Afternoon. Thanks for joining us for another session at our 41st annual J.P. Morgan Healthcare Conference. I'm Brian Cheng. I'm one of the senior biotech analysts covering Roivant Sciences at the firm. Presenting next is the management team from Roivant. The presentation will be followed by a Q&A session. To submit questions, we have floor runners on the floor. We also can use the question portal on the conference website. I'll pass the stage to Roivant's CEO, Matt Gline, for the presentation. Matt, welcome, and the stage is yours.
Thank you, Brian. Good afternoon, everybody. Thank you for coming. Excited to present and then take some questions and, yeah, looking forward to it. We're gonna make some forward-looking statements. For more information, you can consult our forward-looking statements disclaimers. I'm gonna start on page three for those following along online. I'm not gonna spend a ton of time on the past, but I just wanna reflect. 2022 has actually been a very busy year for us. We launched our first wholly owned product in VTAMA, which got approved in May and became the number one most prescribed branded topical in eight weeks, and there's been a number of updates there.
We've made some major changes to our pipeline, including two major collaborations with Pfizer that we announced, one on brepocitinib earlier in the year and one which we'll spend time on and I'm sure again in the Q&A, RVT-3101, our new TL1A antibody. We unveiled IMVT-1402, a next-generation anti-FcRn, and we've done some significant work in the pipeline to extend runway. We've just made a lot of clinical progress. We initiated a phase III study in brepocitinib in DM. We completed enrollment in our SLE study, in a number of other updates beyond those. It's been a really busy year.
This is actually on slide four, probably what I'm proudest of, which is, you know, if you had asked me about our 2023 catalyst calendar at J.P. Morgan one year ago, I basically had one thing on it. We were gonna produce phase III data in atopic dermatitis, which I'm very excited about, but it was a relatively sparse year, 2023 for us. We've done a lot of work in the last 12 months, and we've added a lot of really important catalysts to 2023, such that 2023, in my opinion, is shaping up to be probably the single most exciting year from a clinical data perspective in Roivant's history.
We have data that we already produced last week, which we think is incredible data, sort of move forward a foot in a game of inches kind of data in RVT-3101, our anti-TL1A antibody. We will produce that phase III data in atopic dermatitis in the first half with VTAMA. We will produce additional data from our anti-TL1A antibody, chronic maintenance data from our 52-week portion of the study in the first half. We'll generate first in human data in our next generation anti-FcRn antibody in the middle of this year, and we'll generate potentially registrational data from our phase II- B study in SLE in the back half of this year.
I'm proud of this both because this is an incredibly rich set of clinical data, but also 'cause I think it speaks to what the Roivant model is about, which is finding opportunities and making them work for us as a business and finding uniquely shaped opportunities that we can execute on. I think we've done a lot of that in 2022, and it is what has set us up for a pretty incredible 2023 ahead. I'm gonna spend most of today on our pipeline and on some of the recent and upcoming clinical data.
I'll just pause and I'll say, I think one of the things that's interesting to me, we never set out to be an I&I company, but actually I think we have one of the most interesting late-stage I&I portfolios of any biotech company, certainly of our size and scale. I'm excited to share some of the content of that. We have potential category winners in five out of the seven... I'm on slide 6. 5 out of the seven leading I&I markets. We have VTAMA in psoriasis and AD. We have RVT-3101 in Crohn's and UC. We have brepocitinib in SLE. We have a number of programs in growth markets that aren't yet in the top seven list, which could very well be soon.
Again, a really broad, deep I&I franchise that's come out of the work that we've been doing as a business. I'm gonna start with just a review of the data that we put out last week for RVT-3101, our anti-TL1A antibodies. On page eight, just as a recap. This is a drug that we in-licensed from Pfizer. We announced it just last month. We completed it just last month. It's an anti-TL1A antibody. It's a unique mechanism for ulcerative colitis, Crohn's, and other potentially inflammatory and fibrotic diseases. I'll start by saying we've produced some great data here. It's statistically significant, clinically meaningful data.
