Good morning, ladies and gentlemen. Thank you for standing by. Welcome to the Roivant Sciences Investors Call. At this time, all participants are on the listen only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star on your telephone. You will then hear an automatic message advising your hand is raised. Please be advised that today's conference may be recorded. I'll now hand the conference over to your speaker host, Stephanie Lee. Please go ahead. Good morning, thank you for joining today's call to review the chronic period data for RVT-3101 in the TUSCANY-2 phase II-B study in ulcerative colitis. I'm Stephanie Lee with Roivant Sciences. Presenting today, we have Matt Gline, CEO of Roivant, and Mayukh Sukhatme, President and Chief Investment Officer of Roivant. For those dialing in via conference call, you can find the slides we've presented today, as well as the press release announcing these updates on our IR website at www.investor.roivant.com. We'll also be providing the current slide numbers to keep in mind to help you follow. 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 file with the SEC for more information regarding these forward-looking statements and business risks and uncertainties. We will begin with Matt Gline, who will give us the remarks. With that, I'll turn it over to Matt. Thank you, Steph, and good morning, everybody, and thank you for joining. We are very pleased to host this call and obviously, as you'll hear in a moment, very excited about the data we're gonna share today. We are privileged that this is the, I think, third call this year in which we've shared new positive data, and in some ways, our fourth major study results, all of which have been great. It's a real privilege. I'm not gonna spend a lot of time on preambles, but on Slide three, just as a reminder, we're talking today about the chronic period data for RVT-3101, our TL1A antibody in ulcerative colitis. That situates within what we think is a tremendously exciting late-stage portfolio in inflammation immunology, including our commercial product currently on the market in psoriasis, VTAMA, for which we put out great data in atopic dermatitis earlier this spring. RVT-3101, the drug we're talking about today, brepocitinib, our dual inhibitor of TYK2 and JAK1, and then our franchise in anti-FcRn antibodies, where we expect some important data coming at the end of this summer. Look, we think this is a really exciting overall pipeline, and we think it has the potential to be frankly, one of the largest commercial portfolios in I&I as we go from here. You know, we're very proud of what we've built. Today is an important new brick in that wall. To talk us through that, I'm gonna hand it over to Mayukh, who's gonna remind everybody about the mechanism and then go into the data. Thanks so much, Matt. Good morning, everyone. I'm very excited to take the time to review our results for the chronic portion of the RVT-3101 TUSCANY-2 phase II-B study. Please turn to Slide four. I want to start by taking a moment to review the novel biology of TL1A. There are really two key aspects of this mechanism that underpin our excitement for RVT-3101. The first key aspect is that RVT-3101 mechanistically hits two distinct axes, an anti-inflammatory axis and an anti-fibrotic axis. We believe this is unique as a mechanism and allows for applicability across a spectacularly broad range of indications. As you can see on the left, TL1A is linked to a range of inflammatory and fibrotic diseases affecting multiple organ systems. We now have in hand, across the field, clinical validation in both ulcerative colitis and Crohn's, with SSc-ILD currently being explored and additional indications on the way. The second key aspect is the way in which RVT-3101 actually interacts with the immune system. TL1A is a cytokine that is crucial for amplifying multiple arms of the immune system and the fibrotic cascade. By inhibiting TL1A activity, RVT-3101 corrects pathogenic overamplification in multiple arms of the immune system that we know are individually involved in inflammatory bowel disease. Pfizer had already generated strong proof of biology data from their earlier phase II clinical studies, where they looked at changes in patient samples before and after treatment with RVT-3101. That elegantly showed that RVT-3101 treatment functions as an effective inhibitor of the Th17, Th1, and Th2 arms of the immune system in diseased tissue, functionally combining the mechanisms of multiple therapeutics into just a single molecule. I also want to state again an important point. TL1A blockade via RVT-3101 does not reduce or knock down arms of the immune system. It simply inhibits local overamplification at the site of diseased tissue, and therefore, would not be expected to carry the safety risks associated with immune suppression. What does all of that mean for our program? Going into this week 56 data readout, the hope was that we would maintain our very strong efficacy from the induction period, and that even a few percentage points of improvement in efficacy would be the grand slam case, to borrow Matt's favorite baseball metaphor. Please turn to Slide five. Here are the highlights of the chronic period of the TUSCANY-2 phase II-B study. Candidly, we were completely blown away by the efficacy data we have here. Patients who were assigned the expected phase III dose throughout the entire study, saw meaningful improvements in efficacy from week 14 to week 56, in both clinical remission and endoscopic improvement endpoints. This is also what was already very strong data after just 14 weeks on drug. To call it what it is, this is better than even the grand slam case. We saw really exciting top line efficacy rates at the expected phase III dose, growing from 29% at week 14 to 36% at week 56 on clinical remission, and growing from 36% at week 14 to 50% at week 56 on endoscopic improvement. These data get even more impressive when we look at the biomarker positive population. Clinical remission rates at the expected phase III dose grew from 33% at week 14 to 43% at week 56, and endoscopic improvement rates grew from 47% at week 14 to 64% at week 56. This was all achieved with a remarkably clean safety profile across all doses tested, and importantly, there was no impact of immunogenicity on clinical efficacy or safety. Together, this combination of unprecedented clinical efficacy results and clean safety profile sets RVT-3101 apart from anything in the space. This data, in sum, show that RVT-3101 has truly transformative potential for patients with ulcerative colitis. Please turn to Slide six. Here again is a brief recap of the clinical studies completed to date for the program. The first clinical study for RVT-3101 was the so-called TUSCANY study, which was published in 2021. That was a 14-week single-arm induction study, dosed at 500 milligrams IV every other week. An exploratory biomarker of interest was identified coming out of this study, which showed enhanced efficacy in biomarker positive patients. The second study, for which we reported the week 14 induction data back in January and are reporting the chronic period results today, is the so-called TUSCANY-2 study. This is a 56-week study, which included an induction period and a chronic period. It was placebo-controlled for the induction period, and all arms were dosed subcutaneously once per month. As is the norm these days, this enrolled both biologics-experienced and naive patients. This study built upon the learnings from the earlier TUSCANY study and employed a single prospectively defined biomarker, the same one that was employed in TUSCANY, to see if efficacy would be enhanced in the biomarker positive population. This was a large global study with 245 patients. In fact, this is among the largest