Roivant Sciences Ltd.

Good morning, ladies and gentlemen, and thank you for standing by. Welcome to the Rory Vance First Quarter 2023 Earnings Conference Call. At this time, all participants are on a 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 1-1 on your telephone. You will then hear an automated message advising your hand is raised. Please note that today's conference is being recorded. I will now hand the conference over to your speaker host today, Stephanie Lee. Please go ahead.

Good morning, and thanks for joining today's call to review Roybent's financial results from the company's first quarter at the June 30th, 2023. I'm Stephanie Lane with Roybent. Presenting today, we have Matt Klein, CEO of Roybent, and Mayuk Sukopny, President and Chief Investment Officer of Roybent. For those dialing in via conference call, you can find the slides being presented today, as well as the press release announcing these updates on our IR website at www.investor.roybent.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 FCC for more information regarding these forward-looking statements and related risks and uncertainties. And with that, I'll turn it over to Matt.

Thank you, Stephanie, and thank you, everybody, for joining this morning and for listening. It's only been a short, actually six weeks since our last call, because our last call was for the K. so comparatively a little bit fewer updates, but certainly an exciting quarter end of June 30th and a lot to talk about today. I'm going to give just a brief sort of update on the state of the business as well as an update on the quarter end of the Tama sales. And then actually what we're going to spend the bulk of time on today is we've been getting more questions about Repcitinib, and we've actually got some new data there in Crohn's disease, so we're going to We're going to share that and talk through again a reminder of sort of how we're thinking about that program as we approach the lupus data in the back half of the year and more beyond. And so with that, I'm going to get started just starting on page five. You know, as an overall reminder, we continue to be pleased with the progress we've made in the business. During the 630 quarter, we completed our 10th consecutive positive phase three trial. That was the during two, sorry, during one study, the second study. of V-town and atopic dermatitis, which we continue to be proud of that track record, which has now led to six FDA-approved products across Roivant and the Sumitomo collaboration. As of 6-30, we had just under a billion and a half dollars in cash on the balance sheet, which, as we've guided before, comfortably funds us into the second half of 2025, with a lot of clinical data both generated recently and even more coming in the near future. And we're very proud of our pipeline at this point. We have what we think is among the strongest I&I pipelines with, by our estimate, over $15 billion in peak sales potential supported by VTAMA, but also a number of critical first and best-in-class programs behind it. On slide six, and it's funny because this is a relatively, as I said, quiet moment, but 2022 has been, and I expect will continue to be, an extraordinary year for us as a business. As a reminder, Up till now, in addition to continued progress on the VTAMA commercial launch, and we'll come to that in a second, we've generated positive data in now both large randomized controlled studies, phase three studies, and atopic dermatitis for VTAMA, which, as we've said before, will support our filing for additional indication there at the beginning of next year and approval hopefully next year as well. And then we've also now put out two important data sets, one in January and one in June, demonstrating the efficacy and our overall enthusiasm for RBT3101, our T1A antibody, which obviously has gotten a lot of discussion. That program is obviously one of the most important in our pipeline now. We are currently underway with our Phase II Crohn's study. and in the midst of preparations for our phase three study in ulcerative colitis, which we will share more detail on in the near future. Still coming for the year are two pretty important events. One, which I expect we'll get some questions on, I know Immunivant has spoken a lot about recently, is the upcoming single ascending dose and multiple ascending dose data for IMVT-1402, our next generation anti-FCR and antibody at Immunivant. Obviously, that data, we think, has the potential to show that we have a a best-in-class program there, and we're really looking forward to putting it out. There's a number of other data sets in our FCRN franchise and more broadly in the FCRN field coming in the near future as well. And then, as I mentioned, the topic on which we'll spend the most time this morning is brepacitinib. That's our dual inhibitor of TIK2 and JAK1 at PridaVant. That program has its what would be one of two registrational studies in SLE, a Phase IIb study reading out in the fourth quarter of this year. and actually just a lot going on generally there as well. And it's a program that I think is just starting to get some attention, but it's really sort of earlier on people's radar. So all of that situates on slide seven in our late stage pipeline, which again, we are very excited about in terms of its breadth and in terms of the importance of many of the mechanisms we're working on. And again, there remain programs in that pipeline, like in the Milimab and RVT2001, that are earlier stage, higher skew opportunities that we'll share more about as we get data, which will happen sort of starting at the end of this year with 2001 and beyond with the Milimab. So with that, I'm just going to go into a brief update on where we are on VITAMA, starting on slide nine. So look, we continue to be bluntly very excited about the progress that we are making here. We continue to see Monthly scripts increase. We continue to see docs enthusiastic. We continue to hear a lot of enthusiasm for our AD data. We continue to make payer progress, as I'll talk about in a moment, and continue to see improvements in revenue, which is ultimately the bottom line at the moment. So we're just very pleased with the growth there. We've got now over 11,500 unique prescribers who have written over 200,000 scripts, which is pretty extraordinary for just over a year on the market. It's a really strong start from our perspective. You know, on slide 10, I just wanted to give a sort of payer update. So we're up to about 130 million lives covered, just a tick under 80% of commercial lives, plus 87 million government lives. This is the kind of coverage we dreamed of having maybe 18 months after our launch. This is really exactly where we need to be from a coverage perspective. We are on formulary With all three of the major PBMs, so we're in good shape from a major PBM perspective. We have four additional national health plan formularies. We have a bunch of progress across some of the regional and smaller plans. We are in a great place from a coverage perspective. And the other thing I'll say is the significant majority of this coverage obviously has no prior auth. That's a little bit of a red herring in dermatology where very few drugs are true prior auth, but Most importantly, the majority of it is single step through a steroid with very easy process for that step to be achieved. And so we feel really good about the strength of our coverage, and we think it's underpinning a successful commercial model. You can see a little bit more about that on slide 11. We did $16.7 million in net revenues for the quarter, which continues to be a solid progression in growth quarter on quarter. I feel good about that growth and expect to continue to see it to accelerate with both volume and gross net improvements in the future. Gross-to-net was a hair better, 26% yield over the last quarter. We had pulled, as we said on the prior call, some of the GTN improvements from this quarter, the June 30th quarter, back into the 331 quarter with some earlier formulary additions. So I expect to see GTN to progress sort of linearly on the trend line over the course of the year, and I expect to end this fiscal year, call it in the mid to high 30s from a yield perspective, and still believe very comfortably in we'll be on a trajectory to get to that 50% yield that we and others have guided to as we progress. So the contracting and sort of other payer progression is all sort of moving exactly in the direction we need it to, and we think we're in, yeah, we're in a good shape from a GTN perspective. So that's about it on Vitama for now. I'm sure we'll get some more questions. Look, I think the continued progress there is, is exciting to us and we're excited about all the feedback we're getting. We believe script volumes will continue to increase over the course of this year, especially as our now live DTC campaigns begin to have an impact on volumes. And we're really also looking forward to getting going in AD next year, which is, as you may remember, a about four times larger market opportunity where we have some truly exciting and highly differentiated data. So with that, I'm going to turn it over in just a moment to Mayuk. who's going to do a relatively deep dive here on brepacitinib, our dual inhibitor PIK2 and JAK1. And I think it's a program that has been high on our minds, but a little bit below the line for others just because of everything else going on in our pipeline. But it's a really exciting program. It's a very potent agent, which continues to demonstrate strong clinical efficacy. And one of the many reasons we're highlighting it today, which maybe we'll talk about, is we've generated some data Pfizer had an ongoing study in Crohn's disease that's read out, and once again, the agent has shown great promise in another clinical study. We are unlikely, as you know, to progress it in Crohn's disease, but nonetheless, really excited about the data there and what it means for what we're going to do in some of these other places. So with that, let me hand it over to Mayuk to take it away, starting on slide 13.