It's clinically meaningful at that stage at every dose we tested, and it's data that in our view really advances the field in UC with a great safety and tolerability profile and with enriched response rates in a prospectively defined biomarker subset with about 60% of UC patients. This is obviously a well-validated market. UC and Crohn's are some of the largest I&I markets there are. We think we have potential outside of IBD, given the novelty of the mechanism. This is one of the phase II-B studies ever run in UC. We now have over 300 patients. We've studied in four different doses, including in phase II-B study with a Sub-Q, and we have an efficient phase III program plan that we're excited to share more about in the months to come.
We have an additional major catalyst coming this year, a final set of maintenance data, 52-week data coming at the first half by closer to the middle of the year. This is a drug with a long franchise attached to it. Obviously, the biologics exclusivity, but also IP protection until 2039 plus. This is the clinical data for our pooled data across all of our doses. These are again, extraordinary data, 32% gross efficacy and a 21% delta in clinical remission, according to Modified Mayo in an all-comers population or 37% for the 27% delta in a biomarker-adjusted population or biomarker positive population, a similar set of data in endoscopic improvement. I'm gonna spend most of our time talking about this data, in particular in our expected phase III dose.
We have identified the dose that we will likely carry forward into our phase III trial. We haven't identified what the dose is because our competitor does not have dose-ranging data, we'd like to use that as a competitive advantage in trial design. Suffice to say again, just extraordinary data. I'll point to the 40% gross efficacy with a 30% placebo-adjusted delta according to clinical remission, in the go-forward phase III dose in the biomarker positive population. This class in general, and I know many of you follow Prometheus, which is one of our competitors, has recently put out a lot of extraordinary data in UC, you can see how we stack up here. I think this is the kind of data set, in my opinion, that encourages blue-sky thinking.
It gives you the idea that you can go beyond just UC into other diseases with inflammatory and fibrotic components. That's a functioning part of the unique mechanism for TL1A. This is again, sort of moving a foot in a game of inches. Maybe the last piece of TL1A data that I'll share here, and I'm sure some of this will come up again in some of the Q&A. You know, one piece of data we were particularly proud of is we looked at our biomarker-positive population of patients who are biologically experienced, second-line patients in UC. These are some of the hardest UC patients to treat. Basically, every other therapy stumbles when you go into this line of treatment, and you can see that across the board here.
We almost perfectly preserved our efficacy, still a 41% top line. Notably, placebo patients tend not to respond once they're these sort of second-line biologics refractory patients. The placebo response rate goes away, and we have a 41% delta in clinical remission between gross efficacy and placebo, in this patient population. This is the kind of thing again that changes the field in terms of how UC is treated, and we're excited to have an option potentially for these second-line refractory patients. Notably, we think the drug is good enough to also work in all comers and in a first-line setting. Obviously, that has to get mixed with a, with a, with a favorable safety profile, and we're also really happy with how this looks, from a safety perspective.
I'd say if you just look at this table, and if you just take a step back for a second rather than going through the specific rows, everything on this table is basically placebo-like here. Almost every row on this table is lower for the drug arms than for the placebo arm. A very clean safety profile, sort of despite the extraordinary efficacy. The only other class of drugs that's sort of coming close from an efficacy perspective is like RINVOQ is putting out pretty good data in UC. Obviously, that's a JAK, and JAK inhibitors have a significantly different safety profile. We have a very, very clean drug from a safety perspective. I'll call out one thing here, which is that we have gotten some questions.
This program, as of the early Pfizer data, the phase IIa study has had some immunogenicity, in our study here in phase II-B, a 46% rate of antidrug antibodies and an 8% rate of neutralizing antibodies. You know, we said this on our data call last week. First of all, this is in line with a number of approved biologics, right? Humira has shown ADA rates in the 30s and 40s and even higher neutralizing antibody rates, and Skyrizi is in a similar bucket as well. The other thing I'll say that's important to me is we've seen no evidence of any relationship between immunogenicity and safety and efficacy in phase II-B efficacy or safety data.
