Good day and welcome to the NIU Phase 2 top-line results call. At this time, all participants are in listen-only mode. After the speaker's remarks, there'll be a question-and-answer session. To ask a question at that time, please press star 11. As a reminder, this call is being recorded. I would like to turn the call over to Jeffrey Kalmus. Please go ahead. Good morning, and thank you for joining today's call to review the results from our phase II study evaluating brepocitinib in non-anterior, non-infectious uveitis. We will also discuss updates on our capital allocation and new share repurchase programs. I'm Jeffrey Kalmus with Roivant Sciences. Presenting today, we have Matt Gline, CEO of Roivant, and Benjamin Zimmer, CEO of Priovant. 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 investor.roivant.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 filed with the SEC for more information regarding these forward-looking statements and related risks and uncertainties. We will begin with Matt Gline, who will do the opening remarks. With that, I'll turn it over to Matt. Thank you, Jeff, and thank you, everybody, for joining today on short notice, as with these data calls sometimes. I'm always excited to get on the phone and talk about some exciting data and also to provide some clarity that I know people have been waiting for on capital allocation and capital return strategy. I just want to start quickly with a couple of framing remarks. Ben, CEO of Priovant, is going to do most of the presentation of the NIU data, which is really exciting data. But before that, just on slide 4, kind of as a reminder of where we're at, we had said all along that 2024 was about sort of expansion, clarification, about building for the future for us. I think two really important milestones today against that backdrop, one, which I'll talk about in a second, is I think some real progress on clarifying and advancing our capital allocation and capital return strategy. In particular, very happy we've been able to make some progress in providing some liquidity to a shareholder that really needs it and giving us some flexibility for the future. Then we've gotten a lot of questions over the past few months about what the future of our pipeline looks like. One of the things I've said is, "Well, part of the future of our pipeline looks like the present of our pipeline. We have some really, really great programs." High on that list, brepocitinib. I think that the data that we're going to talk about today in a lot of detail underscores just how amazing that opportunity can be for patients and, frankly, just how potent and active a compound it is. I'm really excited to share all of that soon. First, to get out of the way on slide 5, what's going on from a capital return perspective? We've announced this morning really two things. One is that we've got a board authorization to buy back; the current board authorization is up for $1.5 billion in stock. I'll put that number in context in just a second. The other is that we've reached an agreement with Sumitomo to repurchase their entire stake for $9.10 a share, $648 million in aggregate. That first purchase from Sumitomo will reduce our share count by about 9%. Then the remainder of that $1.5 billion just gives us great flexibility at the current moment, right? The way that we think about it is we're incredibly privileged to have the cash balance that we do. We've said all along that we intend to be disciplined, that we intend to be ruthlessly economic and thoughtful about how we use that capital, and that we thought it was virtually certain that we'd be able to return a meaningful portion of it to shareholders. When we think about this $1.5 billion number, really, what I think about is flexibility. I think it gives us the ability now, if we see opportunities in the market, if we see dislocations in the share price, to really go out and use a lot of firepower. And if we use it up, we certainly have the ability on our balance sheet to re-up the authorization to do more in the future. But also, it gives us the flexibility. We see some truly incredible opportunities for capital deployment on new programs. We've talked a lot about how promising the environment is. I am every bit as excited today as I was on our last quarterly call or more. And so as those opportunities come into relief, we have the flexibility to think very carefully about our capital. But now we're sort of here. We have the tools in our toolkit to do what we need to do yesterday, today, and tomorrow. It bears mentioning this position, our capital position is unchanged by this in the sense that we still have, even if we use the entirety of this $1.5 billion and more, plenty of capital to fund our existing programs through profitability, plenty of capital to expand our pipeline with some of the BD opportunities that I just alluded to, and plenty of capital to continue to return capital to shareholders. I hope this answers some of the questions that we've been getting around how to think about the large concentrated shareholder base. I hope it answers some of the questions about our ability and plans to return capital. Just really looking forward to being able to clarify that and move back on to the important work, which is generating good funds of data. Against that backdrop, I'm going to let Ben speak, by and large, to the brepocitinib data and NIU itself. But if you look at slide 6, just as a reminder of kind of what the pipeline today looks like, I think we remain incredibly proud of our late-stage pipeline. We still have a concentration in NIU, although we're looking in other areas as well. And brepocitinib is one of these molecules, and we've talked about this before, that they come along infrequently. It's an incredibly capable compound with a tremendous amount of data. As a reminder, we have, even before today, six positive phase II studies, over 1,400 patients' worth of exposures. And then today, though, is kind of a special day for us with the program in that today is really the beginning of kind of the Roivant-Priovant, brepocitinib era, right? Prior to today, those six positive studies that I mentioned were all sort of run by Pfizer, largely in advance of us acquiring the program. Even the SLE study that read out last year was a study run by Pfizer that we thought might have fit into our overall picture, but it wasn't a part of our defined strategy. Our defined strategy began with the initiation of our dermatomyositis study when we first brought the program in, and that data is coming next year. But this is the first time we've kind of read out data from a study that we conceived of that the Priovant team, Ben, who you'll hear from and his team, designed and executed. And it's great when you're in that position and the data is just as extraordinary as the data that we're about to talk about. So look, I think this is a drug that matters, or at least it should be a drug that matters. I think this is a disease population that has, as you'll hear, very few other options. This is some of the really, not some of, really the best data that we think has ever been seen in the NIU field. So I couldn't be more excited to share that data with you and to hear more about it from Ben. So I'm going to hand it over to Ben now, and he'll take us through it starting on slide 7. Perfect. Thanks, Matt. Great intro to tee this up. If you turn to slide 8, I'm really excited to share the results of our phase II study evaluating Brepo in NIU. As you see on the slide, and I'll walk through in detail later, this study generated the strongest data that's been generated to date in any study on the registrational endpoint in NIU. We also had great results on a number of important secondary endpoints, particularly certain measurements related to the prevention and treatment of macular edema. We achieved these results in spite of an aggressive six-week steroid taper, which involved pulling patients off 60 mg per day of steroids, pulling them off that completely off prednisone more than twice as quickly as in precedent studies. So really great data against a very high bar for efficacy that I'm excited to walk through in more detail. But first, if you turn to slide 9, I wanted to take a brief step back and provide a bit of additional context on brepocitinib and NIU for those of you who haven't been following the asset closely or aren't that familiar with the indication. Brepocitinib is a dual inhibitor of TYK2 and JAK1. That's really a unique isoform selectivity combination among JAK inhibitors. Looking at the approved and late-stage pipeline, there's very little other therapies that are able to achieve what we do through that dual inhibition in terms of being able to hit type 1 interferon, type 2 