phase II-B studies ever conducted in ulcerative colitis. Please turn to Slide seven. As I think many people in the investment community appreciate, this is a large study meant to answer many questions at once, and we thank Pfizer for running it this way, as it provides us with the richest data set in the field by far and allows us to run a streamlined design in phase III. Here's the schematic for the TUSCANY II phase II-B study. After screening, patients were randomized to one of nine arms, labeled A to I, in the schematic shown here. Patients were assigned to their dose level for both the induction period and the chronic period at day one, and both patients and physicians remained blinded to assignment throughout the study. There was no ability for physicians to electively go up or down on the dose. Whatever arm was assigned was fixed. In January, we presented data as specified in the Pfizer statistical analysis plan. That is to say, the data reflected a pooling of arms that had the same dose during the induction. In fact, that's how we ourselves received the data at the time. Today, in accordance with the Pfizer statistical analysis plan, we will be presenting data both overall and for the most relevant individual dose arms. This is a simple subQ regimen dosed once monthly. There was no loading dose and no IV dose used at any point. As we all know from many historical commercial precedents, the simplicity of a fully subcutaneous regimen without the need for an IV infusion or for induction or loading, will be preferred by physicians and patients. Endoscopy, which makes up one of the components of the clinical remission assessment, was performed at baseline, then at week 14, as noted in the arrows at the bottom of the schematic, which was two weeks after the last dose in the induction period, and at week 56, which was four weeks after the last dose in the chronic period. Importantly, this was a treat-through design, meaning there was no selection criteria, such as clinical response, excluding patients from continuing into and being counted in the chronic period. Most other studies use a so-called re-randomization design, which introduces a selection bias that artificially inflates efficacy rates in the maintenance period in those studies. These data are without precedent in their strength and paint a clear and consistent picture. We look forward to presenting these data in full at a future medical meeting. As we have discussed with the investment community, we believe the detailed results of this study and the insights it provides us are extremely valuable and a major competitive advantage over Prometheus and the rest of the field. For now, for those competitive reasons alone, we will not be disclosing our phase III dose for further subtests. We've communicated this strategy to the investment community ahead of time. Acknowledge this might be a bit frustrating for some, but hope that everyone understands. Again, we look forward to presenting this data from the study in full at a future medical meeting. For today's presentation, we will first be presenting data for the constant expected phase III dose, which is one of either arms D, E, or G. If you turn to Slide eight, and then we'll present data for the overall study, arms A through I. For clarity and for reference, on all slides reporting data, we will highlight which arms or groups of arms we are talking about in a banner at the top of the slide. Please turn to Slide nine. Now let's look at the data from the chronic period of TUSCANY-2. Please turn to Slide 10. First, here's the subject disposition for the chronic period. The major study goal of the chronic period was to understand the degree to which week 14 response rates are maintained and potentially improved with additional duration of dosaging RVT-3101. As was pre-specified in the Pfizer statistical analysis plan, we will be reporting data on the so-called modified intention to treat, or MITT population, which is defined as the full population who received at least one dose of RVT-3101 in the chronic period. We did also look at the data for the ITT population, which were generally in line or varied only slightly from that of the MITT population. As a final note, we were particularly pleased by the roughly 80% completion rate, which compares very favorably to other trials and is consistent with the high degree of patient enthusiasm we have heard from study investigators. Please turn to Slide 11. Here are the baseline characteristics for both the overall population in the chronic period, and then the arm that was assigned the expected phase III dose throughout the study. As you can see, this is an extremely sick population overall on the left, and that the arm assigned the expected phase III dose is perhaps a bit sicker still than the overall population. I'll draw your attention to the differences in, for example, the phase III dose having a higher modified Mayo Score at study entry, 6.9 for that arm versus 6.7 overall. A higher proportion of patients with a baseline endoscopy score of three, which is the highest possible endoscopy score since the scale is zero to three. That's 66% for the constant expected phase III dose versus 54% overall, and a higher proportion of patients exposed to two or more prior advanced therapies. 31% for the constant expected phase III dose versus 25% overall. As many of you are aware, the sicker the population, the harder it is to get a response. Please turn to Slide 12. Again, to help make clear which population we are talking about in any given data slide, you can see the banner at the top right of the slide. Here, it's the constant expected phase III dose arm, all comers, regardless of biomarker status, and all comers, regardless of prior experience with biologics, meaning both biologic naive and biologic-experienced patients. Note that the change values listed throughout may not exactly match the difference between week 14 and week 56 values because of rounding. Now to the figures. For patients assigned the expected phase III dose throughout the study, an additional 40 weeks of data led to meaningful improvement in efficacy off of what were already quite impressive data at 14 weeks. In the left panel, the proportion of patients achieving clinical remission grew from 29% at week 14 to 36% at week 56, an increase of 7%. In the middle panel, the proportion of patients achieving endoscopic improvement grew from 36% at week 14 to 50% at week 56, an increase of 14%. In the right panel, we were very excited to see that the proportion of patients achieving endoscopic remission grew from 11% at week 14 to 21% at week 56, an increase of an 11%. For those who may not be aware, endoscopic remission is an extraordinarily stringent measure of efficacy, requiring an endoscopy score of zero, which means normal mucosa. Most programs in ulcerative colitis don't even disclose endoscopic remission rates because they are so low. Please turn to Slide 13. Again, just to orient people, using the banner at the top right, this is the same arm as the last one, the constant expected phase III dose arm, now just the biomarker positive subset. You can see that the degree of improvement was even greater for biomarker positive patients who were assigned the expected phase III dose throughout the study. On the left, the clinical remission rate grew from 33% at week 14 to 43% at week 56, an increase of 10%. In the middle, the endoscopic improvement rate grew from 47% at week 14 to 64% at week 56, an increase of 18%. Finally, on the right, the endoscopic remission rate grew from 13% at week 14 to an unprecedented 36% at week 56, an increase of 22% and just an outstanding absolute number. We are unaware of any other therapy that has been able to show an endoscopic remission rate any higher than the