We have had an early look at the currently ongoing maintenance phase, the 52-week phase of the study. We've seen a decent number of patients out to 40 weeks and some patients out to 52 weeks. In that data, our neutralizing antibody rate is flat to down, and we continue to see no relationships between immunogenicity and safety and efficacy. Overall, feeling confident about our immunogenicity profile, but it's obviously something that we know that people are watching closely. Look, overall, again, an incredibly exciting program. This was an addition to our pipeline just a month ago.
It's something that investors have focused on quite a bit. We are excited to share the maintenance data later this year and to be a part of this new class of drugs, the anti-TL1 antibodies, that we think are gonna matter a lot both in UC and Crohn's and potentially beyond. I'm gonna go from there to VTAMA. This was another drug that had some major developments over the last 12 months. Drug got approved in May and launched. We'll talk a little bit about those properties. I'll say one other thing I'm proud of here is this was the first novel mechanism drug approved in psoriasis in 25 years. The previous novel mechanism was vitamin D. Even that feels a little like cheating.
Look, it's just exciting to bring a new option to psoriasis. This is an indication that's close to me. I'm a psoriasis patient, and so I know this, I know this space well. We are very happy with how this launch has gone. It is the best-branded topical launch, certainly in modern history. We became the number one prescribed branded topical in psoriasis eight weeks into our launch and have continued to build since then. Patient and physician feedback has been really good. We just, we feel great overall with the reception to the product, and with sort of how we're stacking up in the market. Notably, we're keeping pace on a script volume basis with OPZELURA, which is notable 'cause OPZELURA is an atopic dermatitis, which is a market with four times as many patients.
We announced a few months ago that we've now signed our first major PBM contract. This is a great contract. It gives us exactly the kind of access that we want. It's unrestricted and requires only a step through a steroid that's either an automatic look back on recent history or a physician e-attestation of prior steroid use. A really straightforward, clean profile, and we're really focused on sort of supplanting steroids as the mainstay of therapy. Only needing to step through a steroid is a pretty useful thing for us. We continue to do other contracting work and continue to sign contracts with payers, and we'll announce major PBM contracts as they come.
I think a question you might have had on approval is what is access gonna look like for a novel topical? The answer seems to be that we're gonna get all the access we need and a reasonable commercial P&L coming. This is an important program for us also because we have a major phase III program reading out in the first half of this year. Our atopic dermatitis study will read out. AD is a very large market. And again, we have some really, really phase II-B data from this drug in atopic dermatitis. At week eight, we showed a 49% IGA response rate versus 13% for our vehicle. Really, really good data in AD.
It sets us up well, we think, for the field, especially if we can, if we can come close to replicating this in our phase III studies that we'll read out this year. We have a Japanese partner who hasn't reported the specific data but who reported positive top-line IGA in the EASI75 results in a phase III study as well. That was a smaller study than ours. It was a 275-patient study versus 400 in each of our AD studies. A good deal of comfort that we should have a successful clinical program here, when we read out later this spring. I think the last point I'll make here is, we are really just getting started for these indications, right?
We're doing about 4,000 scripts a week, as you saw on the launch curve. The numbers here are unfathomably large. There are 90,000 topical prescriptions written every week in psoriasis and 320,000 topical prescriptions written every week in atopic dermatitis. The vast majority of those prescriptions are for topical corticosteroids. I'll remind you, topical corticosteroids are tough drugs. They're somewhat efficacious, but they are not safe. You can't use them for a long time. They have short duration of use limits, they cause withdrawal injury, they cause skin thinning, they are fundamentally difficult drugs. That's particularly relevant in the atopic dermatitis market, where most patients are young pediatric patients. Our phase III study goes down to age two.