interferon, IL-6, IL-12, and IL-23, all with a single targeted agent. As Matt walked through before, a great background of clinical data in terms of both safety and efficacy across many different studies and indications. And there's a lot of different directions that we could have taken this. As Matt walked through, the Roivant-Priovant strategy was really about developing brepocitinib as a large orphan franchise across multiple high-morbidity indications. These indications have tremendous commercial opportunity that's largely, or in some cases, entirely uncapped by both biologics and other JAK inhibitors. We think that because of that mechanism I walked through before, brepocitinib is well-positioned not only to be one of the first therapies to market, but also it is well-positioned to really generate best-in-indication data that stands the test of time, even as other drugs may in the future enter the development pipeline. That's because we're able to hit so many of the pathogenic cytokines involved in these diseases through a single asset. So I think the data we're sharing today, from my perspective, really calls for excitement, first and foremost, as relates to brepocitinib's potential in NIU. But I think it also really validates and brings to light this strategy for the drug more generally and increases our excitement for it across multiple other indications as well. Turning now to slide 10, just a bit of background on NIU. This is one of the leading causes of blindness in the United States, a tremendous unmet need. The only nonsteroidal therapy approved is Humira, which has limited efficacy in the indication. And as you can imagine, given the risk of blindness and other very severe symptoms, physicians have a very high sense of urgency to treat. And for that reason, and given the limited efficacy of Humira, a large number of patients are prescribed off-label therapies as part of a general kind of kitchen sink approach to treatment. And in our opinion, this unmet need is one of the most underappreciated commercial opportunities in autoimmune disease. To elaborate a bit on that, at least half of NIU cases, as I note here on the slide, occur in the context of other autoimmune conditions. Really, the current diagnosis and treatment patterns related to that have only developed and really concretized over the past two decades. For this reason, pharmacy claims analyses of Humira prescriptions in NIU, in our view, most likely significantly underassess the current market size, capturing only the idiopathic cases, which is less than 50% of the total, and only patients on Humira without looking at the large number of off-label biologics also used. Our own claims analysis has found about 30,000 patients receiving a biologic therapy for NIU. Prescription rates appear to be growing rapidly. Both his ophthalmologists increasingly embrace the criticality of systemic immunosuppression for treating ocular inflammation and also as other specialists in rheumatology, GI, and otherwise develop greater awareness about the indication, helping to further drive diagnosis rates and treatment rates. And so brepocitinib poised to enter this market with, as I'll walk through momentarily, a potentially highly differentiated efficacy profile, along with very limited competition and orphan pricing, we see clear potential for a multibillion-dollar peak sales opportunity in this indication alone. And slide 11, I'll just briefly go through to reinforce this point, which is that the prevalence and morbidity rates in NIU are very much in line or, in some cases, exceed those in other recognized blockbuster orphan indications. And unlike some of those other indications, we have much less competition here. I think as you think about NIU as a market, I think one way to think about it is really having many features in common with where indications like HS, TED, and MG were several years ago. We're excited to be bringing forward a molecule that has the potential both to be the next approved drug of any modality, first oral therapy, and that has generated data to support a highly differentiated product profile. This brings us now to the NEPTUNE study itself on slide 12. The study enrolled 26 patients who were randomized 2 to 1 to brepocitinib 45 milligrams per day and 15 milligrams per day. This is a study in an active NIU, so patients all had active disease at baseline. Consistent with the treatment paradigm, patients were given a 60 milligrams per day steroid burst for two weeks. And then per protocol, there was a forced taper completely off prednisone by week 8, so a 6-week taper. And then the primary endpoint is the treatment failure rate, which is a composite endpoint of several measures of ocular inflammation and visual acuity. And that is evaluated after week 52 with the primary endpoint at week 24. And we based the study very closely on VISUAL I, which was the active uveitis registration study for placebo. That study and a number of others of similar design that have established it, that have followed it, have established a pretty clear placebo rate of around 70%-80%. And so this is an indication where we don't see a particularly high risk of placebo response. The measures of treatment failure are all fairly objective assessments. And so looking at VISUAL I is a great way to contextualize this data. Just as background, there is a second Humira study, VISUAL II, that was done in inactive patients, which are patients who are basically quiescent at the time they enter. And so that's a very different baseline characteristic and not really quite as relevant a comparison point. On slide 13, I want to go a bit more in-depth on the steroid taper, which is really the one and only material design change we did have from VISUAL I. And as I mentioned before, this was to have a steroid taper that was more than twice as rapid as these other studies. And we did this to actually make it considerably harder for brepocitinib to prevent treatment failure and demonstrate efficacy benefit. The drug needed to have a very rapid onset of action with highly efficacious steroid-sparing benefit to prevent flares while tapering patients from 60 milligrams per day to 0 milligrams per day in just six weeks. Any physician will tell you that absent having a very efficacious steroid-sparing therapy being used, that's going to lead to a flare. And then also notably, brepocitinib, to meet the primary endpoint, needed to sustain steroid-free benefit for over 50% longer than Humira did in VISUAL I to prevent treatment failure by the six-month endpoint. And I emphasize this really just to reinforce that although this was a small study, it was not a small study designed to detect any signal of benefit from the drug. To the contrary, it was a study set up to fail in any world where brepocitinib did not deliver overwhelming evidence of benefit. It was really designed related to that to ensure that there were no false positives. So against that backdrop, we're really excited by the results. Of course, it was important for other features of the study design to be in line with VISUAL I. As you'll see on slide 14, endpoint definitions and IE criteria were consistent. On slide 15, baseline criteria were consistent. Now moving to slide 16, I'll walk through the actual data itself. Again, I'm contextualizing our results in the context of VISUAL I to provide a bit more meaning to kind of how to process these numbers. I've included here two different cuts of the data. If you look on the left-hand side, this was our pre-specified primary endpoint in which discontinuations were imputed as treatment failure and the comparison to VISUAL I on the apples-to-apples methodology there. Then on the right-hand side of the chart, we see the way that the Humira data from VISUAL I is presented on the Humira website. There's multiple different ways that the Humira data is described in certain different formats. This was one of the most Humira-favorable descriptions and was done in a way where their methodology was made pretty clear. So we were able to do what we think is an apples-to-apples comparison there. You see across either one of these approaches, you have the brepocitinib 45 mg doing more than three times better than the placebo arm and more than twice as good as the Humira treatment arm. Really quite striking data. You also see brepocitinib 15 mg doing quite well with a clear dose response. If you turn to slide 17, I'll contextualize that a bit. That good data from the 15 milligram arm is something we expected. By way of context, brepocitinib 10 mg has been studied in placebo-controlled studies in UC and psoriatic arthritis, generated data that was roughly in line with Humira there. So we would expect on the basis of that 15 mg, which is 50% stronger