mid-20s, regardless of trial design. To produce 36% is really extraordinary. Please turn to Slide 14. It's also important for physicians and patients to know that once a patient gets a response, it is likely to be maintained. This is the concept of sustained efficacy. If you achieve success in a given parameter at week 14, what percentage of those patients remain a responder on that parameter at week 56? For patients assigned the expected phase III dose throughout the study, 75% of the patients who experienced clinical remission at week 14 maintained their response at week 56, and 80% of patients who experienced endoscopic improvement at week 14 maintained their response at week 56. What is that really telling us? It's telling us that for patients who saw a response with RVT-3101 at 14 weeks, the vast majority saw that response maintained through the end of the study. As we saw in the data we just reviewed, additional responders get added with long duration of dose.... Anybody familiar with the IBD space is well aware of the unfortunate reality that low remission rates and poor persistence on sex leads to a trial-and-error paradigm, where patients continue to cycle through drugs that either don't work or may provide relief at first, ultimately fail to address a patient's disease. This efficacy package, in total, suggests that RVT-3101 can really change that treatment paradigm for patients suffering with ulcerative colitis. Please turn to S lide 15. Although we focused on the constant expected phase III dose, that is, as it is the most important arm, we want to briefly zoom out to share data from all patients in the chronic period, regardless of dose and regardless of line of therapy. The data overall paint a remarkably consistent picture as to the efficacy of this molecule. The robustness of this data set will be abundantly clear when full data get presented at a future medical meeting. We felt it was important to give you a sense of that here today. On the left, you'll see that the rate of clinical remission was not only maintained but slightly improved from 31%- 34%. On the right, you see that the rate of endoscopic improvement was not only maintained but slightly improved from 38%- 41%. Please turn to Slide 16. For our last key efficacy slide, we want to talk about the performance of RVT-3101 in the biomarker positive biologic experienced population. This is an area of extremely high unmet need that we have heard so much about from both KOLs and investors alike. Efficacy of other agents really drops dramatically in this biologics-experienced population, and it is so exciting that in our biomarker-positive cohort, which covers around 60% of the overall population, we continue to see transformative outcomes and improving efficacy in this extremely difficult-to-treat population. Looking across data from all patients, we saw that on the left, clinical remission rate at week 56 was 34%, an improvement of 5% from week 14. On the right, the endoscopic improvement rate at week 56 was 45%, an improvement of 3% from week 14. These are really striking data that, again, thoroughly outperform anything reported in the field. Please turn to Slide 17. Let's turn to safety. The key takeaway here is that the favorable safety profile previously reported for the induction period is maintained through the chronic period. Shown on the left are rates of adverse events and most common treatment-emergent adverse events seen in the induction period, and on the right are the AEs that occurred during the chronic period. Note that these are non-overlapping periods of time, but the chronic period, of course, is a much longer interval than the induction period. During the induction period, the rates of AEs are effectively the same for the expected phase III dose as compared to all patients on drug, and both are in line with placebo. In fact, AEs were generally lower in the drug arm than they were on the placebo arm. When we look at the table on the right, which is the data for the chronic period, we see rates for the expected phase III dose that are in line with the overall population. Recall, there was no placebo arm during the chronic period. In the chronic period, we saw that RVT-3101 was well tolerated through week 56 at all doses, and in fact, no dose response was observed for drug-related treatment or emergence of adverse events, severe AEs, or serious AEs. Serious AEs were sporadic and determined not to be related to drug. Rates of infection were very low, with no severe infections observed. There was no dose response observed for injection site reactions, with all cases considered mild except for one, which was not at our expected phase III dose. Overall, we're extremely pleased with the clean safety profile we're seeing with RVT-3101. Please turn to Slide 18. There's been a question in the minds of some investors around immunogenicity for the drug and whether there would be an effect on clinical efficacy. We said back in January that we saw no impact on the efficacy data during the induction period, and that on a week 40 update, the neutralizing antibody trend was flat to down. I'm excited to report a very attractive picture now out to 56 weeks. Turning first to ADAs. The leftmost bar shows the clinical remission rate for those patients who are negative for ADAs, and on the right are the clinical remission rates for those who tested positive for ADAs, bucketed into quartiles based on increasing magnitude of maximum titer from left to right. If after 56 weeks of dosing, ADAs were having a negative impact on clinical efficacy, we would expect to see the slope of this curve pointing down as you go from left to right. That is to say, with increasing levels of ADA titers, there would be a decrease in the clinical remission rate. This graph clearly shows that this is not what we are seeing with RVT-3101. Neither the presence nor the amount of ADAs had a negative impact on the long-term clinical efficacy of RVT-3101. Given the lack of a trend line, this seems to be just uncorrelated noise. There is no observable relationship between ADAs and efficacy. On neutralizing antibodies, the rate that we said was flat to down at week 40 went all the way down to zero, in fact, in patients assigned the constant expected phase III dose. Put simply, this data clearly puts the immunogenicity questions to bed once and for all. Between this picture and the safety picture, this is a drug that can be used chronically for the long term. The drug just keeps working better and better over time. This isn't just the best-in-class efficacy and safety profile, it's the best in IBD profile with a mechanism that is extensible into other indications. Please turn to Slide 19. I want to conclude our data slides with a few cross study comparisons to help contextualize this data set. First, an obvious question we want to answer for ourselves was: How does RVT-3101 stand up in terms of the broader landscape of therapies for ulcerative colitis? One challenge when comparing our data to that of other programs is that most studies have utilized a re-randomization study design, where only responders were taken into the maintenance period. This results in a selection bias that overstates the benefit of additional duration of dosing for patients overall. As we've discussed, TUSCANY-2 utilized a treat-through design, where patients continued into the chronic period regardless of their responder status at week 14. Comparison to other studies with a similar design allows the most apples-to-apples assessment of how different molecules behave. Shown here are data from every relevant treat-through study, the recent phase III VARSITY study comparing HUMIRA and Entyvio, as well as a recent 52-week S1P study. Note that the VARSITY study used an alternate definition for clinical