Yeah, thanks, Matt. Yeah. So, yeah, please turn to slide 13. So, as Matt said, I want to take the opportunity to talk a little bit about one of, I think, what I consider one of the sleeping giants within our portfolio. To the extent that ReproCitinib has begun to get some notice from investors, I think it's mostly through the lens of being a pivotal study catalyst for Roivant by the end of this year. And while that is true, we do have the lupus data later this year. I think the lupus story is just a small part of what we're trying to build with brepacitinib. And so I want to go through that story afresh for you here today. The punchline from my perspective is don't sleep on brepacitinib. So put simply, brepacitinib is a unique, highly, highly active dual inhibitor of both TIK2 and JAK1 that has already shown spectacular efficacy in a broad range of autoimmune diseases. So As Matt said, we're reporting here for the first time the sixth consecutive positive phase 2 study for grapacitinib, this time in Crohn's disease, which is a study that is being run by Pfizer and done at Pfizer's expense. And that adds to the string of positive phase 2 studies already reported, now covering, as you see here on the slide, psoriasis, alopecia, psoriatic arthritis, ulcerative colitis, hydradenitis supertiva, and now Crohn's disease. And we'll go through the rest of the material on this slide in greater detail later, but we think that we really have the potential to become the leading oral therapy in loop, given the dual inhibition of TIK2 and JAK1 should provide greater efficacy than inhibition of either one alone. That is a large global study that is designed to serve as one of two registrational studies. And importantly, it is a 52-week study with a 52-week primary endpoint, which is the registrational endpoint that has historically been the most predictive of future studies. Our ongoing single phase three study in dermatomyositis, which will serve as the basis of an NDA filing shortly after data, is coming up to the extent that it now seems a little far off. I think as we round out the year and are sitting in the first half of 2024, it will come into focus as a near-term catalyst to everyone. And that's just the beginning for this program. So we think of that unique dual mechanism and high demonstrated efficacy of breptocitinib really creates a pipeline and a product approach where we can own a series of specialty rheumatology indications, each of which has high end needs and blockbuster revenue potential for breptocitinib. And we'll show that in the coming slides. And then finally, we have a long IP runway here with protection to at least 2039. Please turn the slide forward, please. So as many of you know, the JAK family consists of four isoforms, JAK1, JAK2, JAK3, and TIK2. The JAK family inhibition has proven over the past several years to be an enormously powerful mechanism for treating a wide spectrum of autoimmune disease. While the field has accumulated approvals, starting in rheumatology and moving on to immunodermatology and then IBD, as you see across the top, the underlying biology often remains complex and stubbornly irreducible. Shown here is a simplified schematic detailing a number of key cytokines that have been shown to drive pathobiology of autoimmune disease, along with the key JAK isoforms responsible for mediating those signaling pathways. While early JAK inhibitors were relatively non-selective, more recently the field has trended towards more specific inhibitors, with JAK1 having the broadest applicability and therefore, unsurprisingly, the first to be explored. You can see here in the dark blue band across the middle where JAK1 inhibitors, such as RINVO, and the cytokines that are most directly impacted. Notably, selective JAK1 inhibitors are able to suppress signaling of IL-6 and interferon gamma, two important cytokines linked to autoimmunity that are not suppressed through selective TIK2 inhibition. Now, TIK2 selective inhibitors, such as the TIK2, are now coming onto the scene in a particular set of indications. They cover a different set of cytokines, which you can see in the light blue on the right. Key among these are IL-12 and 23, the latter of which drives the differentiation and activation of Th17 cells in downstream IL-17 production, a key pathogenic driver of many autoimmune diseases. Now, both JAK1 and TIK2 approaches are accumulating a track record of meaningful clinical benefit and commercial success across a range of diseases. RINVOC is already approaching $1 billion of net revenue per quarter, and Sotictu is also projected to be a multibillion-dollar product. But in spite of their many successes, both of these medicines also have their limitations. Sotictu, for instance, failed outright in both ulcerative colitis and Crohn's, while RINVOC has produced lackluster Phase II data in both lupus and NHS. We see this as at least in part connected to the underlying biology. While some diseases may be well-treatable by selective JAK1 or TIK2 inhibition alone, many others involve multiple inflammatory pathways and may require intervention across multiple orthogonal axes to see maximum effect, or maybe even to see a meaningful effect at all. The latter is especially true for heterogeneous, highly inflammatory diseases, which have high patient burden, where clinically meaningful efficacy has to date been limited. So that's what drove our original hypothesis at Roivant, that the field in its current state may not be fully maximizing the power of JAK inhibition, that efficacy might be getting left on the table in certain indications with highly specific TIK2 or JAK1 inhibitors. So in our search for the right molecule to prove out this hypothesis, we unsurprisingly ended up partnering with Pfizer, probably the company with the longest history and deepest experience with JAKs in the industry. In breplacitinib, we found a highly active, safe, and well-characterized molecule with a novel mechanism perfectly suited for what we were looking to do. Simultaneous inhibition of both TIK2 and JAK1, which we can uniquely accomplish with breplacitinib, creates two distinct opportunities to deliver differentiated efficacy. For diseases driven largely by type 1 interferon signaling, that is to say interferon alpha and beta, a dual hit on both sides of the heterodimer shown in the bottom in pink, second from the right in the schematic on the slide, may allow for greater suppression and thus potentially greater efficacy as compared to hitting TIK2 or JAK1 alone. And second, diseases with broad cytokine involvement that include, for instance, both IL-6 and B cell pathways on one hand, and IL-12, 23, and the IL-17TH access, TH17 access on the other, may actually be treatable through repositinib in a way that would not be possible to either JAK1 or TIK2 inhibition alone. So that's the core hypothesis stated in the bottom right. Repositinib will deliver best-in-class efficacy in indications mediated by the TIK2-JAK1 dimer and in diseases requiring broad cytokine coverage. Please turn to slide 15. So what concretely drove our excitement about brepacitinib? So to start, when we looked at a series of standard cytokine inhibition assays, we saw exactly what we hoped to see. So shown here are the results of studies run internally at Pfizer. The left panel looks at type 1 interference signaling, a key driver across multiple autoimmune diseases, and one where both TIK2 and JAK1 inhibition would be expected to have an effect. That's exactly what you see experimentally. The NICE inhibition by the leading cure JAK1 inhibitor and nice inhibition by the leading tier TIK2 inhibitor. And then importantly, Pfizer's experimental data showed that brevacitinib is able to suppress type 1 interferon signaling as well as, or potentially even better than, either rinvoke or CITIK2. This is exactly what would have been predicted in the prior slide. We were benefiting from the double hit and thus achieving a greater inhibition of type 1 interferon signal. On the right, we show two other critical cytokine drivers. So on the top right, You see type II interferon, interferon gamma, which is mediated by JAK1, but not by TIK2. So the pattern of inhibition is, again, what you'd expect. You see that RINVOC and brepacitinib, which both inhibit JAK1, have a relatively higher degree of inhibition of interferon gamma compared to a selective TIK2-specific inhibitor, CITIK2. And then on the bottom right, you see the opposite performance of the single isoform drugs on a cytokine inhibition assay for IL-12 and 23, both of which are TIK2 and not JAK1-mediated. So here you see a nice inhibition by CITIC2, the CITIC2-specific inhibitor, while the action of RINVOC is much more modest. Again, that's exactly as you'd expect based on the schematic we showed in the prior slide. And again, you see that brepacitinib is a very, very good inhibitor of CITIC2-mediated cytokines, outperforming CITIC2 in this assay. So the conclusions here are listed at the bottom. On the left, you can see that brepacitinib should achieve greater type 1 interference suppression And it's possible by targeting either TIK2 or JAK1 alone by virtue of the dual hit. And on the right, brepacitinib can repopulate in a single molecule the cytokine suppression profile of both the leading TIK2 agent and the leading JAK1 agent. Please turn to slide 16. That cytokine inhibition experimental data has translated well into a string of phase two data readouts today. As you can see, oral brevacitinib has demonstrated an extremely consistent pattern of meaningful clinical efficacy in every single indication tested. Efficacy results for alopecia, psoriatic arthritis, ulcerative colitis, psoriasis, and HS were all statistically significant and consistent with as good or better than any other small molecule inhibitor. The HS data, which I'll cover later, was a relatively recent readout that occurred subsequent to R taking over the drug from Pfizer. We're also excited to be reporting today the induction results of a large global phase two crone study run by Pfizer. So I'll provide some additional details in the following slides. Finally, we have another major benefit in the clinical package for brepacitinib. We know what we have on safety as well. So we know that stacking both TIK2 inhibition and JAK1 inhibition does not apparently lead to a safety profile that undercuts the efficacy advantages that we hope to show. Our extensive safety database now consists of over 1,400 patients exposed across 20 different Phase I and Phase II clinical studies for up to 64 weeks, and what we've seen is a well-characterized safety profile in line with approved JAK family inhibitors. Please turn to slide 17. So we're pleased to report today the top-line results from the induction portion of a Phase II study with brepacitinib and Crohn's disease. This is a 151-patient global phase two study. The primary endpoint was the SES CD50, and the key secondary endpoint was the clinical remission rate at week 12, defined as the proportion of patients who achieved a CDAI of less than 150. Both endpoints were highly significantly significant. We think that actually the true efficacy might have been understated on the SES CD50 in this study, as there ended up being a slight imbalance in baseline severity between the arms, which made it harder to achieve that endpoint for the drug arm. That imbalance would not have an impact on the secondary endpoint since the way that that endpoint is calculated only takes into account patients who start with a baseline CDAI of greater than or equal to 220. The punchline here is that this is a trial that I'm sure wasn't on any investor's radar and yet has delivered really strong efficacy. In fact, that 33.5% placebo-adjusted delta on clinical remission which is used as a co-primary endpoint in registrational studies and is particularly important for prescribers, is in fact the highest seen in the late-stage study from any drug, oral or biologic, to date. Please turn to slide 18. So we find ourselves in an enviable position. So we have a highly efficacious molecule that has strong biologic and clinical translation and a variety of large market indications. There are lots of things that we could do with prepacitinib. But our vision with ReproCitinib from the start was to really focus on those indications where we could deliver a step function improvement in outcomes for patients, generating maximum impact for patients and maximum return for our investors. To that end, we asked ourselves, what are the disease indications where the unique properties of ReproCitinib really shine? For us, that came down to a few simple considerations laid out on the left side of the slide. So in the light blue and moving clockwise, the first Where is inhibition of both TIK2 and JAK1 required for maximal efficacy? Here we looked for biologic rationale for dual TIK2-JAK1 inhibition and corresponding clinical validation. Second, in dark blue, which indications have extremely high morbidity or mortality, creating a need for novel therapies that provide a meaningful efficacy benefit? And third, in pink, does the indication have few available treatments, including no approved oral therapies? And finally, of course, we need to be confident that we could run an efficient experiment, minimizing development and regulatory risk. Put those together, and we think that there's an opportunity for representative to become a leading treatment option in a series of large and uncrowded markets. The next two slides will go into more detail on pre-human lupus. But remember, that's just the beginning. Please turn to slide 19. Dermatomyositis is a large orphan indication with a very similar profile to indications like PAH and cystic fibrosis, where oral small molecules have become billion-dollar-plus products. Over the past 30 years, dermatomyositis has become much better understood and characterized in the medical community, and increasing disease awareness and diagnosis has led to higher incidence and