dose than 10 mg to also do equally or, as we see here, better than Humira. And then also just looking in general at normalized dose response data across all the indications where brepocitinib has been studied, over 1,400 patients dosed across many different indications. And we see Brepo 15 mg at roughly 60% of maximum efficacy and over 90% at 45 mg. So again, that ratio of benefit from brepocitinib 45 to brepocitinib 15 mg is consistent with what we've seen otherwise and the relative performance to Humira consistent with what we've seen otherwise. So we think that that context certainly adds to the robustness of the data on slide 16. Turning now to slide 18, starting to go through some of the secondary endpoints to think add even further to the robustness and our excitement about the potential product profile that we're looking at in the event of approval. What we see on slide 18 is the secondary endpoints on each of the four individual components that make up treatment failure. And you see some great data here as well from brepocitinib. No new inflammatory lesions in either eye. Vitreous haze, which is one of the important markers of inflammation. We actually see brepocitinib getting the brepocitinib 45 mg dose arm, the mean improving even after the best state achieved during the steroid taper. So while tapering from 60 mg to 0 over 6 weeks, we're not only maintaining benefit, we're actually improving benefit on that endpoint. And then just looking holistically across these, you see both dose arms clearly outperforming the placebo from VISUAL I. Brepo 45 mg clearly outperforming the Humira treatment arm. Here, I think on these secondary endpoints, you see an even clearer dose response, arguably, than on the primary, which makes sense since these are, generally speaking, more continuous variables than are binary outcomes. So we think, again, both some exciting data here in terms of the potential future product profile and then also really add to the robustness of the replicability of the primary endpoint data looking ahead to a phase III study. Then turning to slides 19 and 20, I also want to talk about an important endpoint outside of treatment failure, which is macular thickness and macular edema. This is an important long-term consequence of NIU. It is a very severe, as anyone who follows ophthalmology knows, it is a very severe problem, one of the leading causes of blindness in uveitis patients. You see on slide 19 our data on macular thickness being quite excellent. On slide 20, we can look at macular edema itself. You see in the brepocitinib 45 milligram arm of the 10 patients who did not have macular edema at baseline, none had developed it by week 24. By comparison, in the VISUAL I study, at the 6-month time point, half of patients in the placebo arm who did not have macular edema had developed it after 6 months. So we think this is really a quite striking result in terms of the potential for brepocitinib to prevent the onset of macular edema. Then similarly, for patients who did enter with macular edema at baseline, there were 7 of those in the 45 milligram arm. And we had a resolution rate of 43%, which, again, is in line with data from leading current and potential UME treatments. And I think the treatment paradigm, in general, can often view treatment of NIU itself and treatment of UME as different. Physicians often will use two different drugs for those. And I think one very exciting feature of this data is we have a drug that's being developed for the broader non-anterior NIU population, but that has the potential, as part of that, to potentially not only resolve but prevent the development of macular edema in the first place. And I think that could be really transformative for the field in a very exciting way. Next, turning to the safety data. All in all, we're very pleased with what we saw from a safety perspective on this study. So if you turn to slide 21, I'll briefly walk through that. Most notably, no deaths, malignancy, or VTE events in either treatment arm. There was one SAE in the 15 mg arm that was a grade 2 hypersensitivity case that resolved following discontinuation of study drug and administration of Benadryl. Notably, hypersensitivity is on the label for approved JAK inhibitors. We've seen rates in other molecules, other JAK inhibitors that are approved in low to single-digit%. In the brepocitinib program to date, this is not the first hypersensitivity, but we've had not all that much. The rate we've seen to date is less than 0.5%, so considerably less, actually, than what we've seen from other JAK inhibitors. This is really not something that gives us any cause for concern. Across the AEs in general, we had no grade 3 events except for one uveitis-related flare in the 15 mg arm and a case of costochondritis in the 45 mg arm, which is a benign sternum pain. So again, all in all, we're very pleased with what we see from a safety perspective. Brepocitinib's safety database, all in all, is very much in line with those of approved and widely prescribed JAK inhibitors, including widely prescribed in indications where the morbidity is not always even as great as it is in NIU. And for what it's worth, this safety data and the rates here are also very much in line with what we saw in terms of rates in the Humira treatment arm of the VISUAL I study. So turning to slide 22 and really tying all this together, we're very excited about this data, both again in terms of its robustness for replicability in phase III, but also in terms of what it says about brepocitinib's potential product profile here. As I mentioned upfront, this is an indication where physicians are focused on treating aggressively. There's high risk of blindness, even for patients who don't go all the way to legal blindness. It's a very severe disease: losses in visual acuity, pain, blurriness, floaters. The treatment paradigm is really to not mess around, given that very aggressive steroid burst, and then just to try to find different steroid-sparing therapies that allow doctors to taper as quickly and sustainably as possible off of those bursts without causing treatment failure. Given the data we've seen in this study, low treatment failure rates, even with the rapid taper, sustained over time, potential benefit not only on inflammation but also on macular edema, we think there's great potential for the drug to be used early in this paradigm. And again, to kind of come back to where I started talking about the indication, given the large number of patients on biologics and the limited efficacy of those, including many that are not even approved for NIU, we think even in the biologic refractory population alone, there's very significant commercial opportunity. And so finally, on slide 23, I just want to talk a bit about this data in the context of looking ahead. And I think that, again, to kind of come back to the overall strategy for brepocitinib in these large orphan indications, it really derives from the fact that these diseases are so severe because there's many different inflammatory cytokines, multiple distinct inflammatory pathways involved. And to generate maximum efficacy, you need a drug that can hit many of those. And as you see in this chart, brepocitinib really does that distinctively. If we think about current or potential future competitors, we don't see them being able to do that in the same way. Starting with IL-17, IL-17 inhibitors have generated mixed data in NIU. That's not just because a specific molecule isn't hitting IL-17 hard enough or is only hitting IL-17A rather than A and F; rather, it's because the TH17 pathway is only one inflammatory axis in NIU. It's relevant, but it's only one axis. An IL-17 inhibitor is going to have no impact on the JAK1 pathway and also no impact on IL-6, which is involved in TH17 signaling but also has other relevance in NIU too, particularly for vascular permeability that contributes to macular edema. We really see that as being a mechanism that's not likely to generate as much efficacy benefit as we see from Brepo. I think turning next to selective TYK2 inhibitors, our view is really obviously, we're enthusiastic about TYK2 inhibition. Brepocitinib itself is a potent inhibitor of TYK2. But I think the kind of sheen of allosteric TYK2 inhibition specifically, so that mechanism can be very beneficial and appropriate in certain indications. I think the sheen as a sort of single solution for all autoimmune diseases has worn off quite a bit lately. We've seen deucravacitinib fail in IBD. We've seen Ventyx fail to meet expectations in psoriasis. And we think NIU is definitely an indication where JAK1 is adding a lot to what we see in terms of efficacy, being able to hit IL-6, which TYK2 does not, also being able to hit interferon