You think about providing a new option with significantly improved efficacy and tolerability for that patient population, it really makes a big difference. You know, a lot of investor and pharma attention in recent years has been on systemic therapy and biologic therapy, but you can see, just look at the markets. These are really topical markets, and it is a huge opportunity, and we are just at the very first innings of what we think we can do here with this program. Needless to say, it's something I'm excited about and something I think is gonna be an important part of our story over the course of this year. I'll hit a couple of other things in the pipeline quickly as I kinda wrap up here. The first is I'll talk a little bit about our anti-FcRn antibody franchise.
This is at Immunovant, a public company that we own 60% of, and obviously you'll hear about this from them as well. And now we have what I believe to be the potentially category-leading franchise in anti-FcRn antibodies. We have two drugs in this franchise. We have batoclimab, our original anti-FcRn antibody, which has shown best-in-class maximal IgG suppression. And we intend to use it in chronic settings. It has a property that it reduces blood albumin levels and therefore causes an increase in LDL cholesterol. We're most focused on using it in indications where we can win on efficacy and where we think that will not be a major liability. What we announced earlier this year is we now have a next generation anti-FcRn antibody as well, IMVT-1402, that addresses the albumin and LDL issue.
There's no minimal impact in albumin and LDL in our monkey data while maintaining that maximal IgG suppression. These are both, by the way, deliverable by a simple subcutaneous injection, a very straightforward injection. What we think is that we can use IMVT-1402 for chronic dosing and indications where an LDL increase might be more of an issue. This gives us an incredible franchise opportunity to go after, on the one hand, bigger indications with chronic dosing with IMVT-1402, on the other hand, rarer indications where efficacy is what's gonna matter most with batoclimab. We're currently studying batoclimab in multiple pivotal trials in MG, GD, and CIDP, among others.
We are generating first-in-human data in IMVT-1402 in the middle of this year, which we think will translate to a direct pivotal path about six months after we generate that data. Now, a question that we get is how does IMVT-1402 deliver the same benefit? You can see it here in the crystal structures for these two binding confirmations. You know, batoclimab binds to a similar part of the Fc receptor. I'm on slide 23. A similar part of FcRn, it binds in a way that interferes with or comes close to adjacent to where albumin binds to FcRn. It impacts albumin binding and therefore causes this reduction in albumin.
IMVT-1402 binds to a similar part of FcRn, that same bottom right corner, but the binding confirmation is such that sort of hangs off to the side and stays further clear of where albumin binds. That's how it avoids an impact on albumin. You can see the monkey data at the bottom here. The chart at the far left shows that at supersaturated doses, we very comfortably hit the same level of IgG suppression at the same supersaturated dose as batoclimab does. You can see at normal doses, we have minimal impact of 1402 on albumin. It's very placebo-like, with basically no impact on LDL at those doses. Pretty comfortable with the profile.
You can see that's in contrast to the blue line there, which is Pitokolab, which we know does impact albumin and LDL. I'm gonna spend just a minute on brepocitinib. This is a dual inhibitor of TYK2 and JAK1, we added to our pipeline in the last year. This is a pretty unique mechanism. It's a dual inhibitor of these two targets. Obviously, TYK2 has been a pretty sort of popular target to pay attention to the last year, especially with sort of TYK2 having been approved by BMS, and with Ventyx and Nimbus also working on the target. Now, this is a drug that we got from Pfizer, and basically our view is the dual inhibition of these two targets.
JAK kinase is the pairwise signal cytokines. There's a collection of cytokines that are signaled by both TYK2 and JAK1. We focused here on diseases because JAK class has some safety liabilities. We focused on diseases with high unmet need where those wouldn't be an issue and where the dual signaling of TYK2 and JAK1 we thought would provide a particular benefit. That means we're most focused right now on SLE lupus, on dermatomyositis. Both of those we have ongoing registrational studies in and some other indications to be announced. Notably, that lupus study has enrollment complete as of the sort of late summer of last year. We know for sure that we will have data from that 52-week study in the second half of this year.