prevalence estimates over time. We've done our own analysis with claims data from 2016 to 2020, and estimates that the U.S. adult prevalence sits at 37,000 patients, consistent with recently published estimates as well. So we're looking at a patient population that is already clearly in the large orphan category. This is not an ultra-rare indication. And as awareness and diagnosis of the disease continues to increase, we expect the number of patients to grow over time. For an autoimmune disease impacting this many patients, dramatic myositis presents a strikingly high disease burden. There is high mortality, with some estimates of up to 40% at five years. The characteristic skin rashes shown on the right cover large percentages of the body and lead to significant pain in addition to disfigurement. The vast majority of patients also suffer from proximal muscle weakness, which can severely impact daily living activities. Many patients end up needing walkers or wheelchairs. Finally, a meaningful proportion of patients suffer from interstitial lung disease. In some, this is a high mortality, highly inflammatory disease, which covers multiple organ systems and will evolve into a large commercial market. On top of that, there have been no NCEs approved in the past 60 years, and there are no oral therapies in industry sponsored late stage development. Steroids, ISTs, and IVIG for many years, with the latter recently gaining formal approval. But again, there's not a single modern drug approved for the indication, and the current treatment options present high safety and convenience burdens, in addition to limited benefits. IVIG, for instance, requires multi-hour infusions for three or more days every month, and is associated with side effects including quite a high rate of thrombotic events. So we really see DM as one of the major unmet needs in all of autoimmune disease. and an opportunity for a modern targeted therapy, particularly an oral one, to enter the market and rapidly become a blockbuster product. And while a number of companies are exploring small proof of concept studies, there are very few drugs in late stage development and no oral therapies in phase three other than brepacitinib. So looking ahead to a product launch of brepo in this market in just three years, we think this has the potential to become a material commercial driver for roivant, as we think about the overall sales across our pipeline over the next five plus years. Please turn to slide 20. We also see this as an indication where the probability of success for Breville is very high. With no modern medicines approved for DM, physicians often experiment with various different therapies to add on to corticosteroids. As a result, through investigator-initiated studies and an extensive body of case reports, there is meaningful clinical validation for JAK1 inhibition in DMs. This aligns with the pathobiology of the disease, which is driven in large part by type 1 and type 2 interferon signal. Given no other JAK1 inhibitors are approved or an industry-sponsored development for DM, even if Repo just matched this level of efficacy, that would set us up well for clear commercial success. But there's also reason to believe that the addition of TIK2 inhibition can further add to the benefit that Repositinib will provide, both to enhance potency of type 1 interferon suppression as well as through suppression of IL-12 and IL-23, which are also involved in DM pathobiology. Please turn to slide 21. Given the high unmet need and our high confidence in clinical success, we took the bold step of moving directly into a Phase III program that involves a single registrational study. Our expectation is that this study, if successful, would support an NDA filing for prepacitinib and DM. The single phase three study is already well underway, tracking to complete enrollment in 2024 with data and a potential NDA filing in 2025. This timeline has us clearly positioned to be the first oral to market by potentially several years, and likely also ahead of a few biologics in later stage development. One idiosyncratic consequence of our decision to move directly into phase three is it means that our next catalyst in DM won't be coming until 2025, but that catalyst could be a major inflection point for Roivant as a business, with a potential billion-dollar-plus product launch immediately to follow. And given this launch would be in an orphan indication with a specialized prescriber base, we would expect the revenue ramp to be significantly steeper than for a volume product like Vitama. So as you think about modeling Roivant's P&L over the next five years and beyond, we think this is a major source of additional value that investors right now may be underappreciating. Please turn to slide 22. DM is the first of many orphan indications where we see a similar opportunity for brevisitinib, and I'll talk about a few more of those in a bit. But first, I want to talk to the other indication where we have an ongoing pivotal study and where we do have a major catalyst coming up later this year, and that's lupus. So lupus is a disease that everyone knows well, and is one that's gotten an increasing amount of attention from industry in recent years. Hundreds of thousands of patients suffer from lupus in the U.S., many with serious and debilitating disease. Only two therapies have been approved in the past 20 years, both injectables. As a sign of how desperate the field is for efficacy, Benlysta is doing greater than $1.4 billion in U.S. revenue, despite very modest efficacy, at between 9% to 14% placebo-adjusted SRI-4. And Cefnalo, which launched recently, is projected to be a billion-dollar-plus product, despite mixed Phase III data. One study didn't show successful significance, while the other showed about an 18% placebo-adjusted SRI-4. Please turn to slide 23. The limited options reflect an unfortunate reality everyone knows. Well, lupus is simply a very challenging disease to treat. It's highly heterogeneous with multiple interconnected inflammatory pathways acting through T cells, B cells, and interferon signaling, and multiple impacted organ systems. To date, most attempts to treat lupus involve a molecule acting predominantly across one of those three axes. Ben Lister, for example, depletes B cells, while Cefnello suppresses interferon signals. Both have generated meaningful but ultimately somewhat modest efficacy. And of course, there's a long history of failed attempts at individual cytokine inhibition, indicating broader cytokine suppression is needed as well. Through dual PIK2 and JAK1 inhibition, Repositinib is distinctively optimized to address all three axes simultaneously. The TIK2 arm modulates T cell activity through IL-12 and the IL-17 TH17 axis through IL-23. The JAK1 arm modulates B cell activity through IL-6, IL-7, and IL-21. And both arms work together to maximally suppress pathogenic type 1 interference signal. Please turn to slide 24. Over the past 18 months, We've had readouts from three JAK inhibitors in lupus, including phase 3 data from Illumion, a JAK1-2 inhibitor, phase 2 data from Linvoke, a JAK1 inhibitor, and phase 2 data from Cetictu, a TIK2 inhibitor. These data provide clinical evidence for the therapeutic relevance of each of JAK1 and TIK2, respectively, in lupus, and as such, increase our confidence in brevisitinib's public success. At the same time, none of these molecules have demonstrated particularly compelling benefits, with the high water marks so far being for TIK2, if you blundered across, and roughly the mid-teens placebo-adjusted SRI4. This is what we might expect, given that unlike brepacitinib, none of these molecules directly targets all three inflammatory axes in lupus. So, we are cautiously optimistic that through dual TIK2 and JAK1 inhibition, brepacitinib can deliver greater efficacy benefits than we've seen from these other oral therapies and become the leading oral therapies for patients and physicians. Please turn to slide 25. We continue to expect top-line results from our ongoing study of brepacitinib and lupus in the fourth quarter of this year. As we've stated in previous earnings calls, this is a large global study using the registrational 52-week primary endpoint, and as such, is designed to serve as one of the two registrational studies. In the event of a positive outcome, we would expect to rapidly initiate a second confirmatory registrational study. I do want to emphasize that while we're cautiously optimistic that repositinib can deliver data that will position it as the leading oral therapy in lupus, our confidence in the probability of success here is not as high as in dermatomyositis. We feel rock solid that we are hitting the pathways that matter, but we as an industry have had mixed success in proving out efficacy on regulatory endpoints such as SRI-4. Lupus is just a challenging indication in that respect, and it was not the core bet that we underwrote when we used in-licensed repositinib. That bet, rather, is the opportunity in dermatomyositis and a string of other large orphan indications to potentially follow. And given the six successful Phase II placebo-controlled studies we've had to date, our enthusiasm about brepacitinib and these other indications will remain, irrespective of our results in lupus. Please turn to slide 26. Turning now to these other indications, I just want to highlight two in addition to dermatomyositis, where we have a rapid potential path to market, with launches that could follow closely behind DMs. A couple to highlight here are non-infectious uveitis, or NIU, and NHS. Please turn to slide 27. NIU, like dermatomyositis, is a large orphan indication with a very high disease burden, with approximately 30,000 cases of legal blindness attributable to NIU each year. Unlike DM, there is one approved targeted therapy, Humira, which has generated over a half billion dollars per year in sales despite limited efficacy and almost no indication-specific promotion. The development stage competitive landscape at NIU is even more wide open than in DM, with no ongoing phase three studies at this time for any oral or biologic. And efficacious oral therapy could easily match the Humira's peak sales in this indication, and with sufficiently compelling data, we could potentially do significantly more. Please turn to slide 28. As with DM, we also have clinical validation of JAK1 inhibition in NIU. The development was discontinued in the U.S., and it generated Phase II data in NIU suggesting JAK1 inhibition may be more efficacious than TNF alpha suppression by Humira. However, the extent and robustness of clinical validation of JAK1 inhibition in NIU is not quite as great as in DM, and so in this indication, rather than moving straight to Phase III, we are conducting a quick proof of concept study. This study also includes dose ranging that would make a potential pivotal study even more efficient. We're excited to report that this study is now fully enrolled with top line data expected in the first quarter of 2024. Please turn to slide 29. HS follows a similar pattern to DM and NIU, a highly debilitating disease with a large organ prevalence increasing over time through increased diagnosis and awareness. Here, too, Humira is the only approved targeted therapy with indication-specific sales of approximately $3 billion per year, again, despite limited efficacy and limited indication-specific promotion. Please turn to slide 30. Unlike DM and NIU, HS does have other oral therapies in later stage development, specifically two JAK1 inhibitors. As you can see on this slide, the Phase II data recently generated by brepacitinib is greater. both in terms of absolute and placebo-adjusted benefit, than that seen from either of these molecules. Prefacitinib's benefit observed in Phase II also surpasses the 42% growth in 16% placebo-adjusted benefit seen in Sumira's Phase III program. Notably, prefacitinib's benefit was robust across both TNF-naive and TNF-refractory patients and was generated despite the study being heavily impacted by COVID-related discontinuations. In fact, the placebo-adjusted benefit among completers was actually 27%, suggesting an opportunity to potentially demonstrate even greater benefit in phase three than phase two. This is further supported by HS pathobiology, which involves not only JAK1-mediated inflammatory pathways, but also the clinically validated IL-23TH17 axis, which is suppressed by TIK2 inhibition, but not JAK1 inhibition. Please turn to slide 31. So, I hope I've been able to convey in some small part how excited we are about the potential for brevacitin. It's a highly active molecule with a unique mechanism of action and long patent line that sets us up to potentially create the leading oral specialty autoimmune franchise in the pharmaceutical industry. Here on this slide, you see how this pipeline and product will build in the coming years. The successful lupus readout later this year clearly tees up a multi-billion dollar commercial opportunity in lupus alone. But even without lupus, we have a rapid de-risk path to a billion-dollar-plus commercial launch in DM, with full enrollment of our pivotal study coming next year, data in 2025, and a potential product launch in 2026. And then there's a rapid pipeline of other large orphan indications to follow, each with blockbuster potential. A pivotal program in HS, NIU, or both could be initiated in 2024. And we have other large orphan indications to follow with potential proof of concept studies planned for 2024. With that, I'd like to thank Ben Zimmer and the rest of the PRIVANT team for all their work on brepacitinib so far. And of course, to our colleagues at Pfizer for both partnering with us on this program, and of course, for all their work in discovering the compound and generating this really rich data set. And I'd also like to thank all the investigators, site personnel, and importantly, the patients who participated in these trials as well. With that, I'll turn it back over to Matt.