gamma, which is very important in TH1 signaling. And so we really think this is an area where JAK1 is doing a lot of the work and that dual inhibition is particularly valuable. And of course, that logic also holds up if you look at other mechanisms like a selective JAK1 inhibitor or a selective IL-6 inhibitor. Each of these do important things but are only going to be hitting certain inflammatory axes. And we think that there's really a tight alignment here between the great data I just walked through and what brepocitinib is doing mechanistically. And that further contributes to our confidence that this is great data, not only by the standards of studies that have read out so far, but also that it is highly likely to stand the test of time. So turning to slide 24 and wrapping up, we're really excited about this and really excited about the potential for what it means for brepo in NIU and other indications. We're excited to be moving ahead with the phase III program, which we expect to initiate later this year. Also, as Matt mentioned in his opening, we're very excited by the progress in dermatomyositis, our phase III study there, which is underway. This is actually the largest interventional study ever conducted in dermatomyositis. That's enrolling very well. We expect to have full enrollment there in the third calendar quarter of this year. And we're on track to have that readout in 2025. This is another very exciting large orphan indication that I think meets many of the same opportunity traits that I walked through earlier for NIU. And so slide 25, won't belabor these points since we've already gone through them. But again, great data, really excited about its implications both for phase III and a potential product profile as well as for other indications. Thanks so much. Thanks, Ben. Appreciate it. And obviously, again, just tremendously exciting data that we are really pleased to put out today and excited to see the progress in the program and looking forward to that phase III study starting or phase III study starting later this year. So with that, I'll say thank you, everybody, for joining. We're, again, excited about the progress in capital allocation, excited most of all to deliver clinical data that will matter to patients. And looking forward to taking your questions. So I will hand it back over to the operator to begin that. Thank you. If you'd like to ask a question, please press star 11. If your question hasn't answered and you'd like to remove yourself from the queue, please press star 11 again. Our first question comes from Brian Cheng with JP Morgan. Your line is open. Hey, guys. I'm sorry. I'm taking questions this morning. Congrats on the buyback and the NIU data. First, a housekeeping question. What is the latest fully diluted share count after the repurchase of the Sumitomo block? Thanks, Brian. Thanks for listening, and thanks for the great questions as always. After the Sumitomo block, based on the 12/31 number, I'd say either a basic share outstanding number, I think about 733 million, or I'd say on a treasury method dilution, about 790 million is probably the way to think about that share count. Okay. Going back to one of your slides, you talk about further repurchase using a potential combination of open market, tender offers, and private transactions. After the Sumitomo block, there's still about $900 million or so still open to a combination of those. How are you allocating those three methods? And is there a strategy to loop in investors that have been keen on your story for some time? And I have a quick follow-up. Thank you. Yeah. Perfect, Brian. Thank you. Look, I think, first of all, as I said in this part of this discussion, we're just excited to have the flexibility to take advantage of whatever comes our way. So I think we don't have a sort of programmatic plan to it's going to be a third, a third, a third, or something like that. I think our view is, as with Sumitomo, if there are large shareholders looking for concentrated liquidity at an attractive price, that's a conversation that we continue to have on a regular basis with those shareholders. I think uniquely now that we have this program in place, we can and will be out there anytime that there's a dislocation in our value that we think doesn't reflect the value of the business to take advantage of it on behalf of the shareholders who are with us long term. And so I think that's a change. It's something we've always said we would do once we got ready for it. And now we're positioned. So I think that's something we'll be out there in the market when that happens, taking advantage of it. And then I think more generally, we're going to be opportunistic about how much of that to deploy, when to deploy, and whether to go above and beyond what we even currently have authorization for. So I'd say stay tuned. And in terms of continuing to sort of cycle the shareholder base, look, I think we are really pleased with a lot of the progress we've made in bringing new folks into the story. And I think there were at least some people who were kind of waiting to see clarity on this point. I think some people were waiting to see clarity on our pipeline strategy. I expect those things to come into relief, some of it today, some of it in the near future. And look forward to continuing to talking to those people and continuing to try and place Roivant stock with folks who want to be holders for a long time. Thanks, Brian. Yeah. Just to unlock on the NIU piece. So very good data there. But it's interesting that the NEPTUNE study has a more aggressive steroid tapering than we saw compared to the NEPTUNE phase II and also the phase III VISUAL I for Humira. So how are you thinking about your phase III? Is that going to be a similar approach as NEPTUNE where you are deploying a more aggressive steroid tapering? Or does it not matter at all with more just a traditional steroid tapering? What's your latest on it? And thank you for taking my question. Thank you. I'll give a quick thought, and then I'll hand over to Ben in case he's got sort of more to say. Look, I think, first of all, I think the design and Ben hit this in his comments. The design of a steroid taper in the phase II was in part designed to make sure that we did not see false positives in the study by being very assertive. Now, the data we showed was extraordinary. And so I think it makes us sort of think carefully about what we want to do in phase III. Mostly, I think we'll comment on phase III design once we've had a discussion with FDA. But Ben, anything you'd say about sort of general principles? Yeah. I mean, I would echo kind of have more final thoughts after FDA engagement. I would say there's really two unique values of the steroid taper. The first is in the context of this phase II data having a very high bar to clear as I walked through. But the other is thinking about, from a physician perspective, the value of being able to have evidence that a drug can work in this way and to get patients off steroids faster. I think that is something that will be of high value to physicians. I think physicians are going to be very excited by what they see here. And it's potential. And I think that, again, I think that steroid-sparing benefit in terms of getting patients off steroids faster is a very high value. So I think we set this very high bar for ourselves. Given we've cleared it, I think our default is not going to be to back down from that but move forward with, again, what we hope will be a product profile that is highly differentiated for this among other reasons. Thanks, Ben. Thanks, Brian, for the questions. Thanks, Sam. Thank you. Thank you. Our next question comes from David Risinger with Leerink Partners. Your line is open. Thank you, Matt, and Kim on the announcements. I really liked slide 11 in the presentation today. I have a number of questions. Let me just go one by one if that's okay. First, for the planned NIU trial, the phase III, are you considering including a Humira arm in order to show superiority and force payer coverage? That's my first one. Yes. Thanks, Dave. Thanks for listening. Thanks for the question. I should let you know your audio is breaking up a tiny bit, so just FYI. But I think I've got where you're coming from. Look, I think on the one hand, our data here is striking. And I think we know what we've got, as it were. It's a phenomenal dataset. I think that cuts both ways from a trial design perspective in the sense that, to be honest, with data that's striking, I'm just not sure I'm not sure with data that's striking for disease with this level of morbidity, I'm not sure we're that worried, to be honest, about payer coverage. But it's a thought for the future. I think it is relatively unlikely