You said that tier two might be less meaningful. Are you saying that 12 weeks may not be enough to fully drive the separation?

Yeah, thanks. I appreciate the question, Brian. And just to reiterate, I just like, look, I think first of all, it's hard to know exactly what the tail will be at the end of dosing at the end of week 16. So that's like one piece of this. Obviously, period two is blinded, so we don't know now anything about what's in there. So that's all sort of a part of that. Look, I'll say the other thing is, and just to reiterate what I said earlier, I think given that the period two primary endpoint is losing an ACR 20 response, if you imagine a patient who has achieved an ACR 50 or an ACR 70 response, even if they start worsening on the first day of period two, you know, it just takes some time to give up that level of response. And so that's where I'd say, like, the quality of the data in period two is, the quality of the data in period one is it's always counting against period two, irrespective of the pharmacokinetic effects of withdrawal of the drug. So I think it's, you know, remember, every ACR 70 responder is an ACR 50 responder is an ACR 20 responder. So it just takes time to come off that hill. but we have people who've achieved a lot of benefit.

So that's that.

Thank you.

Thank you. And our next question will come from Dennis Ding with Jeffries. Your line's open.

Hi, good morning. Thanks for taking our questions. For PHILD, I'm curious what are your thoughts around Phase 1B data and, you know, the interpretability of that data in the small number of patients? Specifically, why did the 4-milligram color outperform so much relative to the 2-milligram dose on CGMP and also cardiac output? And, you know, I wonder if you're expecting a, you know, if you should expect a big increase in cardiac output since Moseley is locally delivered to the lungs and it's not really a systemic. Thanks so much.

Thanks, Dennis. I appreciate the question. Look, I think the first answer is 4 is twice 2. So there's just a lot more drug being delivered. The second point I'll make is, remember, there are 170 patients across the Healthy Volunteers program. And so while the specific study that you're referring to may have been a small number of patients, we have a large body of evidence at this point across Mosley being administered in a lot of different settings. And I'd say the dose-dependent improvements in CGMP were broadly consistent across all of that data. The dose-dependent improvements in PVR were broadly consistent across all that data. So I think we generally think we know what we've got.

I think with single dose, you saw real robust growth and immediately right away in CGMP. I think the thing that was exciting for us is it demonstrated that the inhaled approach was really buffering us from a systemic result, and that was really important for us. And I think we'll see that as we go forward. This inhaled approach is so important because you can get the drug to the well-ventilated parts of the lung without worrying about those systemic effects. And so I think that's the biggest takeaway, was we saw cardiac output, we saw MPAP reductions. These are the things you want to see, but these were single-dose studies. So now we'll see them in much more robust fashion in our phase two.

Yeah, the other thing I'll say, just because it occurred to me as Drew was answering that question, is, look, I think one of the things that makes PHILD exciting as a commercial opportunity is it really requires inhaled therapy precisely because of this effect. And so, you know, the competitive landscape will be thinner, and the ability to develop drugs for this market will be more challenging, because you need to sort of thread the needle on systemic vasodilation, and so we feel that gives us an advantage as well, and frankly increases the level of need for the patients, so look, I think it's all setting up in that Thanks, Dennis. Appreciate the question.

Thank you. And as a reminder, please limit to one question. Our next question comes from Derek Archilla with Wells Fargo. Your line's open.

Good morning. This is Jacob on for Derek. Thanks for taking our question, and congrats on the 1402 data. So real quick on safety, just want to clarify, there were no LDL changes or other events of interest observed, right? And then secondly, given the strong activity in period one, how is this informing your trial design strategies in the future?