Thanks, Mayuk, appreciate it. And obviously, thank you for that deep dive into the program. Some questions about it, but also just wanted to set people up for the month and, frankly, years ahead with it. So looking forward to more there. I'm going to go very quickly through the rest here and then open up for Q&A in just a minute or two. Starting with on slides 34 and 35, while we're not going to spend any time today on the CL1A data, it occurred to me as we were finalizing this presentation that the June 30th quarter was the quarter in which we had generated 56-week maintenance data, and that it felt weird not to at least nod to that extraordinary data set. So we've had a couple of calls on that topic so far. The TL1A program is an incredibly exciting opportunity, and we continue to look at this data and find new things to like about it, including the continued improvement into 56 weeks and some of the things that set us up really well for the phase three programs. So more on that to come. As a reminder on slide 36, We are now underway, including first patient dose with our phase two study in Crohn's. The goal here is to get, as I've said before, dose ranging, quote unquote, out of the way prior to beginning phase three in a way where when we look at all of these timelines and stack them together, we think we still have an opportunity to be effectively first in class in Crohn's disease by going quickly from this study into a phase three study in Crohn's. So we're very excited about the opportunity for T01A in Crohn's in addition to UC and look forward to sharing more data next year when this study concludes. And then lastly, on the late stage portfolio on slide 37, I talked about this a little bit at the beginning. Obviously, we collectively, likely led by Immunomance, are going to have an opportunity to get back together in the next couple of months to talk about updates on our FCR enfranchise. Most notably, we are expecting imminently within the next, you know, I think Minivan has said September for the single-sending dose data and October and November for the multiple-sending dose data, data that we think will validate the best-in-class potential for IMVT4102, our next iteration anti-FCRM. As a reminder, the hope there is to show that we can continue to suppress IgG to a best-in-class level while also avoiding the impacts on albumin and LDL. that have been seen with the TOCLNAB. It's been a busy year for the FCRN field, and the other thing I'll point out is that we just recently saw data from a competitor, F-gartigimod, in CIDP, which was really great data that both continued to underpin and validate the FCRN mechanism. It's now worked basically everywhere it's been studied and showed a potential in a new market, including one where we have an ongoing Phase IIb study of a relatively similar design. to the eugenics one that just ran out. We'll have some top line data from that study next year. And then the last thing I wanted to briefly shine a spotlight onto on slide 38 is just we continue to make progress on our various discovery efforts. I've got a slide here on Vant AI, which is a rapidly progressing effort that we have to use certain advanced machine learning techniques, specifically on induced proximity and protein degradation. One note here, we had previously had a number of efforts in this area, including one at ProteaVant. We've now effectively collapsed the ProteaVant induced proximity effort into Vant AI and have sold the balance of our ProteaVant shares to our partner SK. And so Vant AI is now the sort of instantiation of our principal bed at RoiVent on induced proximity and protein degradation. And we are really excited with the early progress there, including some great hiring And notably, we've now got Michael Bronstein as a scientist. He's one of the really the lions in the field of of molecular modeling using machine learning. And so we're really excited to have him on board and some other great hires there as well. But we'll talk more about soon. Real progress coming. We'll get back on the phone as we've got we got to share. But keep keep an eye on this space as it were. I'll wrap up very quickly on slide 40 with a brief financial update. Financial picture continues to evolve as we'd expected. Revenues and so on we've talked about. Cash most notably good into the second half of 2025 as we had discussed before and continuing to keep an eye on that and on managing it across our portfolio with various opportunities coming soon. With that, I'll stop. Slide 42 is the catalyst map. We've talked about some, but not all of these things coming. And just an exciting balance to 2023 ahead. So I'll say thank you to Mayuk, to the team, and to everybody, including patients and investigators, who helped make this quarter what it was. And I will turn it over to the operator to open the line for Q&A. Thank you, everybody.