Based on the clinical data that we have for the class, we know that the TYK2s like deucravacitinib have done well in SLE. We know that baricitinib, a JAK1, has produced good data in SLE, and we know that we have in cross-trial comparisons against each of those two drugs quite a lot of data to suggest that we are a bigger gun, that we're able to deliver pretty significant efficacy. There's an opportunity here to deliver some pretty extraordinary data in SLE that could matter quite a bit to patients. I'll wrap up here and make sure we have some time for Q&A, but I'll just say again, 2023 is gonna be a big year for us. We have a ton of really important catalysts and data coming.
We've got expanded reach of VTAMA with continued coverage as well as continuing to grow commercial volume. We think that'll matter. We think it'll be something that'll sort of show the world what a topical can do. We have our phase III readout in AD which we talked about earlier. I think, you know, if positive, it would pave the way to a very large additional market, much larger than psoriasis for VTAMA. We have the 52-week maintenance data for RVT-3101. That'll be the first 52-week data ever generated from an anti-TL1A antibody. We are the only anti-TL1A antibody currently working to generate data like that, and we know the world will be watching that data very closely, and we're excited to share it.
We have, I just mentioned, the first in human data for IMVT-1402, our next gen anti-FcRn antibody in the middle of the year, which we think if it validates the best in class IgG suppression and the clean albumin and LDL profile, has an opportunity to sort of establish ourselves with the best anti-FcRn antibody in the field. We have the potentially pivotal readout in brepocitinib, the dual TYK2 and JAK1 that I mentioned before, which again could serve as one of two registrational trials in a large market with high unmet need. I'm excited to deliver those catalysts and many more in the year and years to come. Excited to continue to engage with investors and to continue to build the business, and we're really pleased with the progress we've made in 2023, 2022.
Thank you very much, and, I'll sit down now and then Brian and I can do some Q&A.
To submit questions, please feel free to use the question portal on the conference website. We also have floor runners for those audience who are in the room today. I'll kick off with more high-level questions. You know, you've got a lot going on. You know, recently you have the TL1A event that was just announced with Pfizer. How should we think about just your overall strategy based on the portfolio that you have today? Is there a specific focus or, you know, theme that you would like to see as we look beyond, let's say, next year, you know, into the next two to three years or so?
Yeah. Thanks, Brian. Look, I think, it's been an interesting environment the last 12 months in the sense that on the one hand, we are quite capital rich, and it's been a very fertile environment for finding new opportunities. I think the Pfizer TL1A deal is a great example of that. We are really pleased with that sort of opportunity space. On the other hand, the capital markets candidly have been extremely tough, and so we've been focused on preserving our capital and on a very high bar for new opportunities. I think all of that remains true as a backdrop matter for what we're trying to achieve.
As I said at the beginning, we didn't set out to build an I&I franchise, I think we are incredibly proud of the late-stage I&I franchise because we think it's one of the best and one of the most catalyst rich in companies of our size and scale. You know, I think we continue to like those targets and those indications, I think we continue also to feel like the best thing for us as a business is to be opportunistic. I think we have a ton of great data, including a number of different pivotal studies reading out over the next couple of years. I hope that coming back in the next few years, VTAMA will not be our only commercial product.
Likewise. Maybe first focus on TL1A. We've gotten a lot of questions about TL1A recently. I think it was especially on the back of the deal announcement, Prometheus data came out and then your data came out as well. It was sort of back-to-back news flow. One question that I've been getting is that, you know, why did Pfizer give that away with no upfront costs, no milestone attached, especially when they had already seen the data, right? What drew your team to work with their team on TL1A and, you know, is there any, you know, is it a competitive process to get this TL1A asset?
Yes. The first thing I'll say is they didn't give it away. They're a great partner of ours. They own 25% of the JV. They own Europe and rest of world. We have U.S. and Japan. I think that's consistent with our view, which is that Pfizer, and part of this is a question for them. Pfizer's got some real P&L constraints with LOEs coming in a number of major products in the next couple of years, and they have to make difficult decisions around R&D prioritization. This is a program they really believed in, and they wanted to preserve as much value as they could while finding a partner.