that we would have a Humira arm in a phase III trial design. But to be candid, those discussions are still in the future with FDA. And we're still sort of plotting ourselves out. So I think that's kind of where we're at. Okay. Thank you. And then just looking ahead regarding Brepo and dermatomyositis, could the FDA issue accelerated approval on a single Phase III trial if the results are highly compelling? Or will a second successful Phase III trial be required before approval? Just to be clear, and I think we've said this before, but just to be very clear about it, our expectation is that the ongoing dermatomyositis phase III program is registrational. That is, this is the last study we'll need to run. Yeah. I think that's the key point, is that our study was designed and powered to serve as a single phase III study. We've had engagement with FDA on that point. Obviously, as with any single phase III study, we'll need to generate really excellent data to meet the standards. But this is an orphan indication. Dermatomyositis, no modern targeted therapy is approved at all. So we think that certainly with great data, there's going to be a lot of excitement to have this drug on the market as quickly as possible. Got it. And then finally, how are you thinking about pursuing additional potential indications for Brepo beyond dermatomyositis and NIU? I'll say simply, we have a lot of ideas. And Ben and the Priovant team come up with new ones on a very regular basis. So I think stay tuned. And every time we read out positive data with this compound and look at it, it makes us feel like we should be doing more with it. So I think absolutely on the table. Great. Thank you very much. Thank you, David. Appreciate it. Thanks for listening. Thank you. Our next question comes from Yaron Werber with TD Cowen. Your line is open. Yes. Thanks for taking my question and congrats on the data. So I have one for NIU and then one on dermatomyositis. For NIU, are you contemplating also doing a study in non-active NIU as well, just to round out the label? And then secondly, for DM, it sounds like we should think that the data that program is getting a lot of attention from KOLs, which is good to see. It sounds like it's going to be a 52-week endpoint. So I'm thinking sort of data in second half next year. Am I thinking about this correctly? Thank you. Yeah. Thanks, Yaron. I'll hand it to Ben to answer both those questions. Yeah. So first on NIU, I think that in general, I would say that the kind of treatment paradigm and way physicians think about active versus inactive NIU has been evolving. And these are not two separate patient populations. An inactive patient is just an NIU patient where their disease is under control at that time. An inactive patient is an active patient whose disease is under control at a given point in time. So again, I think that we'll kind of have final details on what our phase III program looks like after we engage with FDA. But as a general matter, our perspective, and I think the KOL perspective, is that the active patient population is really what matters and mirrors how they're engaging in the real world. And important to note, the Humira label itself does not distinguish between active and inactive NIU. And then on dermatomyositis, I think your inferences are reasonable. It is indeed a 52-week primary endpoint. And yeah, we're looking at Q3 roughly for completion of enrollment. And so I think that can kind of do the math on the back of that. But your inferences seem correct to me. Can I maybe just throw up a couple of follow-ons? So on both DM and NIU, is this a market that you guys would want to commercialize yourself? And do you have a preference to commercializing sort of US and what to do ex-US? And then maybe just secondly, the remaining $8.50 or the buyback, is there any chance that you'll try to do, as you said I guess I'm trying to get a sense with SoftBank. I don't know how much you can share with us on some of the dialogue there. Thank you. Yeah. I'll take those in reverse order. Look, on the remaining $50, again, we're going to be opportunistic. We talk to our large shareholders regularly. The question of what SoftBank would or wouldn't do was mostly a better question for them than for us. They continue to be, as best we can tell, excited about the story but also have sought liquidity over time. So we'll see. But we certainly have the flexibility to have a conversation with them or to be in the market at any moment of dislocation. On the commercial question, look, I think the short answer to your question is, yeah, look, I think these are indications we would be excited to commercialize. They are indications of high morbidity. They're orphan diseases with relatively concentrated prescriber bases. One of the nice things about NIU is many of these patients are treated at specialty uveitis sort of focused centers. So we know who the docs are. The docs are incredibly excited about new therapies. There just isn't a lot in the pipeline or not a lot that's been delivered. So I think it's absolutely the kind of market where we could do it ourselves. The only caveat I'll give is the same caveat I give whenever I get any of these questions, which is that we are ruthlessly economic in thinking through these things. But it's a big opportunity. And I guess the one thing I'd say in a plug for it is you had called out or maybe David called out slide 11. I think, so if I say, our view is that NIU is a significantly underappreciated market in terms of the size and opportunity right now. It looks, on even a little bit of scratch-the-surface inspection, a lot like some of these other markets like HS or TED or myasthenia gravis where until new therapies entered and until patients and doctors really started thinking about what things could look like, people just undercounted the opportunity. I think we expect to prove out something similar in NIU. So it could absolutely be an opportunity where commercializing ourselves gives us a chance to see that play out. Thanks for the questions. Thank you. Our next question comes from Yatin Suneja with Guggenheim. Your line is open. Hey, guys. Thank you for taking my question. So two questions for me. First one is on Brepo indication expansion. Obviously, you have NIU and DM in the works. How should we think about indication expansion? And then does this open up broader ophthalmology opportunity? And are there indications in the ophthalmology space that you can pursue? So that's one. The second one is maybe just a little bit more about the capital deployment. How would you rate, let's say, buyback versus BD versus returning cash via dividend, just if you can opine on that, and then the type of BD, the size and scope that you are considering? Thank you. Yeah. Perfect. So I'll take these in reverse order again. On the capital allocation question, I think one of the things I like about the way we're set up here is even in the context of existing buyback authorization, we have a lot of flexibility over the coming weeks and months to make decisions on a daily basis. And I think there are prices and situations where it's 100% going to make sense for us to buy back stock. And there are BD opportunities where it's 100% going to make sense for us to allocate capital there. And we're fortunate to be in a position where it isn't really either/or. And to be honest, I wouldn't view us either as committed to using the full $1.5 billion if BD opportunities come up that make us want to do something else instead. Nor would I view us as limited by $1.5 billion in a world where we see dislocations that we can take advantage of that go beyond that size. It's just a conversation with our board. On indication expansion for brepocitinib, and I'll hand it to Ben to see if he's got things stayed well. But look, I think when you have data this good and frankly, this consistent with supporting the sort of parameters of the molecule itself, it makes you want to think bigger. It makes you want to think of other things. I think you could imagine we're looking at any severe high morbidity orphan disease where inflammation is the driver. For example, where Humira is used off-label or whatever, whether there's a lot to do in Ophtho versus other places, I don't have a sort of a. There's certainly a lot to do in other places. There may be additional opportunities in Ophtho now that we have a sense that we're going to have a presence there. But Ben, what else would you say? Yeah. I would echo all of that. I would just add that we'll definitely think about commercial synergies as we think about indication expansion. I think one thing to bear in mind for these orphan indications is, and that was alluding to this earlier in response to the last question. You have