Thank you. Ladies and gentlemen, to ask a question, you will need to press star 1-1 on your touch-tone telephone. To withdraw your question, press star 1-1 again. Please stand by while we compile the Q&A roster. Now, first question coming from the line of Brian Chen with JPMorgan. Your line is open.

Hey, guys. Thanks for taking my question this morning and the walkthrough on Prebo. Maybe first on Prevost, given what we saw from other JECs in SLE specifically, how confident are you that Prevost can perform better than Ducra specifically in SLE? Is there anything that you would want to flag from the baseline characteristics in the ongoing phase 2 design to ensure that you can show the differentiation and also make sure the placebo rate is low? Then I have a follow-up. Thank you.

Yes, thanks, Brian. And maybe I'll take one second of that question and then also hand it over to Mayuk to see if he's got further comments. Look, I think in terms of the confidence in SLE, and I think you heard Mayuk say it, on the one hand, I think there's strong biological rationale that hitting both TIK2 and JAK1 should provide a meaningful benefit. And so I think that's an important point. And then I think the second important point is understanding the bar correctly. And I think if you look closely at the Ducra data, look, I'm not going to say Ducra is not an impressive agent, but really I think the way to read that data is probably sort of mid-teens blended efficacy. And I think if you look at the three milligram dose where they showed something more impressive than that, I think there was a pretty significant sort of patient population imbalance that suggests to us that mid-teens is really the bar to beat. You know, as far as the baseline characteristics, you know, I think, first of all, as a reminder, this is a study that Pfizer designed and ran. We think it's a pretty well-designed study, and we've been watching it closely. There were certain things that we didn't control. And as Mayuk mentioned, look, lupus is a scary indication for trial execution. But we feel overall pretty good. And, you know, I think that our study design, for example, was designed to try and flag some more severe baseline criteria. which is historically correlated with success, but we'll obviously see how that plays out later this fall. Mike, anything you'd add to that?

No, not really, Matt. I think you nailed all the points I would have made.

Great, thanks.