They needed to find a partner who was gonna be willing to share an upside and allow for an interesting and unusual deal construct, which is something we pride ourselves in being able to do, while also a partner who they were confident was gonna be able to execute on the program, which is something that Pfizer, based on all of their past collaborations with us, knows that we can do. I think once you start thinking how many companies are in that sort of unique intersection of willing to do something flexible that solves Pfizer's problem while also being able to execute on the program successfully, I think there are not too many companies at that intersection. Truth told, we don't think it was much of a competitive process.
We think the relationship that we had ultimately carried the day there, and we're really thrilled to be working on it.
I think last week during the call, you talked about how you already had seen some of the data from the maintenance portion from the from the study. How should we think about the potential effect of the ADA in the chronic period? You know, since 3101 only targets the trimeric form of TL1A, can you talk about the potential differentiation from competitors?
Yeah. Look, the first thing I'll say is I suspect that a big part of the reason why we are getting these questions is. We did the deal with Pfizer, the immediate reaction from the street was, "Well, obviously this means the class sucks, because otherwise why would Pfizer do this deal?" Prometheus put out their data, it was very good. The answer was, "Well, obviously this means that Roivant's drug sucks, because otherwise why would Pfizer do this deal?" We put out our own induction data, I think it was very good data.
The immediate reaction was, "Well, then there must be something hiding in the maintenance data, because otherwise Pfizer would do this deal." I do hope once we report the maintenance data that we get to the bottom of the stack of turtles, and there's nothing beneath it, because I think it's a great drug, and I don't think there is anything in the data to suggest a problem. You know, from an immunogenicity perspective, and I said it before, we've gotten a look at a decent amount of maintenance data, not all of it by any stretch.
That data sort of confirms our view that or affirms, I should say, our view that there is no relationship apparent between immunogenicity and that's NAB's radius or whatever, and safety and tolerability, and that it looks like the NAB rate is flat to declining over time, which is obviously all encouraging. That's what I hope to report out when we report the final data. You know, I don't think there's a huge difference between the fact that we bind to the trimer and they also bind to the monomer. That's something that could have mattered in either direction in theory, right? The monomer could have been an antibody sync. It could have been helpful. The active form of TL1A is the trimer, you'd think that's what matters.
Truth told, in my opinion, it just, it seems like it's fine either way. Their data are also pretty compelling.
I guess from the data perspective, you know, it seems like It works in both the all-comer population and the biomarker positive population. What's the latest thoughts on just how you would move forward into phase III? Would you only focus on biomarker positive? What could be the next rational step for you?
It's a great question. Look, I think there was a version of this data where the placebo-adjusted deltas for the class were in, like, the low teens, and the biomarker was necessary to have a compelling drug, right? You get a 10-point delta, you'd be in the twenties, you'd be like, "Okay, we've got a drug here." That's not the world we live in. The world we live in is that TL1A is clearly an important target in an all-comers population, and the 20% deltas that we have are, in our opinion, sort of strongly justify that this drug should be developable as a first-line all-comers drug, not specific to the biomarker population. That's definitely how we see it. That said, the biomarker is interesting. Our biomarker, in particular, covers a pretty broad range of the patient population.
It covers 60% of eligible UC patients, which is quite a number. We look at it and we see, we see opportunities in both settings. I think you can bet that our phase III program will not focus just on the biomarker. It'll focus on an all-comers population, but that we will study the biomarker prospectively and that we think it provides an opportunity for competitive commercial differentiation, especially because our biomarker covers, let's say, a larger portion of the patient population and still delivers a pretty impressive delta relative to our sort of all-comers patient data.
Great. Maybe switching gear to VTAMA. You're now over seven months now, right, into your VTAMA launch in plaque psoriasis. What are the key dynamics that you're seeing? With the first PBM contract secure, can you shed some light on how that's opened up access for VTAMA?
