Roivant Sciences Ltd. (ROIV) September 2026 Conference Transcript

Good afternoon. Welcome back from lunch. To introduce myself, my name is Richard Wagner. I work with Jason Gerberi. I'm the U.S. large-cap pharma name. I'm based in London. On behalf of my colleagues Chi Fong and Dina Ramadane, covering analysts for Roivant and Amunivant, respectively, I'm pleased to welcome Matthew Glein, CEO of Roivant, for a 40-minute fireside chat. Thanks for coming. Roibon has achieved several key milestones this year, including positive phase 2 readout of your once-daily inhaled SCG, mostly Cigulat, and PHILD, and approval of your TIC2-JAC inhibitor, Repositinib, and Dermatomyositis. We still have multiple readouts coming up before year end. To help level set the discussions, what would be the company's top priorities in the next four months? Yeah, perfect.

So, look, it's been a period of a lot of progress for us. It's been a great 12 months behind. We just, as you mentioned, got Breb Sitnip now with Raya moved, and we're making some real progress on the SGC franchise. Look, coming up to the next 12 months, very busy 12 months ahead. Obviously, one of the most important things for us is with Breb Sitnip now on the market, we're in the early innings of that launch. What we wanted to go as well as we possibly can have it, And so there's a lot of work going into making that successful. We have some major clinical data coming in brebacitinib, including between now and the end of the year in non-infectious uveitis, where we haven't given specific guidance on when, but relatively soon we'll have data from that phase three program. And if that's successful, we then file for registration there. And that would be a second potential registered indication for Listeria for brebacitinib. And then, you know, after that, or in addition to that, we have a bunch of data sort of going on as it were for our fcrn programs at immune event including later this year uh updates on both the cle program as well as probably more importantly the ttra the late-line recur arthritis programs where we'll talk about our development plan there and our path forward actually putting out some good early data earlier this year and the next year for moon event is a huge year uh with the registration data right less importantly by city gravis and much more importantly graves disease. Those are sort of upcoming data. And then other than that, I'd say major priorities here are getting everything else up and running to sort of start new studies for pulmonary hypertension program and to initiate new indications for all of the other drugs as well.

Thank you. That's a great introduction. So I'd like to start with brepacitinib or brepo. You mentioned one month into the launch and dermatomyositis. What can you say about the launch experience? How is it tracking with your internal expectations so far?

Well, our both internal and externally disclosed path there is slow and steady. That's what we said over and over and over again. The truth is we're three weeks in, so there's really very little to say that's productive. I'll say what I think most investors know, which is if you talk to treating physicians, at least the KOL community, there's a ton of enthusiasm, and that is certainly translated into our early experience. But what that means in terms of scripts and coverage and everything else. It's just too early to know, but we feel great about what we're doing and optimistic that we're going to have a good outcome there. But slow and steady remains the guidance. Look, first time there has been a novel therapy launched into ratomysitis in a very long time or ever. And so it's hard to know the unknown.

You mentioned Scrib. So what type of launch metrics can investors expect on the earnings call? Will you present patient numbers, enrollment forms?

Yeah, what we've mostly said about this is that we're focused on the launch itself and focused on net sales as the ultimate judgment. We have not given specific guidance on what metrics we're going to provide. I'm sure we won't be able to help ourselves from providing some subset of that stuff. But the honest answer is it feels like companies have mostly not been rewarded for providing a lot of detail and guidance on this. And so I think, you know, I think mostly we're focused on having the launch itself go well, having the patient experience be positive, having the reimbursement piece be positive, and letting the sales speak for itself over the medium period. Good, thank you.

Do you see any read-through from the evolving competitive landscape for the commercial opportunity for Bravo and DEM?