And maybe just one more follow-up on ImmunoVans 1402 data coming up next month. Just to prep us for the top line coming up, can you walk us through how we should gauge the profile at top line in terms of one IgG suppression compared to botoclomab and FGAR? And more importantly, the impact on albumin and LDL given the potential variability in the LDL assay?

Yeah, thanks. Thanks, Brian. Great question. Obviously, one we're getting a lot right now, and I'm sure Immunovant's getting a lot too. I think Immunovant's spoken a fair amount on this point publicly. I think on IgG suppressions, Look, we believe we have an equivalently potent molecule here, and we'd like to see equivalently deep IgG suppression is the short answer. Remember, comparing apples to apples versus as close as we've got to equivalent time points and things like that. But in general, I think we'd like to see really the same level of deep IgG suppression, and certainly we'd like to feel like we're going to be able to suppress IgG comfortably deeper than F-cartigimod can. So that's on the IgG suppression points. You know, on albumin and LDL, obviously there's – a lot of speculation and discussion on this point. The facts are that the variability of the albumin assay is about 5% and the variability of the LDL assay is 10 plus percent. And so I think within first approximation with relatively small studies, you want to be comfortably within both of those. Smaller is generally better. And my sense is that if the albumin impact in the SAD is relatively modest, that the LDL will follow, and that because of the variability in the LDL, it'll be easier to see if you've got a few weeks of compounding data after multiple injections. So I'm mostly looking to the albumin in the SAD data. I haven't seen really any of this yet, so I can't say what it's going to look like, but that's what I'm keeping my eye out for.

Thanks, Matt. Thanks, Madhuk.

Thank you. One moment for our next question. And our next question, coming from the line of David Riesinger with Lyric, Elon is open.

Good morning. Thanks very much, Matt and team, for all the updates. So, I have questions for both Matt and Mayuk. Matt, could you provide an update on the evaluation of potential monetization of assets? and also provide an update on the pursuit of new product acquisition opportunities. And then I'll pause and follow up with a question or two for Mayuk.

Thanks, Dave. I appreciate it. And I figured we would get some version of that first question. Look, I think we are in a privileged moment in terms of the amount of clinical data we have generated and will generate soon. That data is both deeply informative to our own strategic future and also exciting to potential partners, acquirers, and so on. And it's flattering to be the focus of attention. It's made me wonder a little bit how exactly public speculation happens. But anyway, it's flattering. Look, I think the short answer is on the monetization side, we're value-oriented and we're going to have to make these decisions carefully. knowing that a number of our late-stage programs are really rare opportunities with huge potential, and so we don't take any decision on them in either direction lightly, with the dollar sums at hand being very large and the opportunity for patients being very large. Certainly, I wouldn't expect us to make any decisions of substance on this point until we've started to get some of the Immunovant data in, just because that's a pretty important strategic catalyst for us as we think through what the future of Roidman could look like across the breadth of our portfolio. You know, on the new opportunity side, I will hand that over to Mayuk, actually, but I guess the one thing I'll say is this has been a phenomenal asset sourcing opportunity and environment for us. Obviously, a year ago today, we would not have been talking about TL1A. We also wouldn't have been talking about 1402. We hope we've proven that we see some pretty interesting and unique things and that we can bring them in. And I'll say we've got things on our racket right now that are just as exciting to me bluntly as anything in our late stage portfolio. And I hope we can convert some of those and the next year we'll be talking about them as well. But Mayuk, anything you'd add to that?

Not really, Dave. I mean, look, I think that this is, as Matt said, this has got to, you know, our sort of normal course of business to be out there looking for new and high value things. I think that work is ongoing. I feel really good about, you know, as Matt said, things that are a racket. Stay tuned.

Cool. Thank you. I appreciate the question.

Thank you. And then just to follow up. So, Mayuk, thanks for providing the comprehensive vision for brepacitinib. Could you discuss the decision not to pursue a number of indications despite compelling results, including Crohn's? And then if you could also discuss SOTIC2's inverse dose response in SLE and whether there are any potential implications for brepo in SLE or no. Thanks very much.

Sorry, I missed just the last part of that question, Dave.

So, yeah. So, on the last part, the slide shows an inverse dose response for SOTIC2 in SLE. So, as the dosing went up for SOTIC2, the efficacy went down. Just wanted to see if you had any comments on that and whether there may or may not be implications for BREPO as a dual agent in SLE. as it's dosed up. And as I understand it, you're testing 15, 30, and 45 milligram doses.

That's right. Matt, do you want to take the indication question?

Yeah, sure. I mean, look, I think, Dave, it comes down to, and this was sort of the inherent thesis in Brepo as well. I think at the moment that we acquired Brepo from Pfizer, it was sort of just in the thick of the sort of turning point on JAK inhibitors because of labeling. And I think our view has been, in the face of very compelling data, as you point out in Crohn's and in a number of these other indications, that the competitive landscape there is such that the JAK labeling may be a disadvantage difficult to develop through. You know, I think if you take Crohn's, for example, you know, I think that's an interesting question in the sense that clearly As we continue to study RINVOC in IBD pretty aggressively, and also the allosteric TIC2s have struggled a little bit there. So I think we'll get some more data on that later. I think we'll continue to reevaluate those questions. That said, I'd say the other thing about our view is I think with the data that, frankly, the TL1A class is putting out in IBD, we're not sure exactly where a JAK will fit in the future treatment paradigm. understanding the obvious benefits of being an oral. But anyway, look, I think the affirmative bet we're making here is that orphan indications where the JAK liabilities won't be a problem with the unmet need is highest is sort of the place where it makes the most sense for us to pursue, for us to pursue BRAPO.

Yeah, I mean, I think just to add to that, look, I think we're always going to be, I think, kind of dynamic in our understanding and really sort of, you know, this sort of comes down to, in a certain sense, an embarrassment of riches in terms of just the clinical data set and the breadth of potential indications we can go after. I think, as Matt said and articulated on the call, you know, our sort of primary thrust, as it were, is in these, you know, orphan indications for which I think we feel like our ability to separate versus other options is as great as the competitive intensity is the least, et cetera. And that sort of really allows us to kind of have this specialty rheumatology and own that area for ourselves. And so, you know, I think we've got a lot of different options here. And I think it's important to decontextualize over the next couple of, you know, data sets that we get in both lupus and IU and then MFDM coming right after that. And tell me your question on SOFTIC2. So look, I mean, I think obviously this is sort of the, you know, sort of the inherent sort of uncertainties around just, you know, relatively small endpoint estimates as well as this sort of, you know, lupus clinical trial readouts generally. I think that our own view is that there's not, you know, not really likely. The truth is not an inverted dose response in that particular study. I think there are reasons to believe that, you know, in essence, this could be like a little bit of a reflection of just like slight imbalances, imbalances, you know, between the various dose arms. So, for example, you know, we think that the, you know, the three milligram BID arm, the one that produces the sort of highest print head, you know, more subjects receiving sort of triple combination standard of care baseline compared to other arms. And then that's a 12 milligram, you know, once daily arm had higher dropout rates, et cetera. And ultimately, I think if you look through sort of sedictive, just generally, it seems like they're quite close to saturation, you know, at the three mix. There's not really kind of like a true reason to believe that there's sort of more juice in there at the higher doses. And then finally, it seems like, you know, mid-teens, it's kind of blended across these three values. It seems to be consistent with how Bristol themselves seem to be powering their phase three as well.