remission, unfortunately cannot be directly compared on that metric. Certainly, our data looks stronger than every comparable study. That's all the more impressive when you further account for the fact that these other studies had a less sick and less pretreated population, with a higher proportion of biologics-naive patients. For example, in the VARSITY study, if they were exposed, had only been treated with a TNF inhibitor. TUSCANY-2 studied a more refractory population. In sum, we believe that the efficacy shown for RVT-3101 at the expected phase III dose compares quite favorably, regardless of biomarker status, with a further enhancement in biomarker positive patients. Please turn to Slide 20. We also wanted to focus on a concept that has been generating a great deal of interest in the KOL community, combination therapy in ulcerative colitis. Recent strong data from the VEGA phase II study, which was conducted only in biologics-naive patients, is shown here in pink. VEGA combined an intensive regimen of an IL-23 dosed intravenously in combination with an anti-TNF during induction and continued patients on the anti-IL-23 subcutaneously in maintenance. It was suggested that combination therapy could be the only way to break through the low efficacy rates in the current landscape of approved therapies. We were excited to see that RVT-3101 not only surpasses the bar set by VEGA, but does so as a monotherapy. In blue is the data for the expected phase III dose in biologics-naive patients, as that was the population studied in VEGA. Note, like TUSCANY-2, VEGA utilized a treat-through design. The results here fit with what the biology of TL1A blockade predicted. We saw a 50% clinical remission rate and a 69% endoscopic improvement rate in frontline patients, regardless of biomarker status. RVT-3101 is functionally combining the mechanisms of multiple therapeutics in a single molecule. By preventing aberrant overamplification rather than reducing or knocking down different arms of the immune system, RVT-3101 is able to have this effect without inducing immunosuppression and its associated risks. I want to make sure that this data doesn't get lost in the nuance of discussion around combination. These are really strong data. With such profound efficacy, we believe RVT-3101 has the potential to become the frontline therapy of choice for every new, newly diagnosed ulcerative colitis patient. Please turn to Slide 21. I hope I've been able to convey at least a small part of our enthusiasm for this mechanism and for this molecule, one we believe has the potential to be best in class across IBD, as well as a broad range of additional indications. It is also clear that we are well positioned to be first in class and well positioned to go to market with the most attractive commercial presentation. Over 400 patients have been dosed with RVT-3101 across all studies completed to date. In addition, we have about 250 patients worth of induction data, over 200 patients of maintenance data out to one year, all with a subcutaneous formulation. Over 250 patients of dose-ranging data across both an IV and three subcutaneous doses. Over 200 patients worth of data showing enhanced efficacy for a prospectively defined biomarker, covering around 60% of the overall population, the same biomarker that is locked and will be used in phase III. We will be ready to go to market with a simple auto-injector dosed once per month with no IV loading dose, no off-body subcutaneous infusion, or any of that complication. What does all of this mean? It means that we are uniquely ready for a streamlined, simple phase III program. We don't have to guess at a dose or bring more than one dose into phase III. We don't have to guess at how a subQ may behave in phase III based on limited IV and bridging data. We don't have to go into phase III with a different biomarker than was characterized in phase II. Please turn to Slide 22. Finally, it's worth bringing this data package back to the implications for this mechanism. We commented back in January that the really strong induction data encouraged some blue sky thinking for our program. A remarkable amount has changed in just the last six months. Prometheus reported really strong induction data in both UC and Crohn's disease. We reported our really strong induction data. Prometheus Biosciences was acquired for close to $11 billion. It's clear that Merck and others have recognized that TL1A blockade could be the next potential super class of therapeutics. First, we start with inflammatory bowel disease, which is already a $15 billion category in the U.S. alone, growing. This is, as everyone appreciates, a large commercial market in spite of efficacy that's modest and durability that's modest for existing options. The phase II data set indicates that we can achieve high-end efficacy combined with a very favorable safety profile. We have a drug that can be used to treat all patients, I mean everyone, regardless of line of therapy, regardless of biomarker status, regardless of disease severity. This data set makes us want to go after every segment of this market. This data set shows that patients will be able to stay on drug chronically, with efficacy that increases over time and a continued benign safety profile. Finally, at long last, we have the promise of bringing precision immunology to the field to further enhance efficacy. That is something that physicians and patients want, and it's something that we think will be useful with payers as well. All of this is really just the beginning of what's possible. Again, it all comes down to the unique mechanism of action of TL1A blockade. Its ability to simultaneously act across multiple arms of the immune system, correcting dysregulation at the site of diseased tissues. This sets up a very different way to think about treating inflammatory disease generally, where you can have a single molecule potentially recapitulate or even improve upon standard of care therapeutics that can each can target only a single or a small number of related pathways. TL1A blockade can do this with a remarkably clean safety profile. We've shown the potential in IBD. The real power of this approach extends more broadly to any indication where TL1A has been shown to play a role in amplifying cascades and driving disease. To get a sense of the blue sky potential, on the top right, here are just some examples of extraordinarily large inflammation-driven indications, where TL1A has already been shown to play a role, and where, in many cases, there remains a great unmet need for drugs with better efficacy and a benign safety profile, just like in IBD. These five indications alone currently constitute more than $50 billion in annual sales in the U.S. alone. Then on the bottom right, we have the other access to which TL1A blockade can exert therapeutic benefit, its ability to modulate fibrotic cascades. This not only contributes to efficacy in inflammatory diseases like IBD, which have a fibrotic component, but also opens up indications for which there is a real lack of effective therapies and a tragically profound unmet need, diseases that have features of intestinal fibrosis, pulmonary fibrosis, or liver fibrosis. Please turn to Slide 23. With that, I'd like to summarize a few key takeaways. First, RVT-3101 has generated the largest and most comprehensive data set by far in ulcerative colitis. Unlike others in this space, RVT-3101 is de-risked and ready for phase III study. A single dose has been selected, there is no IV to subQ translation risk, and we are locked with our biomarkers. Second, RVT-3101 has demonstrated outstanding efficacy, regardless of line of therapy, with efficacy that improves over time. The vast majority of responders maintained their week 14 induction response through week 56, the