quite concentrated prescriber bases in tertiary centers of excellence. There's high overlap between the KOL community and the investigator community and the eventual prescriber base. And so I think that there's actually a sort of different kind of commercial synergy that one gets even across different specialties by kind of having this really exclusive focus on these different large orphan indications. So I think that's another factor that we're going to bear in mind as we think about synergies as well as specialty overlap. Thanks for all the great questions. Thank you. Our next question comes from Corinne Johnson with Goldman Sachs. Your line is open. Good morning, team. Congratulations on the good data here. This is Graig on for Corinne. So to start us off here, do you see any read-through based on efficacy or safety that this study in NIU may have on the phase III study in Dermatomyositis? Thanks, Graig. Thanks for listening. And thanks for a really good question. Look, I think two things. One is, at some level, I'm not a superstitious person. Some say you're not surprised by great data. But remember, we already had six phenomenal studies in Brepo and other indications. And so we knew it was a highly active compound. And we had good reasons to believe that this mechanism would work well in NIU. I think this data certainly reinforces just how sort of potent the compound can be or how big a gun it is. And so I think in that sense, it adds to our confidence. And then look, I think it's also nice to see, for example, the level of activity on the 15-milligram dose in this study that probably gives us some additional confidence there. Anything else, Ben? Do you have? No. I would just say that I think we have high confidence in the dermatomyositis study given the totality of data we have on Brepo. And I think NIU only adds to that. And I do think one feature that NIU and DM have in common is they are both selected by Priovant and Roivant on the basis of really carefully looking at the alignment of the pathobiology of the disease to the mechanism of Brepo and to the distinctive attributes of dual TYK2 JAK1 inhibition. And so I think seeing that kind of mechanistic alignment in NIU has played through to not only our seventh successful indication but an indication where we have some of the best data, I think, can kind of give us confidence that this mechanistic alignment with pathobiology can really flow through into the clinic. I think that in combination with the totality of other reasons to have confidence around Brepo and dermatomyositis make us only even more confident. Got it. That's helpful. Maybe just one more, but can you provide a little bit more color on how you're thinking about pricing the agent? It's premature until we see the data in all of the indications or at least some of the indications in phase III where we're going to carry it forward. But look, I think these are orphan indications with high morbidity. And this is great data. And so we think we're delivering a lot of value. I guess that's how I view it for now. But stay tuned as we get a little bit of a clearer picture of what we look like. Thank you. Thanks, Graig. Appreciate the questions. Thanks for listening. Thank you. Our next question comes from Andy Chen with Wolfe Research. Your line is open. Hey. Good morning. Congrats on the data. Two from me. So first of all, can you talk about why uveitis is not a competitive indication? I hear you on the 30,000 claims data receiving off-label biologics. But we've also seen pharma companies getting good data here, and they choose to not go into uveitis. Just can you talk about your confidence behind uveitis as an indication? And also a second question, just going forward, can you talk about the possibility of a combination therapy in uveitis? Are you going to allow Humira background patients? Because now we're in the post-Humira biosimilar world. There might biosimilars that might be just much cheaper in the future. Are you thinking about that as a potential segment of the patient population? Thank you. Yeah. Thanks. Both great questions. And thanks, Andy, for listening. And welcome to the call. Look, on competition, I guess what I'd say is I can't think of a lot of examples of pharma companies who have run successful NIU studies with good data and then have decided not to pursue it. There have been other studies in the past. Some of them have been underwhelming. There was a study in filgotinib which looked interesting. But as I'm sure you're aware, that drug wasn't pursued for other reasons unrelated to this. There was a study in IL-17 a while ago that was, again, interesting but not extraordinary. And we'll get some more IL-17 data, I think, later this year in a phase II. But again, based on what we've seen, I think so far, it's not obvious they're going to be able to deliver this kind of benefit. So when you say, "Why isn't it a competitive indication?" I think the answer is even Humira, which is really the only approved therapy of a recent generation, has treatment failure rates of 50% or higher depending on how you count them in many contexts. And I think it's just been a tough bar. It's been a disease that has resisted successful development of agents with anything like this efficacy profile. So I think we feel really good about sort of where we'll fall out there. And to be honest, three, four years ago, HS was also not that competitive an indication. And I think as people have come to appreciate the market dynamic there, it's gotten more competitive. I guess it seems possible to me something similar will happen here. But I think we're just early in the curve of what sort of potent drugs can do, seeing what really potent drugs can do in NIU. As far as Humira background therapy is concerned, I guess I'll hand to Ben to answer as well. But one thing I'll say is just given the high treatment failure rate that Humira and every other biologic has shown, I think it's less I don't know that I would have a problem necessarily with patients who were "on background Humira." But I think the real point is that it's not a good enough therapy. It still leaves a lot of room on the table. And remember, these patients are acute. They're at risk of developing risk of blindness. Patients are just going to want to be on the thing that works best. But Ben, anything you'd add there? No. I think, again, we'll kind of have the final study design to share after the end of phase II meeting with FDA. But it's a general matter, I think, that the phase or sorry, the final phase III study design after the meeting with FDA. But I think it's a general matter, the phase II study that's generated great data. And I think a basic principle of drug development is that you have great data in phase II to base the phase II on that. And so I think that kind of the first principle we'll be approaching going forward. Thanks. A great question. Thank you. Thank you. Thank you. Our next question comes from Louise Chen with Cantor. Your line is open. Louise Chen with Cantor. Your line is open. Hi. Thank you for taking my questions. Congratulations on all the progress today. First question I wanted to ask you is if you could give more color on this multibillion-dollar peak sales opportunity for Brepo, how do you get there? What gives you confidence that you can get there, especially if you're going to launch on your own? The other question I wanted to ask is when will we hear an update on that undisclosed asset that you've been working on? Last question is just when will you have an update on potential business development deals? Is it something we'd hear in the second half of the year or its first half of the year if possible? Thank you. Yeah. Thanks. So I'll start with the last of those questions, which is, look, I think we continue to feel every day blessed to be in the position that we're in in this market for opportunities. We have never seen a better opportunity set than the one we see right now. We don't have perfect control over when those opportunities materialize. So I can't say for sure whether it's next month or a few months from now or six months from now. But just suffice to say, we are sprinting in a lot of directions at once. On the update on the undisclosed asset, look, the short answer is it's unlike NIU. It's a particularly competitive area where there's another drug with a similar mechanism. And so our view is to get our phase II started before we provide full color. We are going to share that update in due course, probably a little later this year. It will come sort of around the same time as our phase II starts. Sorry, your first question was how we get to billion-dollar peak sales in NIU. Look, I think there's a few ways to cut that question. One is, and sorry, you said