I know you mentioned that this is likely one of a couple registrational trials, but this is do you think this data changes that uh thanks derek uh great questions both uh although i'll remind politely for the other analysts we're trying to keep to one given the number in the queue but i appreciate both questions and i'll take both of them uh first of all on safety uh in fact um what i can say here is not just uh in this study but across now hundreds of patients dosed across 1402 studies uh the dmc has been watching that issue and we have seen no impact on albumin or LDL across the hundreds of patients dose from 14.02. So while I don't have the very specific data to share for this study numerically, I think the answer is we've seen literally nothing on albumin or LDL from 14.02. And then, look, given the level of activity in period one on trial design, I think the answer is we're going to have to take this data when we get it. We're going to have to look closely at it, and we're going to have to have a conversation with FDA about where we stand and what we need to do. Obviously, the stronger the data from the first study or from this study overall, the the more compelling that conversation is, and, you know, so I think we're excited about this data. Our belief is that we should be able to run a lean program from here, given the patient population we're focused on, given the level of need in this patient population, but that's a conversation we're going to have to have together with FDA in the months to come. Thanks for the question. Thank you.

Thank you, and our next question comes from Samantha Semenko with Citi. Your line's open.

Hi, good morning. Thanks for taking the question, and congratulations on the data this morning and all the progress. Now that you have this first data in RA for 1402, I'm wondering also how we should be thinking about the CLE data coming up in the second half. Will that readout include the entire 52-week study, or will that just be the 12-week randomized portion? And what magnitude of treatment effect do you think would be meaningful here?

Thanks very much. on the first question thank you appreciate the questions on the on the data that will just be the 12-week period that's what we'll have by then so that's we'll be able to share and in terms of what treatment effectively meaningful look I'll say two things one is we will have an opportunity to continue to talk about what we expect to see from that study over time and we'll probably do a little preview of that data before it comes secondly CLE is a little bit different to some of these other indications, and that it is commercially more competitive, and there's other mechanisms coming, and so I think the bar for us is not just sort of per se clinical meaningful. I think the bar is like, do we think our data is good enough to support a program in the face of where the landscape is headed? And so we're going to look closely at that data, we're going to look at what we see, and we're going to make a decision based on the totality of the data, but I think the bar there is pretty high, and I think we can do that going in. Thanks for the question.

Thank you, and our next question is going to come from Thomas Smith with Leering Partners. Your line's open.

Hey, guys. Good morning. Congrats on the really stellar RA data here for 1402. Just wanted to ask one, if I could, on the Pivotal Graves program. Any updates you can share with respect to patient enrollment? I think you were initially kind of gating some of the scale-up activities and trying to get a sense for how the early enrollment trends were going, but just wondering if there's anything that you could share there in terms of pace, cadence, and maybe patients being enrolled, anything differing from initial expectations? Thanks so much.

Thank you. Yeah, it's a great question. Look, I think the short answer is we had a pretty high bar for ourselves when we started the study, and we didn't exactly know because there hadn't been a lot of development in I think we can now say enrollment's going great. We're on track. We'll have the data in 27, as we previously discussed, and a lot of enthusiasm and a growing amount of enthusiasm as we continue to add sites as docs continue to get comfortable with the study so I think overall really happy with how that program is evolving uh and I'll just again take the opportunity to say I think all of our VANT teams at this point are executing at a really high level from a cleanup enrollment perspective and I think that's that's been a real driver of value for us thank you thank you and our next question is going to come from Alex Thompson with Steve for your lines open.

Congrats on the day. This is Patrick Olson on for Alex.

I guess just kind of building on, you know, the path forward here in RA, you know, looking at period two, I guess if your 300-milligram arm performs, you know, just as well as 600-milligram, you know, how are you guys thinking about your dosing strategy going forward in phase three?

It's fun to sit here and think about, like, what happens in the phase two study. we see as good, first of all, it's a randomized withdrawal study, so it's like trying to figure out exactly what it would look like for 300 and 600 to perform equivalently. But look, I think overall it's just too early to say we've got to look at the data. This is a patient population with extremely significant unmet need, and without, I mean, to say without a lot in development is an understatement. I think like basically we are plowing a new course with this patient population, so I think we've really got to look at that data and get an outcome from it. I think the inclusion of 300 and 600 in the study was important because FDA, especially in new indications, especially in indications like RA, is likely to want some dose-ranging information. But I think we're going to have some flexibility and we're going to get safe. You know, historically, there has been separation in IgG reduction, obviously, between 300 and So, you know, we'll see how that translates in this population. But I think we've got a lot of options here. Thanks for the question. I appreciate it.