end of the study. Third, our biomarker has the ability to select for the roughly 60% of patients that could see significantly enhanced efficacy from RVT-3101. This is exciting for patients and for physicians who are desperate to break out of the trial-and-error paradigm that currently defines treatment in IBD, which we talked about earlier. Finally, there are multiple avenues for additional growth. In Crohn's disease, we recently started a phase II dose ranging study, designed to rapidly give us dose and biomarker information for a streamlined phase III. We ultimately expect time to market to be in line with competition, and we plan to fully prosecute the biology of TL1A at Innovation in additional indications to be announced in the future, that can show the true breadth and versatility of this new super class of therapeutics. Finally, some important thank yous. First, we'd like to thank the investigators, the site personnel, the Pfizer study team, and importantly, the patients who participated in this trial. Without all your efforts, these results would not have been possible. Once again, I'd like to thank everyone at Pfizer more broadly for discovering and developing this molecule and their trust and collaboration with us on this program. It's the latest in our long-standing partnership, covering multiple different programs over many years.... Both Pfizer and we feel strongly that this is a great compound and an exciting mechanism, and we are truly privileged to run with it and help bring it to patients in the years ahead. We are excited to have the opportunity to fundamentally transform millions of patient journeys with this program. We are confident RVT-3101 will have tremendous impact on patient care. With that, I'll turn it back over to Matt. Thanks, Mayukh. Appreciate it, and thank you everybody for listening to that. We're obviously very excited about this data. I'm looking forward in just a moment to taking some Q&A. I'll wrap up very quickly on Slide 24, just by reminding everyone that 2023 is just a crazy year for us at Roivant. This is the, as I said at the beginning of the call, really the fourth major data set we've put out this year with the TL1A induction data, two AD studies, and the two atopic dermatitis studies both coming before it. We have a number of other major data catalysts, including multiple studies in IMVT-1402 and batoclimab, our FcRn franchise, as well as our lupus study in brepocitinib. A big second half to the year ahead, a really exciting and we think successful first half of the year. Most importantly for today, a drug in RVT-3101 that we feel very, very good about taking forward, and that we are excited to deliver to patients. Well, thank you, everybody. I'll echo what Mayukh said in his note of thanks. Appreciate your joining this morning, and with that, I'm gonna hand it back over to the operator to begin Q&A. Thank you. Ladies and gentlemen, to ask a question, you will need to press star one one on your telephone and wait for your name to be announced. To withdraw your question, press star one one again. Please stand by for our first question. Our first question coming from the line of Brian Cheng with JP Morgan. Your line is open. Hey, guys. Congrats on the data, thanks for taking my question this morning. Can you give us a directional sense of the next step toward a phase III study in UC for the remainder of the year? How will the registrational program here look like compared to what we typically see? Are you still shooting for all comers? You mentioned that, you know, there's the optionality of biomarker positive patients. How should we think about this optionality piece? I have a follow-up. Thank you. Yeah, perfect. Thanks, Brian. Those are great questions. Thank you for joining this morning. You know, I think, I'll answer the latter of your questions first. We are absolutely still expecting this to be an all-comers, all lines of therapy phase III study that is designed to get the broadest possible applicability of the drug to patients, irrespective of biomarker status, irrespective of biologics experience. What we will do is we will study the biomarker in our phase III as a sort of secondary endpoint, with an idea that we can generate and produce that data and use it as an additional option for physicians and patients as they're sort of deciding on their treatment paradigm. Also with the ability to prescribe the drug, regardless of biomarker status. We think in particular, that may be helpful commercially and with payers in providing some optionality, which I think was the meaning behind that comment. As far as the path forward, first of all, we will meet with FDA shortly here. That's obviously gonna be the most important step here in locking in the trial design. We expect to communicate about our exact trial plans after that meeting is done, and we're sure what we're doing. That said, our expectation is in line with what we shared before, that we're gonna go straight to a phase III program here. That the trial design will look like a modern UC program, probably relatively similar to what was done for etrasimod, and that we'll begin it as soon as possible. I think, our competitors have given guidance around early next year. I think, we'll be in line with our competitors. Great. Maybe just one more follow-up. You have indicated the number of possibilities beyond UC and CD this morning. I think this backs the next question of, you know, what's your latest stand on potential collaboration for RVT-3101 in other indications? Also, what could be the cadence for the next set of indications here? Yeah, thanks. Thanks, Brian. Look, I think the first thing to say is this data, as I said, with the induction data, encourages blue sky thinking, encourages thinking about all of the places in which an anti-TL1A antibody could work. Obviously, Mayukh mentioned we've already begun the study in Crohn's, but even beyond IBD and in other inflammatory and fibrotic conditions, I'll share an update there as soon as we have it. Suffice to say, we are springing at this program from every direction, including figuring out the ways to generate data beyond IBD. Mayukh, anything you'd add there? No. No, no. On the partnership question, look, I don't have much to say right now about it. I, you know, I think, we are really excited about the mechanism. We're really excited about the drug. We know there's a lot of enthusiasm in the world for it, and we're committed to doing whatever is best for the drug and best for patients. Great. Thanks, and congrats on the data again. Thanks, Brian. Thank you. Our next question coming from the line of Corinne Jenkins with Goldman Sachs. Your line is open. Maybe I'll tee off on his most recent question. You know, you talked about addressing a broad spectrum of disease with a single phase III program. Are there any implications to the size of the program that you'll run in order to kind of demonstrate efficacy across, for example, naive and experienced patients, the biomarker positive group? I'm just curious, how are you thinking about that? Yeah. I guess the short answer to that question is, look, it's gonna be a robust program, as all UC programs generally are. We are confident it ought to be smaller than our competitor's program, simply because they will still have to do, dose ranging and other work. I don't believe that powering for any of these subsets is gonna wind up being the rate limiter on size. I think it's just gonna be the overall needs of the program for approval. Mayukh, anything you'd add to that on size? No, not really. I mean, look, I think given the really robust efficacy results we've got here, I think, as Matt alluded to, I don't think that this is gonna be an extraordinarily large study. It's gonna be a typical UC study, very streamlined, and