brepocitinib generally. It's easy to get to billion-dollar peak sales in brepocitinib generally. But even in the context of NIU, I think there's a few ways to cut that question. One is you just look at the patient population, the morbidity, and the level of efficacy of existing therapies. The truth is, I think it would be hard-pressed to name an indication that had a patient population and morbidity of this level that had a new therapy come in with data that was this much better than the standard of care and that didn't, frankly, find itself on a path to being a billion-dollar market. Humira is growing solidly double digits a year. NIU is doing at least $hundreds of millions today, having been on the market not that long and, again, growing at a pretty good clip. Humira is a different animal here. It's much less efficacious. It's priced for different indications, etc. So it's a pretty different story. I think on top of that, NIU—and this is an important point that we're going to do more work on and also just publish over time more work that we've done on it. NIU is an indication where the claims data definitely underestimates the rate of prescriptions for NIU for a drug like Humira because about half of these patients have significant comorbidities. It can be hard to tell, right? A patient gets an RA diagnosis. Then they get an NIU diagnosis. Then they go on Humira. A lot of the existing claims databases would look at that patient and assume that that was an RA script, when, in fact, we think it's pretty clear once you look more closely at these data, a lot of those scripts are NIU scripts. So I think even in the existing data on NIU, there's actually a suggestion that a blockbuster therapy is possible with a less efficacious therapy. Once you get beyond NIU, even Dermatomyositis, these are large orphan markets with high unmet needs that support orphan pricing. It just doesn't take that many patients to get to a really big opportunity. And with data like the data we're generating, we just feel highly confident. Yeah. And I would just echo that last point. I think in each of these alone, let alone across multiple of them, the percentage of if you think about overall prevalence of 70,000 or more patients with non-anterior NIU, 40,000 adults with dermatomyositis at orphan pricing, the absolute number of these needed to kind of get to blockbuster levels is not that high penetration rates. And with the data that we've generated in NIU and hope to generate in DM, we actually think we can get high penetration rates into these populations. And then in terms of the question of commercializing ourselves, which I know is part of your question as well, I'd kind of come back to some of what we were saying earlier. But I think that these orphan indications are really, in some ways, optimally suited for obviously, Roivant overall is a commercial stage company. Priovant is not. But for kind of even looking just at the Priovant level at a kind of first-time commercial launch, given that you're looking at a very concentrated prescriber base with high overlap with the KOLs and clinical trial sites. I think there's a lot of precedent in orphan disease for biotech companies making the transition to commercial and launching therapies very successfully there. Thanks. A great question, Louise. Thank you. Thank you. Our next question comes from Douglas Tsao with H.C. Wainwright. Your line is open. Hi. Good morning. Thanks for taking the questions. And congrats on the data. I guess two questions from me. First, in terms of NIU, I understand your point in terms of physicians not necessarily discriminating between active and non-active disease. I'm just curious if there could be a dynamic similar to what we've seen in the TED market where the FDA did not care but payers did sort of impose restrictions based on what the clinical trial data was in terms of what they were willing to reimburse. And then just a second question in terms of capital allocation. Obviously, you're going to still have a significant cash balance, which I understand you will use some to sort of fund ongoing R&D. But just curious if you can provide some thoughts about how you're thinking about deals. I know you're still excited. But do you have perspectives on size of deals that you're now looking at? Has that changed versus what you've done in the past? Thank you so much. Yeah. Thanks, Doug. Those are both great questions. I appreciate it. I'll take them in backwards order. On capital allocation, I think the short answer is no change from our previous discussion on this topic. We are in a rich, rich, rich opportunity set. The rub with Roivant has always been that we're stingy with upfront dollars and everything that comes with that. So we're not always a great M&A buyer, although never say never. And what we prefer to do with partners, often with larger pharma companies who are less focused on upfront cash and more focused on risk-sharing and an opportunity to do great if we do great, I think you're going to continue to see us looking at those kinds of opportunities first and foremost. But again, in the grand scheme of things, I think everything's on the table. In terms of opportunity size, certainly nothing about today's announcement changes our appetite at all. I think we're still looking for programs where, frankly, where our capital is a competitive advantage among others and where we can go out and, in some cases, run large phase III programs that many competitors wouldn't be able to readily fund because we have more than enough capital to do so. On the active versus passive question on the payer point, look, I think the short answer to that question is, first of all, we are going to have long-dated follow-up that'll give us a clear sense of continued efficacy in these patients sort of well beyond the acute or early presentation of the disease. I think it's important to understand the biggest patient need here is at that moment of active disease where they're at risk of significant progression, at risk of blindness, etc. I think we want to make sure we're focused specifically on that opportunity first and foremost. I think if we can deliver data, anything like the data we've shown today in that population, I am not concerned about the commercial dynamics. Great. Thank you so much. Thank you. Thanks for the great questions. Thank you. Our next question comes from Neena Bitritto-Garg with Deutsche Bank. Your line is open. Hey, guys. Thanks for taking my questions. I apologize. These have already been asked. I missed the first bit of the call. I guess the first question is just how do the results today impact your desire to do additional deals in the ophthalmology space? I know that's not a space that you've prioritized previously. I guess any thoughts on that would be helpful. Then second, any thoughts that you can provide on what a placebo response or treatment failure rate may have looked like given this study design? I know we have the placebo group from the VISUAL I study. Just given the faster steroid taper, I guess any thoughts on what the placebo treatment failure rate may have looked like in a study like this? Thanks. Yeah. Thanks, Neena. Great questions. On the first one, we've never been sort of indication first. We've always been opportunity first in the way that we look at opportunities. So I don't know that there's a big change in how we think about therapeutic focus based on this data. I think the short answer is if and when we're launching Brepo in NIU and we're out talking to these ophtho centers, if there are additional ways to make use of that commercial spend, we'll certainly think about it. And as Ben mentioned, there are synergies that go beyond ophtho. Sorry. On the question of placebo response rate, I think we hit on this. And if you look at slide 16 in the deck, I think in the VISUAL I study, on an apples-to-apples basis to how we looked at our data, they had an 82% treatment failure rate in the placebo arm. That's with a lower bar that is with longer steroid therapy. So I think our expectation is that the placebo response rate would have been worse than that or, again, a higher treatment failure rate. And to be honest, I think we were a little bit worried about a situation in which our data looked facially comparable to something like the Humira, but we thought that indicated a better drug because of a more aggressive steroid taper. I think the fact that the data was so clear makes this an easier discussion. Ben, anything you'd add to that? No. I mean, I would say, yeah, kind of in VISUAL I and looking at the few other studies that have had kind of similar design to this, we really see that 70%-80% placebo rate quite consistently. And with our much more aggressive steroid taper, as Matt said, we