Thank you. And the next question comes from Prakar Agrawal with Cancer Fitzgerald. Your line's open.

Thanks for doing my questions, and congrats on these impressive data. So maybe on the RA front, given the sample size is quite large, but ultimately this trial was open-label, and some of the ACR responses can be susceptible to open-label nature of the trial. So maybe just if you can expand, if you have any data on some of these secondary endpoints, which might be less susceptible to open-label design of the trial, And what would give, how much efficacy degradation would you assume as you move from an open label to more of a placebo-controlled trial in a registration trial? Thank you.

Yeah, thanks. This is, look, it's a great question. It's obviously what was on our mind from the day we first saw the data. I think it is certainly helpful that we're talking about ACR 50 and ACR 70 responses and just ACR 20 responses. I think once you get to that level, sort of spontaneous placebo-style remissions of those kinds are less frequent. We don't have any of the secondaries or additional markers to share. We've been looking at that data hard, and we feel excited about the data based on what we've seen in terms of everything hanging together, but that's about all we're able to say at this point. I think that's about all we know at this point. One other thing is we have the way the study is designed, the people doing the joint assessments are blinded, so they are doing the assessments without knowing anything about the study, what patients are on, where in the study they are, whether they're on drug or placebo. That's obviously only one component of the total here, but it is one way for us to get a little bit of objectivity into a study that is otherwise at this stage open label, and that is helpful and pretty objective. Thank you.

Thank you. And our next question comes from William Pickering with Bernstein. Your line's open.

Hi.

Congrats on the updates and thanks for the question. On Moseley, you also have a phase two open label with patients on background to prostanol. What are you hoping to see in that study?

And then how are you thinking about broader evidence generation strategy to support reimbursement of Moseley in combination with prostanol? Thanks.

Yes.

So, in the combo study we have patients on background tropopinol obviously in the main phase 2b we don't have patients on background tropopinol and the reason we set this up this way is because we know that polypharmacy is going to be is going to be a part of the landscape and so in the phase in the subsequent study that we run we're likely to have some proportion of patients on background tropopinol as well and it felt like going into that state study with no experience treating patients on both drugs was for a variety of pretty obvious reasons a liability and so I think the combo study is in part really a safety study it's just designed to make sure these things can be administered safely together we will learn from it the information that will help us design the stratification rules help us understand better who's going to be on what in the in the subsequent study but I think you know I think beyond that it's hard to say at this point and that's become a study still in pretty early days so we don't have much to say about it through anything to add to that I think that's exactly the case.

We decided not to go on top of inhaled treprostanil in the first focus study. We were initially looking at our drug in single-engine activity in PHILD, and we wanted to have some time to understand that population, understand Mosley. Also, as you know, treprostanils do have a sticky issue with cough, and we wanted to make sure that our drug would have a clear path to be able to demonstrate its tolerability profile, which I think has been relatively impressive. So with that, in the later days, we decided with the team to go a little deeper and look at Mosley on top of inhaled troposinol, given the confidence we had in Mosley after seeing it in our focus study, of course, in an aggregated setting. So with that as a backdrop, as Matt said, we're only in the days, but we actually don't expect there to be much of an issue there, but we definitely want to understand that from a dosing and safety perspective. Thanks, Paul.

Thank you. And the next question is going to come from Douglas So with H.C. Wainwright. Your line's open.