we'll be able to cover kind of every corner of the market within that study. All right. Maybe one more from me. You alluded to it, can you more specifically contextualize the sustained clinical remission rate data as it compares to other available therapies and real-world treatment in UC? Yeah. I don't have a lot of specific data to call to mind. I'll give it to Mayukh in a second, who may be able to give a little more context. I guess the one thing I'd say is, as I'm sure you're aware, many of the other clinical trials earlier in these diseases were re-randomization designs, where basically the way those designs work is during the induction period, clinical responders are identified, and then those responders are carried through on therapy, and the rest aren't. I guess, in my way of thinking, the sort of sustained remission rates here are a more stringent version of that, where you're cutting the data at the first approximation in the induction period on remission instead of response, and looking at sustained response, sustained remission rates. In some ways, I think that makes it sort of at least useful to contextualize the randomization data. Mayukh, anything you'd add on sort of contextualizing the sustained remission rates? Yeah. I mean, I think broadly speaking, look, this is kind of another one of those things that we don't have a lot of comps for, but sustained efficacy metrics across the field are typically in the 50%-60% range. To be printing 75% and 80% numbers here is, again, pretty remarkable. Great. Thanks, guys, and congrats on the data. Thank you, Corinne. Thank you. Our next question coming from the line of Louise Chen with Cantor Fitzgerald. Your line is open. Hi. Congratulations on the impressive data and all your successes this year, and thanks for taking my questions here. I wanted to ask you if you think the efficacy could actually extend beyond the 56-week period, or how do you think about that? Secondly, with the data you saw today, how do you think this could change the treatment paradigm for UC? Last question is there any read-through from the UC data you've seen into your Crohn's study? Thank you. Thanks, Louise. Appreciate the questions as always, appreciate your joining. You know, on the first question, efficacy beyond 56 weeks. I'll ask Mayukh. I'm not aware of too many studies that have studied UC treatment beyond a year, I don't think there's a lot of comp data for that. That said, I think if we look at the trajectory of the data, it continues to improve, I think there's a possibility that patients will continue to benefit, especially frankly, on some of the... You know, we talked a little bit about endoscopic remission, especially on some of the really difficult endpoints where we continue to see an effect on the disease. That was your first question. Sorry, I'm blanking on the second question. Um- How could it change the treatment paradigm? Yes. Sorry. Thank you. You know, how many more frontline usage? Yeah. Thank you, thank you, thank you. Look, I think, look, I think there's a couple of answers to that. First of all, obviously, it's a privilege in UC to begin with, that we are now using clinical remission and endoscopic remission as like the endpoints that are effectively the point of the realm. That's what people are thinking about, is what amount to clinical cures for these patients at some level. And, you know, I think now that we have a monotherapy agent, which in the biomarker population is you know, comfortably in the forties or above, in terms of these endpoints, I think you're looking at a different world for these patients and for our ability to treat them. I think the first thing is just it really raises the efficacy bar, and I think that will have a real impact on how patients think about these diseases as diseases. So, you know, I think that's the first answer. I think the second answer is, this is really one of the first late-stage potential applications of a biomarker in immunology broadly. And I think it's gonna be interesting to watch how it plays out and to better understand how treating physicians think about that and how it can fit into the treatment paradigm. Obviously, the way we're running the program is flexible to that point, but I think it's gonna be an interesting thing to watch commercially, interesting thing to watch scientifically. Mayukh, something to add? Yeah, I was just gonna say, I mean, just in terms of, like, the treatment paradigm, look, I think based on this data set, and if this data set has recapitulated phase III, I think this really will transform that paradigm. I mean, keep in mind, Louise, that, you know, patients at present typically go on a drug for between six and 12 months only, and then drop off, right? That's because, you know, either it didn't work very well in the first place, or you had efficacy and you lost it, or there's, you know, something to do with the safety profile of that drug. I think this program, RVT-3111, has none of those, none of those issues, right? We have strong efficacy data out of the gate. That efficacy gets better over time. We have extraordinarily high efficacy in the frontline setting. We have high efficacy in the second-line setting, where we know that existing options simply don't work, very well at all. Everything suggests this efficacy should improve over time. I think you had a question on Crohn's, right? I think the last question was on translation to Crohn's. Yeah. Yeah. Look, yeah. Go ahead. We think it's predictive, is the answer. Look, we think Crohn's and UC are pretty similar diseases. There's a lot of, a lot of biology and mechanism, sort of, reasons for overlap, particularly the fibrotic prong here. Obviously, Crohn's is also a fibrotic disease. arguably even more of one. Yeah Ulcerative colitis. Yeah. Then to be candid, obviously, we were pleased to see Prometheus's data in Crohn's earlier this year. It was an open label study, but it showed good efficacy in the context of other trials and so on. Look, I think there's a lot of reason to believe that this will, this will translate. Obviously, we're excited to see the actual data from that study next year. Thank you. Thank you. Our next question coming from the line of Robyn Karnauskas with Truist Securities. Your line is open. Hi, thanks for taking my question. It's very rare that the data's so good we don't have a lot of questions. Congrats on that. I guess one of the key things I think that people are trying to get to is the additional indications, and I know you had a question on partnership, but how do we think about spend and how you allocate how bold do you go to start looking quickly and aggressively, and how does that influence spend? Then I have a follow-up. Yeah, thanks, Robyn. Look, thanks for listening. Thanks for taking the question. I appreciate the commentary on the data. Obviously, we're excited about it, too. You know, I think the first thing is, one of the great things about TL1A and one of the great things about this data set is IBD is a very large opportunity. There's no question that even IBD alone, this is a really, really large, sort of, transformational potential. We're focused on that now and focused on not giving up any ground. It's a competitive race. We're focused on getting those studies up and running. We're focused on being first in IBD. That said, this data is really compelling and works... Clearly, TL1A works across a variety of anti-inflammatory and anti-fibrotic axes, and as we've said a few times, we think there's a lot of other opportunity. I think right now what we are thinking through and working on aggressively is proof of principle to lay out the sort of shape of the playing field, right? How broad can we go? Looking at fibrotic disease, looking at inflammatory disease, thinking about the