Got it. Thanks very much.

Thanks, Dave. Appreciate the questions.

Thank you. And our next question coming from the line of Robin Karnakas with Truth Securities. Your line is open.

Hi, guys, and thanks, Mayuk, for doing all the work for me on lupus and brepo. It was a fantastic presentation. A question on capital allocation. First, just on brepo, when you think about how, you know, whether to spend more on these orphan drug indications, can you just remind us of the Pfizer agreement and how much, if there's anything they contribute? And then bigger picture, you talked about making capital decisions after seeing at least initially some of the data from 1402. And you've got so many moving parts just this year and next year with many drugs and decisions you'll have to make. Can you just walk us through how you're going to think about that? Would you start thinking about that after SAD? And how long might it take you to come up with a game plan for what you're going to do for Rayvant for spend? Thanks.

Yeah, on the first question on REPO specifically, the answer is the lupus study itself was very heavily subsidized by Pfizer. So our cost there was a fraction of the total study cost. And that obviously made it an attractive setup for us. The rest of the costs associated with other indications are ours to bear. Pfizer does not contribute. They are protected from dilution at their 25% stake, up to a dollar cap, frankly, relatively similar. to the mechanism at TLEVANT with the DLNA program. So in terms of other orphan indications, NIU, DM is all our cost, et cetera. Those are capital allocation decisions for us, the same as any other. But SLE in particular has been highly subsidized through the end of this current study. If we decided to run another study, that would also be ours to fund. More generally, I guess I probably, insofar as I said, we wouldn't think about it until we saw the UNEVANT data. That was probably an overstate. have spent a lot of time thinking about capital and capital decision-making as we explore the opportunity set, and I agree there's a lot of moving pieces coming. You know, I think the SAD data will be informative. I think the MAD data will be informative. I think we're going to learn other things from the FCRN field, including some RA data from J&J, from our own GRAVE study, et cetera, through the balance of this year. You know, I don't know that there's going to be like a single tipping point obvious moments where before which we can't make any decision and after which we can. I think it's more of taking the facts as we have them and trying to understand in which direction things swing over the coming months. That said, we have the best version of this problem, I think, in the sense that we just have lots of different options for capitalizing the business going forward. And so I think we're frankly picking among good choices at this point.

Okay, great. Thank you.

Thanks, Rob. Appreciate the question.

Thank you. And our next question coming from the line of Louise Chan with Cantor. Your line is open.

Hi. Thanks for taking my questions here, and congratulations on all the progress this quarter. So I wanted to ask you on brepacitinib, one thing people have been asking us is how you think about pricing if the drug is approved? And I know it's a little bit early, so if you can't talk about specifics, maybe you could tell us the bookends and how you're thinking about it and what you might comp it to. And then on VTAMA, the reimbursement work you did on psoriasis, how much can that be leveraged to the atopic dermatitis opportunity so that you can move quickly on uptake on that one? And then one more here on brevisitinib. Can you be a little bit more specific on when this year we'll see the data? Is it early, mid, or late fourth quarter? Thank you.

Yeah, thanks, Louise. On the two Brepo questions on the timing, I think it's safe to assume mid to late fourth quarter is probably the way to think about that. On pricing, I mean, I'll hand it to Mayuk, but I think my short answer to that question is at this point, there's a pretty wide breadth of possible indication spaces between SLE and DM and so on. So it's probably premature, but I'll hand it over to Mayuk.

Yeah, I think the punchline is we're thinking about this principally as sort of a, you know, call it an orphan drug pricing band, you know, given the sort of indication set and sort of what makes sense, you know, in both of these. I think that that is, you know, potentially compatible with pricing in lupus as well if the efficacy data is really strong.

And then on the VTAMA access question, I think the short answer is yes. That is, a lot of that work can be heavily leveraged, and I would expect the sort of process with payers to be significantly streamlined, given that we're all on formulary. Obviously, there is still work to do. It's not like it's instantaneous and automatic, but I would expect it to be a faster, more straightforward, and frankly, much more predictable process where I have, look, I think there were some real unknowns about how coverage was going to materialize prior to our launch. And I think at this point, we are pretty confident that we are going to get comfortably covered with reasonable rebates by the payers. Thanks, Louise.

Thank you. Thank you. And our next question coming from the line of Dennis Ding with Jefferies. Your line is open.

Hi, good morning. Thanks for taking our questions. I just had one on AminoVans. So on the upcoming 1402 data, can you just remind us the study design and how long is the follow-up for SAD and MAD? And interestingly, you know, how often is albumin being measured? And as a follow-up, you know, maybe given your comments around the assay variability and that, you know, there could be different time points at which albumin is measured. And, you know, just also appreciating the fact that albumin reductions can go up and be down at some points and others. And I was just wondering what are some, you know, what's a good outcome for you guys in SAD and the MAD on the albumin front? Thank you.

Thanks, Dennis. I appreciate these questions, and obviously it's an area of a lot of focus, so it makes sense. Look, I think on study design, there's a fair amount about this in the Immune Event Corporate deck and in ours as well. You know, on the SAD study, it's 6-1402 plus two placebo patients per I forget exactly how far out it's measured, but it's at least a few weeks. And then on the MAD study, it's 10, 14, or two in two placebo patients, and it's weekly dosing for four weeks, and again, with a several-week tail at the end. We've got pretty frequent data points, I'd say, as a reasonable benchmark. If you went and looked at, like, some of the Botoclumab data we've put out, I'd say, like, the measuring points are pretty similar. And so, you know, I'd In fact, we follow these patients out a lot more than a few weeks, and there's sort of a number of measurements within 10 days, and then it starts to get a little bit more spaced out in the SAD study. So, again, there's a fair amount of data in the immune event deck on this point. In terms of what good looks like on albumin in the SAD and the MAD, against a backdrop of smaller is better. I think, you know, again, with a 5% variability in the assay, I think we'd hope to be comfortably within 5%, and I'd say any of the agents, frankly, that show a 5% or less impact on albumin seemed to be pretty well set up from an LDL perspective. So I think, you know, it's hard to say exactly how things would sort of compound from the SAD study to the MAD study, but in general, you know, I'd say lower is better within that 5% bar is probably what I'm looking for.

Got it. Thank you.

Thanks, Dennis. Appreciate the question.

Thank you. And our next question coming from the line of Corinne Jenkins with Goldman Sachs. Your line is open.

Good morning. This is Craig on for Corinne. So as you referenced earlier in the call, this can be a pretty tricky indication. So on that, what do you view as the bar to support continued study in the indication?

In SLE you said, yeah?

Yes, that's right.

Yeah, look, I think the way we are currently thinking about the program, understanding that it's kind of a balance of the factors, is Ducra is the bar to beat, given that they have the Cleaner Tick 2. This would count as one of two pivotal studies, we believe, if successful. So the data from here would already make it onto the label. It's a 52-week study. So it should be relatively predictive of a future study as well, given the way that it's set up. So I think we have the best possible setup, understanding that there has been some complexity in SLE trials before. You know, in terms of the bar, I think it's a balance of the factors. But I think, you know, you've heard us say that we think Sotictu is a mid-teens drug. And you've heard us say that we'd like to be better than Sotictu. So I think that gives you sort of some indication for where our head's at, but we're going to have to look at, you know, there's multiple endpoints and things like that. So, you know, I'd say, you know, mid to high teens sort of and whatever that trend looks into across the other places to look.