Mostly no. I guess the sort of most sort of obvious version of that question is Argenix put out their myositis data, whatever it was, late in the summer. You know, I think prior to their receiving that data set, my sense is that their expectations for DM were relatively muted, and they had had more hope in IMNM. Indeed, they hit a p-value in the IMNM subset of patients as well as for the study overall and did not get a p-value in the amount of myositis subset. That said, I think their data in DM probably exceeded their own internal expectations. And, you know, it's clear from their body language and their voice that they would like to see the product approved in DM ultimately. I think they've been a little bit equivocal on what that's going to take from a clinical development perspective. But I think a reasonable expectation is they'll have to run a study around myositis, potentially some sort of small bridging study, similar to what they did through a negative MG. but we'll have to we'll have to say our view commercially all along has been look this is an orphan indication with very high morbidity reasonable mortality a lot of unmet need um i think a rising tide is is is going to lift all boats here in the sense of like my hope is that they get approved i think their approval will be good for us i think brevo remains in dm specifically excuse me the drug in pole position um but i think uh you know i think I think it'd be good if they got approved as well over time. And, you know, I think their data was, you know, reasonably impressive for what they could review was a secondary indication of myositis.

Okay, good. So turning to non-infectious luteitis, what outcome would you define as a good outcome for reposition?

Yeah, so this is another indication where there hasn't been a lot of medical innovation, and so there's a lot of them that need. This is the third leading cause of blindness in the U.S. It's a pretty devastating disease, and tolerance among the ophthalmology, could be brought home information, is very low because it can lead to blindness and permanent damage. You know, the only sort of approved, quote-unquote, novel or next-generation therapy is Humira. There's about 50,000, a little bit less than 50,000 NIU patients currently on DNFs. Our Phase II data was very, very good. I'm a rough-shot comparison. And the primary endpoint in these studies is time to treatment failure, which is what it sounds like. And in the Humira studies, placebo was three months and change. And Humira itself had like, I think, 5.6 months time to treatment failure. In our phase two study, we didn't have a placebo arm, but our high dose was greater than 12 months on average treatment failure. That was as far as we measured. So a pretty significant difference from the Humira experience. I think that leaves a lot of room. I think even if we do not wind up being in the phase three program sort of quote unquote better than Humira and Crestron comparisons, it may not matter that much in the sense that Humira has a pretty high treatment failure rate and he's basically generally looking for new options relatively early into treatment. So I think we're going to have, as long as we're statistically significant, we should have a drug and a good commercial opportunity. And then within that, the better the data, the better we look comparatively. I think the better our chances are of earlier adoption earlier in the treatment cascade yeah that was my next question where where would you see a position commercially given that the tnf biosimilars are available yeah look i think you've got to assume that the default expectation here is that we live in a humeral refractory or tnf refractory population both from an access perspective and frankly the fta's general stance on jack inhibitor and jack inhibitor related mechanisms in tnf approved indications is that a tnf is the is the right first bet i think there's two important caveats to that one is until we've seen the data it's just impossible to know and i think because this indication can lead to blindness because power drop information is very low i think it's possible if our data is good enough that docs will push aggressively for earlier line uses and that may help both with the fda ultimately end with payers and i guess a reminder of the question more tns Seville, et cetera. In a world where docs feel like they need to get patients through a TNF in order to get them onto an efficacious therapy, where data is very good, I think you could just see TNF use increase as docs are trying to cycle patients onto brepsidin over time. So I think we'll have to sort of see how that plays out. But I think a reasonable base case expectation is that we live in a sort of TNF refractory world. And again, there's 50,000 NIU patients on TNFs. Many of them have inflammatory comorbidities like an RA or an IPD or something like that. But anyway, if you're on a TNF or any of those indications and you've developed an IDF, by definition, a TNF, there's nowhere to go with some of the patients on something else. Okay.

You mentioned soon, having the phase three soon. Can you narrow it? We have not given guidance beyond second half is the official guidance on it. We announced that the 52-week study had fully enrolled sometime prior to November of last year. so that was just you know squarely in the second half of the period the second half now so yeah okay i have not seen any data okay no data announced um so turning to uh 1402 the fcrn you mentioned um and uh you set up the uh different uh readouts very nicely so starting with difficult to treat uh ra collecting the randomized uh period two data yeah uh in the second half of 26, you've guided to sharing a comprehensive update. Also caution that period two may not look as great as the open label period one data. So can you speak about the potential data scenarios if you hit or not in period two and what would be the implications for the path forward?