different paths forward, so that we can get a sense for what the tree looks like. In the broadest possible version, it will impact spend, but that'll be for a great reason. Namely, if TL1A winds up working across a variety of inflammatory and fibrotic conditions, we will want to develop it broadly, and I am highly confident that we will have many different ways to make sure that development takes place. Otherwise, I think from a spend perspective, until some of that proof principle is developed, you can think of the significant majority of spend here as related to IBD. The only thing I'd add to that and staying on sort of our plans here, but I think that there is a way to prosecute some of these questions with in essence, a relatively limited amount of capital spend in the proof of concept stage. Got it. The other question was just, I was curious, when you outlined three possible doses, you know, was there a dose response? Like, why not disclose the dose? Is this for competitive reasons, or have you decided on which one it is yet? Thanks. That's it. Yeah. We are locked in on dose. We have a lot of very helpful information about dose response. We think it is helpful for FDA. We think it is helpful commercially. We think it's helpful for making sure we run a low-risk phase III program. The only reason we have not shared it is competitive. Is that Prometheus did not run a dose-ranging study. Merck is presumably still trying to figure out exactly what they want to do from a dosing perspective. They're gonna have to kind of carry those questions and answering those questions, you know, in phase III, which ultimately makes for a, you know, less simple, less clean study design than I think we're expected to have. Got it. All right. Thank you. Just to clarify, I guess one last, I think embedded question there. Yes, we have the dose we're gonna use in phase III. That's the expected phase III dose. That's, you know, that's a constant dose that we identified in the induction phase. It was the same, you know, thing that we reported in January and then now in the chronic phase. Thank you. Our next question coming from the line of Doug Elsa with H.C. Wainwright. Your line is open. Hi, good morning. Thanks for taking the questions. Congrats on the data. First, Matt, I think you spoke, or Monty, you spoke about how you're thinking about phase III and powering, and that would be, you know, obviously it's going to be an all-comer study. Just curious, in terms of the biomarker population, are you thinking about getting that powered and powered sufficiently so that you could get it included in the label? Yes, is the short answer to that question. The biomarker covers 60% of the patients. It's not gonna be that hard to get it powered for inclusion in the label. Absolutely, yes, our expectation is it would be powered for inclusion. Okay. Would you anticipate enriching the population just to make sure. I mean, it doesn't sound like it will be hard, but just to make sure that you do have a proper number of patients, both biomarker positive as well as maybe you know, sort of, all come or non-biomarker positive patients? Yeah, Doug, we won't enrich. We don't think we need to enrich. We have a very good sense. There was no enrichment done in either of the prior studies, and we think that we have a very good bead on the 60% in an unenriched population. Okay, just one follow-up for me. Just curious how the data at week 56 compared to the week at week 40? Obviously, we did continue to see some improvement from week 14 or 16. Not enough coffee this morning. The induction phase. I'm curious, did we continue to see the trend lines up, or did it reach sort of maximal efficacy by week 40? Yeah. Thanks, Doug. I haven't had coffee yet either, so I'm sympathetic, but I'll hand it over to Mayukh to answer the question. Yeah. Yes, the punchline is we did continue to see improvement. You know, keep in mind, of course, that at week 40, we don't have endoscopies, right? That was only done at week 14 and at week 56. We're sort of missing part of that equation, but in other parameters, we absolutely continued to see improvement. One quick follow-up. I mean, would there be reason to think that further out, we would continue to see further gains, you know, in for patients? I guess I'll flip it around. I'd say, our data gives us no indication that we have plateaued. I think it's reasonable to expect continued improvement. Okay, great. Thank you very much, Matt. Thank you. Our next question coming from the line of Neena Bitritto-Garg with Citi. Your line is open. Hey, guys. Thanks for taking my question, and congrats on the data. Just to follow up on the biomarker positive patients, I didn't hear this on the call, but could you tell us what the sustained clinical remission rate and sustained endoscopy improvement rate was for patients that were at the expected phase III dose, who were biomarker positive? Can you also remind us in terms of the actual biomarker assessment, how easy that actually is to do clinically? I think you've said before, you don't need an actual separate companion diagnostic, but just from a practical kind of commercial perspective, how easy is it to actually identify the biomarker patient population? Thanks. Yeah. Thank you, Neena. Thanks for listening, and thanks for the questions. You know, as far as the assessment, we haven't commented on specifically how it's collected, but we've said it's not gonna be any kind of commercial liability, so we think it'll be straightforward, is the answer. Then, look, I think the short answer on the sort of sustained remission rates is broadly consistent. Mayukh, anything you'd like to add? Yeah, broadly consistent, better than the sort of bar that I alluded to earlier in the call, across all of those metrics. Got it. Thank you. That's helpful. Thank you. Our next question coming from the line of Dennis Ding with Jefferies. Your line is open. Hi, good morning. Thanks for taking our questions, and congratulations on the great data. Two quick ones from me. You know, when you look back at the induction data on a modified ITT basis, remission was 29% in all comers and 33% for the biomarker positive, and these are all at the phase III dose. I recall back when the data was reported in January, the induction data, that the delta was closer to around 10%. How should we interpret this and the utility of a biomarker, of a biomarker, you know, approach, given this data? Or, you know, is this or is this just a dynamic of small numbers and variability? My second question is around, you know, phase III. What strategies can you take to minimize a placebo effect? Thank you. Yeah, thanks, Dennis. I appreciate the questions. They're good questions. On the first one, I'll say, first of all, this is not a function of mITT versus ITT. The differences between those two were truly minimal and just related to really a couple of patients different in exclusion. The delta here relative to the data we reported in January, was that it's a different cohort of patients, right? These are only the patients who were on the phase III dose for a whole for a full 52 weeks, while the data we reported in January, which is as sort of Pfizer had given it to us, was all of the data for all of the patients on the phase III dose during the induction period. This is a smaller subset of patients. As you can see, if you compare the baseline characteristics between the two, this is a slightly sicker population, and so, you know, the numbers are probably a little bit lower for that reason. Overall, I think when we take a step back and look at the totality of the data, and I think this will be clear when we present it all in the medical meeting, our view on the biomarker is fundamentally unchanged from where it has been here. We think the biomarker