Got it. That's helpful. And maybe just a quick one. You highlighted for the first time that you've achieved payer coverage with government-covered lives. I guess, how should we think of the, I guess, doctor adoption of these patients following this update? Is it going to be a similar timing as the commercial covered lives? You've kind of highlighted it's around six months in the past.

Yeah. Look, the truth is that the psoriasis market is sort of 80%-ish commercial anyway. So even though we've got a lot of covered lives there, it's a smaller chunk of the patient population. So, you know, I think now that we've got coverage, they're government patients that they'll sort of accrue over time to better GTN yields and so on. You know, I think in general, I just expect to see steady improvements in GTN from here on out as we get closer and closer to that 50% bogey over the next 12 months and beyond. And I think the government lives will contribute to that, but I don't think it's, sort of going to be like there's some kind of step function specifically associated with the government lives.

Got it. Thank you very much.

No problem. Thank you.

Thank you. And our next question coming from the line of Yaron Webber with .

Great. Thanks for taking that. I have a couple of questions on . And just remind us, AA, . What are your plans sort of with that indication? And then secondly, for HS, can you file, can you just conduct one pivotal? Is that sort of sufficient or do you think you need two? And then I guess finally, at what point can you present or as far as you're going to present the data from the studies? I mean, the studies are positive, obviously. I'm talking about Crohn's and HS, but just so we can also understand the overall profile safety-wise. I mean, there's obviously a lot of data out there, but just so we see the full data. Thank you.

Yeah, perfect. Look, I think the first answer is on alopecia, we have no, like, current plans to progress in alopecia. That's an interesting indication. Our data looks promising, but our view is sort of the same as for the other slightly larger indications. So, you know, I think not sort of on our near-term roadmap, but obviously with the quality of data we have, we'll be watching everything. You know, on the other questions, you know, first of all, on HHS specifically, look, I think it's premature. We haven't sort of discussed it with FDA in detail or anything like that. We don't have a concrete plan there. So I'd probably rather not box this in on a particular study design. That's probably what I'd say there. Mayuka, anything else you'd say in terms of those other points? Or you may be sort of slightly closer than I am to the Pfizer publication timelines.

Yeah, so I think not too much more to add. I think, you know, that current study in particular, you know, still has a maintenance portion to come along with it. You know, look forward to seeing more at a future medical meeting. And then the HS study actually has been published at this point, so we can send that to you, Jeroen.

And Pfizer's got discretion on the publication on Crohn's.

Yeah.

Thanks, Yaron. Appreciate it.

Thank you. And our next question coming from the line of Douglas Saw with HC Winwright. Your line is open.

Hey, Doug. You might be on mute. Can you hear me now, Matt?

Sorry about that. Yeah, perfect. Starting with the TAMA, I'm just curious, as you have successfully added to the coverage for the product, do you anticipate making any changes to the sort of copay card or the sort of access program, consumer access program as it is now, Or do you anticipate waiting until getting approval in AD before making any changes?

Yeah, thanks, Doug. That's a great question. Look, I think for the moment, we have no immediate plans to change the copay card. It's sort of set up in a way, as I'm sure you appreciate, to work well for us as people migrate from uncovered to covered. And, you know, unlike some of the other cards that were set up initially, some of our competitor programs or other new topicals had like, you know, $10, $10 programs or whatever, where the uncovered side of the card was low in order to attract trips at a time when coverage was spottier. You know, we always had a slightly higher copay on the uncovered side. It was frankly set up to carry us into the AD launch and beyond. You know, we evaluate this stuff constantly. And our focus right now is, you know, the high prescribing docs feel really great about the product. And what we're really focused on is taking the docs, we're writing two scripts a month and turning them into five and 10 script a month docs. And I think the sort of goal of whatever changes we make would be to sort of keep that process in motion. But the short answer is I think the copay card actually works reasonably well. To be honest, if there's something I think we're sort of working on, it's, I think at this point, the actual quality of coverage is better than the perception of coverage. I think these docs have been burned a fair amount historically on challenging coverage in Durham. And we actually have quite good coverage. It's easy to obtain. Many, many of their patients, as you can see from the presentation, will be covered. I think many Derms, frankly, have not, like, caught up with that reality yet. And so a lot of the educational work we're doing is just trying to make sure people understand that picture as well as we can possibly help them understand it.

And, Matt, you sort of touched on another point. I'm just curious your perspective on how do you – or what's the plan right now to sort of help accelerate the writing from sort of your low prescribers, right? I mean, because it sounds like, you know, your script base is fairly concentrated and obviously to sort of take it to the next level, you're going to need to increase that depth. What are the things that you're able to do to get people to go beyond just writing that first initial script? And are you aware of what is keeping them from only writing just a couple of scripts right now? Thank you.

Yeah, thanks, Doug. Look, it's a great question. It's quite literally a billion-dollar question, so we spend a lot of time thinking about it. You know, I think the short answer is we've already taken certain steps. We've got now – DTC was something we were pretty conservative about up until we got to this sort of good payer coverage position. So within the last month or two, we've really sort of started to ramp up the DTC campaign, and that should take months more to really fully sort of make it into the script volumes. but it's something that we are watching to drive volumes that way. There's other things too. There's, you know, one property is these patients don't go to the doctor very often. And so frankly, if you were a, if you were a hypertrophic dermatologist, you've been waiting for the VTAMA launch for many years. If you were a local driving dermatologist, you sort of showed up, maybe you wrote a few test scripts or you write a few test scripts every month, but you actually haven't seen very many patients back in your office. who you put on Vitamma a year ago. And so, you know, I think one thing that works in our favor is just time. It's just docs sort of seeing repeat visits from patients who they put on, you know, earlier in the launch. And I think that will cause a compounding effect for us. And then we continue to sort of keep our ear to the ground and work on, you know, whatever the questions I mentioned, the coverage question is probably one of the most important messaging questions that we're working on right now. It's just helping docs understand that, This isn't like other topical, but it's going to make a difference for their patients and it's going to be easy for them to use in a way that some of the other historical launches have been more challenging. And so I think that's where a lot of our focus is. I'd say in the doc hall that I've been closest to, frankly, the number one point is this payer coverage point. It's just docs are a little gun shy about where things are on the payer side. But we hear other things that we continue to work on. And in general, I think docs who are familiar with the product are pretty happy to be using it. So we're just trying to get get everybody else to build some experience in muscle memory. Remember, these docs write steroids in their sleep, so it just takes some time. But we'd love to see faster.

Okay, great. Thank you so much. Thanks, Doug.

Thank you. And I'm not showing any further questions in the Q&A queue at this time. I will now turn the call back over to Mr. Matt Klein for any closing remarks.

Great. Well, look, I just want to say thank you to everybody for listening this morning. Thank you to our team. for all the work this quarter and beyond. I'm really looking forward to the next couple of months here. I think we're going to have some important opportunities to get back together. And, yes, thanks all, and have a great rest of your summer. And we'll be back here soon to talk about some more exciting updates. So thank you, operators. Thank you, everyone, for listening. And we'll talk again soon.

Ladies and gentlemen, that's our conference for today. Thank you for your participation. You may now disconnect.