Yeah, look, we're super happy with that contract. I think it was always a question when we first launched the drug. We felt the profile of the drug was good enough that we were gonna get covered and gonna get covered with easy access. Obviously, that's something that I think the street kinda wanted to see from us. I'm now very confident based on the quality of that contract and the sort of context of other payer PBM conversations that are going on, that we're gonna have. You know, it may vary a little bit by contract. There'll be a spectrum, but, like, we're gonna have good access across the board and the patients are gonna be able to get VTAMA. That's an important milestone, honestly.
That's something that we sort of crossed over sometime this fall, sort of our internal confidence in that fact. I think that means that from here on out, it's an execution story on the payer side and a volume story in terms of getting out to as many patients as we possibly can. Yeah, it's a great position to be in. We're very fortunate.
Previously you talked about DTC is also a part of your push for VTAMA to push into plaque psoriasis. Where does that fit in? I think, at least from my point of view, I think I saw some commercial for VTAMA. Are you still ramping it up? How does that fit into your, you know, as you secure more PBM contracts in 2023?
Yeah, sure. It's a great question. Look, DTC is a part of the dermatology landscape, and many, if you watch TV, especially if you watch, like, network TV or cable or whatever, many dermatology products are heavily advertised. The Dermavant team is extremely experienced and has a lot of creative thoughts on how to sort of produce targeted DTC opportunities that will hit the specific patient populations we care about. Obviously, the business model for VTAMA is a little bit different than the business model for like a SKYRIZI. It's a different price, it's a different sort of patient population. I think you can imagine the Dermavant team is focused on tailoring the strategy to the nature of the product.
you know, the other thing I'll say is, we've done a little bit of DTC, I think enough to have a sense that it works pretty well and that it sort of patient demand is responsive to it. Obviously, DTC drives demand, but you wanna make sure you're driving demand for, let's say, commercially important scripts. We do sort of think a little bit about tailoring the DTC strategy to keep pace with the payer conversations so that you're not necessarily driving script volume to patients who don't yet have insurance coverage.
How does atopic derm fit into your strategy?
I mean, atopic derm is, as I said, it's a huge market. It's 320,000 prescriptions a week, and it's a market that is in some ways where psoriasis was 20 years ago, with just sort of DUPIXENT and some of the very first systemic therapies, becoming available. You know, one thing I'll say about the payer coverage, you were asking about access. These categories are in some ways sort of upside down for payers. These systemic therapies are very expensive. Prior to the introduction of VTAMA, it was quite difficult to control access to them because corticosteroids have relatively short duration labeling. Even if you wanted a patient to go through a bunch of corticosteroids, they could fail them relatively quickly just by following the label guidelines. There wasn't really a good tool.
One of the great things about VTAMA is no duration of use restriction on the label at all, so patients can be on it chronically, and if it works for them and they're happy, they can stay on it. You know, I think getting into the AD market early in that sort of journey before systemic therapy has sort of taken hold for as large a patient population is a great moment for us. The other thing about AD is, AD is a market that is driven heavily by young pediatric patients, infants, toddlers, really young people. You know, that's a very safety conscious for obvious reasons market. Tolerability matters, safety matters. Some of our competitor products historically have stumbled based on, like formulation issues and patient experience because young children care about that stuff.
You know, I think we have an excellent formulation and really strong safety data, at least in psoriasis. In our pediatric max use PK study, we studied our drug in young children with atopic dermatitis with body surface area up to 90%. Picture that for a moment. These are quite sick children, and we saw very little systemic exposure and really no safety or tolerability issues to speak of in that population. I think that will be an important aspect of our drug in addition to what we hope will be strong efficacy.
Maybe just switching gear into Immunovant. That's the company that you own, you own about 60%. As we look into the sector, one key data catalyst is argenx data for upregulator efgartigimod in CIDP.