Hi. Good morning. Thanks for taking the question. I think we're wrapping up the data that are progressing. Matt, I'm just curious, in terms of the RNA data, if you've had a chance to sort of talk with some of the key KOL clinicians on the data and I'm just curious what their sort of feedback is um and if they were more focused on the depth of response than you saw or the breadth of response and obviously you kind of have both so you know you didn't necessarily have to choose but if there's anything that was striking from the initial data set thank you thanks Doug um so look we have uh obviously a bunch of KOL was involved with the study um therefore we have those conversations continuously and with some of the important ones for the

field who have been on multiple of these studies as well. I think in general the answer is they're super impressed. I think one KOL told our team roughly is a quote, you can't fake ACR 70s like this. The opinion of one physician, I think it's true at some level, but ultimately we'll have to see what the rest of the studies show. But look, I think docs are excited. They're excited about the depth of responses. They're excited about what this could mean. And look, I think the most important thing is these are physicians who they're treating these patients. They have no options. Many of these patients are very uncomfortable and in a lot of pain. I think they see a new option for this population, and they were hoping for something that worked even a little. And obviously, this is beating that far handily. So I think there's a lot of enthusiasm.

Thank you. And our next question will come from Dina Ramadane with Bank of America Securities. your lines open.

Good morning. Congrats on the data this morning and thanks for taking our question. Just a quick one from us. On the non-responders, could you provide maybe some more color on these non-responders in period one? Was there anything you could maybe point to, such as prior lines of failed therapy or baseline characteristics, such as maybe antibody levels that were the reason for not responding to 14.02. Thank you.

Yeah, so we're looking at that in detail now just to try and get some further comfort and understanding about what's going on. I don't have anything to say about it now, but that's exactly the kind of analysis that we're running. And, you know, you said non-responders. Just a reminder, 72% or 73% were ACR 20 responders. So we're also looking at some of the people who got to 20 but not 50 and just, like, trying to get a better sense of... Thank you.

Thank you. And our next question will come from Iris Gow with Guggenheim. Your line is open.

Good morning. This is Iris. Thank you for taking my question. Congratulations on the data, and happy birthday to your MADS father. My question is also on sporting O2. Are there any more colors on what proportion of patients were refractory to rituximab, and maybe NTR6 can use their MOAs are relevant in seropositive patients? So let's get back with you. Thank you.

I don't have that in front of me. It's a good question. We have cleaned some of that data. We had a bunch of IL-6, of IL-6 refractory patients, but we're talking about, I don't And so, look, overall, we don't have that to share right now, but I think the answer is that the population is consistent with heavily pretreated population. They've been on multiple lines of therapy. Many of them have failed things in addition to Jax and TNF. So, you know, all of those different mechanisms are in. We may eventually share more data on sort of what those different subsets look like, but I think we're particularly enthusiastic about the JAK and TNF combined failures. Remember that over 10% of these patients have failed more than three lines of these advanced therapies. Thank you.

Thank you, Eric. Thank you. And our next question will come from Sam Slutsky with Lifestyle Capital. Your line's open.

Hi, good morning. This is Kate on for Sam. I appreciate you taking the question. So I know the strength of period one data has made period two all the more challenging, particularly on ACR20. But looking to period two, is there a delta versus placebo potentially on other endpoints that would excite you commercially?

I don't think phase two is really about commercial value at this point. I think phase two is about better understanding the characteristics of the patient, seeing erosion of efficacy, starting to understand, you know, to separate out drug effects from other things. So I think, you know, I think it's not so much that we're looking for some commercial bar in phase two. I think the quality of this headline data is such that even if it degrades, we're happy with it. And, you know, I think, you know, even in subsequent studies, I don't know that we're, like, shooting for this bar per se. This is just a great foundation from which to build something pretty exciting and all right.

Excellent. Thank you.

Thank you. And that will conclude today's Q&A session. And I will now turn the call back over to Matthew Klein for closing remarks.

Look, thank you, everybody, again. Appreciate it. There were a lot of questions there, so I appreciate everyone's forbearance in helping us get through it all and in limiting a number of questions, which is a great favor to the people lower in the queue who need to come up with questions if theirs has already been asked. So thank you again to everybody for playing along with that. An exciting day for us and exciting data to be able to put out. So thank you again to everybody who makes that happen from the Vant and Roivant teams to the patients and investigators. It takes a village and it's a great outcome and something that we can really build from here. And once again, happy birthday to my dad. Thank you everyone for listening and we'll talk again soon. Have a great day.

This concludes the conference call. Thank you for participating and you may now disconnect.