delivers a real clinically meaningful benefit on the order of what we shared in January. We think it will be helpful commercially. Again, still no intention to limit the study to just biomarker patients, but we think docs will appreciate having the option. That's on the on the biomarker question. Anything you'd add to that, Mayukh? No, not really. I mean, I think, you sort of pointed out one kind of, you know, one data point, but if you look again in the data- Yeah ... E ven across, like, all the different metrics, all the time courses, you just see a really clear and consistent sort of pattern of enhanced efficacy in the biomarker-positive population. That's true. Even in the data we shared today, like, the endoscopic improvement data looks really, really good, and the endoscopic remission data is frankly remarkable. Yeah. It's an unprecedented level. On placebo, you know, I think, obviously, the proper execution of the phase III study is high on our list. Frank, if you want to just share any thoughts on execution there? Sure, happy to. I think one of the things that we benefit from is, you know, that this is the largest study in this mechanism to date, and we have site-level performance from the entire Pfizer study, from both induction and maintenance. We can say which sites were, you know, really good sites. ... How did they perform? How did those patients perform? I think that level, you know, site-level intelligence gathered, you know, from so many sites, from so many patients here, really gives us a leg up into thinking about how we minimize placebo effect, going into phase III. I think the only other point I'll add on placebo, just as a baseline thing to keep in mind. Look, I think our placebo rate in the induction phase here was normal, probably at, like, the higher end of the band of normal, but pretty normal. Look, I think our data was exciting in that context. I guess I'm feeling pretty good about kind of where we shake out there. It's also just worth, you know, reminding, as we talked about in January, that the placebo rate that we printed, yeah, like, while Matt said it was sort of normal or maybe upper end of normal, it was also the smallest of the arms in the induction portion of the study. In a certain sense, the uncertainty around the point est that the ability of a placebo responder to kind of move that percentage up, you know, was higher. Beyond that, I think, you know, as we talked about, you know, back in January, the, you know, the placebo patient cohort was actually the least sick of the cohorts in the study. I think, you know, back then, kind of looking across all the induction portion, induction arms, we really saw our placebo arm being, you know, being the least sick, our expected phase III dose arm being, you know, being, you know, a bit sicker and sort of overlapping with the Prometheus dose arm and then Prometheus's placebo arm being kind of the most sick. Wonderful. Thanks, Matt. Thank you. Our next question coming from the line of David Risinger with SVB Securities. Your line is open. Hey, good morning. This is Brian on for Dave. I guess first off, congrats on the data. I just had a quick question. I kind of wanted to understand, what proportion of the patients here were on background therapy and, how many of them, if any, did you have discontinued background therapy in the maintenance period? Thanks, I appreciate the question. Thanks for listening. I'm gonna ask Mayukh to take that on the specifics, but they're good questions. Yeah. across the study. Sorry, I'm just kind of looking here quickly, but, you know, something on the order of, I think, really, around 40% of patients were on steroids at baseline. Over the course of the, you know, the maintenance period, there was, you know, sort of tapering was encouraged, but not mandated. You know, roughly, again, broadly speaking, roughly half of the patients were able to reduce their steroid dose. Excellent. Thank you so much. Nothing other than corticosteroids was in this background therapy. Great. Thank you. Thank you. One moment for our next question. Our next question coming from the line of Yaron Werber with Cowen. Your line is open. Hey, guys, good morning. This is Joyce on for Yaron. Thanks for taking our question. I'll just add my congrats on the data. Maybe just looking at another slice of the data, are you able to comment on what you saw specifically in the biomarker-negative patients? Maybe what was the magnitude of the delta there between the biomarker-negative versus the biomarker-positive cohorts? Maybe just more broadly, how are you thinking about competitive positioning on the biomarkers between you and your competitor, Prometheus? Thanks. Yeah, thanks. I appreciate the question. Thanks for listening. You know, I think, the short answer is, we had compelling efficacy in biomarker-negative patients. That was broadly consistent across arms and so on. The reason we haven't reported it on the phase III dose is just 'cause you start to get to relatively smaller N, once you compound these various effects, and the fact that the biomarker population is significantly, negative population is significantly smaller than the biomarker-positive population. I'll say we saw compelling efficacy for biomarker-negative patients across cohorts. And feel broadly good about this drug, both as an all-comers drug and for biomarker-positive patients. We have sort of a good understanding of our performance in those groups. In terms of positioning versus the competition here, I think everything we've said before still obtains. This data shows that we have an effective biomarker that clearly separates from the all-comers population and offers an incremental benefit to patients in identifying responders. We think it's gonna be an important tool. We think on the curve, it will deliver, based on what we've seen so far, and obviously there's more data to come from our competition. What we've seen so far, we think a sort of broadly, comparably efficacious biomarker in a larger patient population, which we think will be more attractive to physicians and patients. That's sort of at a high level, I think, how we position the biomarker. Yeah, I'd just add to that. I mean, look, I think we're, again, we're locked and loaded. I think we've got this huge data set that builds upon the earlier clinical study as well, and we've got our biomarker set, and we see this again, you know, pattern, kind of no matter how you slice it, of enhanced efficacy on top of an already great base, you know, all-comer data set in the biomarker-positive population, covering 50% of patients. Really, I'd say that the question really is probably one more for Prometheus and Merck or Merck, I guess, at this point. They're playing catch up, and right now they're, you know, they're not locked and loaded, and they're starting with a much smaller biomarker-positive cohort. Thanks. That's super helpful. Great. Thank you. I'm showing no further questions in the queue at this time. I will now turn the call back over to Mr. Matt Gline for any closing remarks. Great. Look, thank you to the operator, thank you to everybody who dialed in this morning and listened. Again, I'll echo Mayukh's thanks to the Immunovant team, the Telavant team, the folks at Pfizer who are our partners, and all the investigators and patients who worked on the program. We could not be more excited to be carrying this forward. It's a privilege to work on a program like this one, and a privilege to have produced all of the data that we've produced so far this year, and I'm looking forward to more data coming in the balance of the year. Thank you, everybody, and look forward to talking to you all soon. Ladies and gentlemen, that does end our conference call today. Thank you for your participation. You may now disconnect.