Yeah.
coming up soon. Where you stand today, how do you see the potential read-through from argenx data sets to, you know, Immunovant's FcRn programs? Maybe just remind us, the audience, what is specifically that you're looking for from the 1402 read sometime later this year?
Yes. As far as CIDP data is concerned, look, the one thing I'll say about about argenx's data is IgG has been a superb biomarker for clinical efficacy in the FcRn class. If argenx shows good data based on their IgG suppression, we ought to also show good data based on our own IgG suppression. As you know, we can get to deeper IgG suppression, and so there's a chance that whatever efficacy they show at their level of IgG suppression, we can do better. I think that read-through was interesting, and I think it'll be interesting kind of where they fall out on that spectrum. Obviously, CIDP is also an indication where the field is learning rapidly about study design.
I think we'll learn a little bit from their results around sort of the clever study design that they've chosen, which we think is sort of an important milestone for the field. As far as what we are expecting from our own first in human data this summer in 1402, our monkey data suggests that we get the same kind of best in class IgG suppression in 1402 that we do with batoclimab, and that we get no or minimal impact in LDL and albumin. My hope is that we would just confirm those facts with 1402 in humans. If we do that, we think we have paths straight to pivotal studies based on that data, and the clear dose response that other FcRn antibodies, including batoclimab, show.
Have you considered pharma's offer on your Immunovant shares?
I don't think I can comment on whether we have gotten offers from pharma companies or not. Look, obviously it's an area that has attracted a lot of pharma attention. J&J bought Momenta a number of years ago. Look, we think it's an important class and there's a number of people out there with important immunology franchises and, you know, I hope and expect they'll take note, and we look forward to those conversations.
Okay. Maybe lastly on Priovant. Data coming up in the second half, in the fall. What should we really be looking for? Just remind us how does that compare to the JAK approach alone versus the type two alone?
Look, SLE has been a tough indication for a lot of companies over the years. Studies are hard to run. Execution's really important. And this is a study that was in part designed by Pfizer, so we didn't have sort of complete control of it. But overall, the biological hypothesis here is very strong, right? We have good data from JAK1. baricitinib put out pretty good data in SLE. We have good data from TYK2's. Deucravacitinib has put out good data in SLE. The overall quality of the data that we've got is high.
You know, this is a relatively coarse analysis, but in cross trial comparisons between Brepocitinib and deucravacitinib or baricitinib in each of psoriasis, psoriatic arthritis, UC and alopecia, where we have data about our compound and one or the other or both of their compounds, we are superior in sort of a cross trial read in each of those scenarios. I think like from a coarse grain perspective, there's reason to believe that we should be able to deliver some of the best data the world has seen in Brepo. It's also known that Brepo is mediated by some of those cytokines that are pairwise signaled by JAK1 and TYK2. I think there's also sort of a biological rationale there as well. What do I hope to see?
I hope to see, yeah, strong SRI-4 responder rates that justify onward development of the product.
What would we classify as strong?
Well, existing approved therapy, I think, is like 10%-14%. deucravacitinib showed data that on a pooled basis is maybe in the, you know, teens or low 20s. I think, I think baricitinib showed data in the teens as well. I think better than that.
Is this data set enough for you to file in SLE?
This would be one of two registrational studies. One of the important things in SLE is, don't run three studies when you can run two. Don't run two studies when you can run one. So we need to do two here, but this would be one of the two if successful, we believe. We've set it up that way.
Okay. Maybe just, before I let you go, you have multiple catalysts upcoming in the very near term. How should we expect just the cadence of catalysts?
If every year can be like 2023, I'll be very happy. We're gonna continue to do work in the business to add programs, to work on our capital allocation, to work on our development plans. I'm happy with what we did in 2022 to produce the 2023 that we have ahead of us. Yeah, we're gonna work on continuing to generate important data that matters to patients every year.
Great. I think we're at the top of our time together for the Q&A session. Thank you so much for joining us today at the conference. Thanks, everyone.