would expect something that would be even higher than that. Again, in this case, higher being worse. That said, I think one of the nice things about this data is even if we're wrong about that and what the placebo rate would have been is more like 70%-80%, it's still, as you see on slide 16, fantastic data against that bar. Thanks for the great questions. Thank you. Our next question comes from Robyn Karnauskas with Truist Securities. Your line is open. Hi, guys. Congrats on the data. I just had a few drilled down into the market. So just trying to figure out what the real opportunity is. So a couple of questions. Number one, what percentage of patients do you think are actually well-controlled and stable on Humira? And the second question would be if there's comorbidities and someone has RA, and obviously, if Humira might address both a little bit, maybe UV not as much. Going back to the combo question that was asked earlier, how do you see the drug being used? Do you think a safety study is needed for docs to be comfortable combining the two given their immunosuppressants? And then I have a follow-up. Yeah. Sure. On the first question, look, I think the easiest answer to that question is at the 6-month time point where these studies were at, the week 25 time point where the study ran out, Humira, on our stats analysis, had a 62% treatment failure rate. And that includes either people that have discontinued or people that had effectively worsening of disease in various axes as we talked about earlier. I think at a bare minimum, you'd think of, of the limited group of patients on Humira, 62% of them are not well-controlled by virtue of either treatment failure or discontinuation. And my suspicion is the number's actually greater than that, that because those treatment failure rates are what they are, first of all, there's a lot of patients who aren't going on Humira because it's efficacious but not that efficacious, as it were. Also, there's a lot of patients who just never make it quite to that corner of the treatment paradigm for various reasons. We think there's a big opportunity. That's on how well-controlled these patients are. Anything you'd add to that? No. I think that's right, is that they're not that well-controlled is the punchline. And the patients on off-label therapies, there's no evidence that these therapies necessarily work beyond anecdotal evidence. And so we'd see the failure rates there and then being even higher. On the comorbidities point, I think the answer is yeah, Ben, you can take this. Go ahead. Yeah. I was just going to say I think that there's generally a recognition for these patients where the etiology is in the context of other diseases, that treatment of the eye needs to lead. I think that's something that physicians across specialties would agree with when you're talking about risk of blindness. And again, even when it's short of blindness, very severe visual problems, I think that this is something that obviously ophthalmologists, but I think also rheumatologists and others would have a very acute awareness of. Rheumatologists, obviously, have a lot of experience thinking about systemic autoimmune diseases across multiple organ systems and thinking about which organ systems need to lead. The ophthalmologists, of course, are going to be particularly focused on the eyes. And so we really think that that's kind of for these patients what leads the treatment paradigm. And then the treatment of the other, perhaps less severe symptoms in other organ systems follows. And look, in this phase II study, the patient, we have to treat where they are. We don't have the phase III conversation with FDA yet. So I can't say exactly what we're going to do in phase III. But in the phase II study, patients were allowed to be on stable ISTs, for example, because that's just who the patient population is. And so I think we'll see probably something similar in our phase III study with more to come. That's helpful. And then last question is you talked about 30,000 on biologics with 5,000-10,000 that are not on therapy. And seeing these trials, so many people have been diagnosed with uveitis but not treated for many, many, many months, which I assume would open up the opportunity if there was a real potent drug out there that works. So why are patients not on therapy? And do you have a sense? I know it's probably early with your market research. Would a doctor prescribe this sooner? What do they need to see in phase III or duration of safety to get more comfortable with treating people on the spot? That's it. Thanks. Yeah. Look, I think there's sort of two separate questions here. One is taking the sort of acute, active patients who need immediate therapy. Look, I think if you show up to the doctor's office and you're having a flare-up or maybe it's your first presentation of NIU, what are you going to want against the backdrop of a disease that could cause blindness? You're going to want the biggest gun now. And so I think one thing is the water is a little bit muddy in the current world about what that is, frankly. Humira is a great drug, but docs like doing steroid injections and other things depending on where the disease presentation is and so on. I think this data is at least this data is clarifying, right? This is very good data. I think if you're an acute patient, certainly, you're going to want a therapy of this kind. I think as you talk about sort of moving into the sort of broader treatment paradigm, I guess there's a few things. One is, look, not to miss the point, it's a once-daily oral therapy. It's a med like any other. If your patient has never been on an injectable therapy and you're not sure what that's like, this is just like any other pill that you take. I think there's a change in sort of treatable paradigm just based on mode of administration. I think the other thing that'll matter is seeing the kind of efficacy benefit out to 24 weeks, 52 weeks in a bigger study. For example, Ben referenced the sort of macular swelling data. I think if something like that persists out 12 months and you're seeing patients on other therapies developing recurrence, developing swelling, developing things that could lead to blindness over time, I think docs are going to want people well-controlled on Brepo for a long time if that's what we see in that data. Yeah. I think broadly speaking, kind of what you see in NIU is that steroids work reasonably well. They don't always work, but they work reasonably well. The biologics don't work very well. So you have docs kind of constantly trying to get patients off steroids onto biologics, but the biologics not always doing what they need to do. And so that's why you kind of see a lot of that cycling. A lot of those patients are maintained to some degree on steroids, including frequent bursts or even just medium to high doses administered chronically. I think that, of course, has its own side effects. For systemic steroids, those are obviously well-known. Also important to note that steroid injections, which are used for NIU particularly as a treatment for macular edema, carry arguably even worse side effects than systemic steroids, including very high risk of glaucoma. So yeah, I think to kind of echo Matt's point, I think the biggest problem in NIU is that there's just not drugs that work well enough. Our hope is that Prevacid and NIU can be that. Okay. Thanks, Robyn. Thank you. Those are great questions. Thank you. We're going to continue to do work to try and focus people on the size of the opportunity here because, again, it's just not one of these indications where a lot of that work has been done to date. Stay tuned for more of our claims analysis and so on. Thank you. If there are no further questions, I'd like to turn the call back over to Matt Gline for closing remarks. Yeah. Thanks. Thank you, everybody, for listening again on such short notice. We have great covering analysts. We appreciate it. I want to thank, obviously, Ben and the entire Priovant team who worked really hard on the study. I want to thank Pfizer as our partners. And then I want to thank all of the investigators and, frankly, most of all the patients in the program who have entrusted us with their care. It's an exciting day to be able to put out data of this quality. It's exciting to be able to say at the same time that we've cleaned up at least sort of some of the overhang from our existing shareholders and that we have the firepower to continue to work on that problem. And I just couldn't be more excited for many other opportunities to get on the phone together in the coming months. Thank you all, and have a great, great day. Thank you for your participation. This does conclude the program, and you may now disconnect. Good day.