So as a reminder, this is sort of an interesting study. So this was a study of of our NTF-0 antibody, MT4202, in late-line treatment refractory RA. So these are patients who have failed at least two sort of biologics classes in RA. So think IL-6s, TNS, JAK inhibitors, et cetera. Many of them, I think, 60% have failed in JAK inhibitors, for example. So these patients have a few other pharmacotherapeutic options and are quite sick. And the study we ran was a randomized withdrawal trial, open-label run-in period, followed by, for those who had achieved an ACR-20 response in period one, they were then re-randomized, either the lower dose, or they either stayed on drug, went to a lower dose, or dropped off altogether on the placebo. That was sort of a blinded randomized withdrawal period. Now, the period one data that we generated, the open-label data, was very striking. So of the patients in period one, about 70% of them achieved an ACR20, about 50% of them achieved an ACR50, and about 35% of them achieved an ACR70. Now, if you think about the period two population as denominated in that 70% of the ACR20 responders, that means like almost two-thirds of the period two patients had an ACR50 or greater response, and almost half or about half had an ACR70 response. The primary endpoint in period two was loss of ACR 20. So you've got all these patients who have achieved an ACR 70 or an ACR 50 who, in order to be primary endpoint responders, have to drop down below ACR 20. It just feels like a pretty high bar to imagine hitting statistical significance in period two, given the depth of response in period one. So what that means is what we said at the time about the period one data. I think period two, from like a data perspective, is probably less informative than it could be because the period one day it was so good now the good thing is the likelihood that we're even an open label study acr 70 spontaneous remission spontaneous acr 70 responses don't like occur in this ra population very often so that we look at period one day we're like okay we have a drug like this is very likely some signal here i think we'd like to see some amount of separation in period two data that patients who went into placebo lose response ideally faster than the patients who are still on drug. There is some tail pharmacodynamic effect where the drug in the first few weeks of that period is still working. The randomized drug period is only 12 weeks long. So it's hard to know exactly. We'll see if we'd like to see some separation or just like make us confident about phase three. Other than that, I'm not sure we're going to learn that much from the clinical data here, given what we saw in period one. So I think like success here looks like no red flags that would stop us from running a phase three study. And then the real question mark isn't so much, what is the period two data? The real question mark is, what is the development path forward for the drug in this subset of RA patients? It's a subset of RA patients for which there have been vanishingly few clinical trials run. There's one or two ongoing now, mostly in like T-cell engager or CAR-T kind of therapies where there's B-cell depleting therapies where the risk profile looks pretty different. I think the question for us, for the agency, is what are you going to try and make us do? What are we going to be comfortable with? And they're a pretty wide envelope from relatively small hundreds of patients, like a few hundred patient studies to the typical thing in RA development would be multiple 1,500 plus patient RA studies. It would be surprising to me if FDA in this late-line population wanted us to run something more like that program, but we won't know until we talk to them. And I think the big update leader is going to be like, what have we aligned on with FDA? I think it is imaginable that FDA could dig their heels in in a way that would make us question the program overall, but the most likely outcome is we get comfortable with some kind of middle ground and we go forward. Do you think you could bottle on a single phase three? I think that is a question we will have to discuss with FDA. The room division is historically relatively conservative on that point, but again, this is a patient population with few options, and the data from the open level 1 period, at least here, was impressive enough that it's certainly a conversation worth having. But I'm not sure where it's the answer here. Thank you. I do think we will see other drugs in this patient population approved with comparatively small and comparatively few studies because some of those drugs will be CAR-T's and T-cell engagers where there will just be a preference to expose as few patients as possible in the clinical setting without an obvious risk-benefit discussion to that kind of risk. And so, you know, I think we have that going for us as we go in front of the agency. We're like, they're clearly going to be focused on streamlined studies in this patient population, which I hope we can take advantage of.

Thank you. There's also the cutaneous lupus or CLE POC headline data at the end of the year. You've described CLE as a commercial hurdle as well as a scientific one. What would 14.0T need to demonstrate for the company to commit capital behind a phase three program?

Yeah, it's a good question. And we've always described, and frankly, we described EGTRA the same way as well before we had the data. CLE really is an option bet that is like it was never intended to be a part of the thesis kind of a thing. it was about the upside skew. And to your point, that's in part because, look, CLE is not just about the state of the field. There's a lot coming. There's the BDCA2 from Biogen, there's TLR78s, including from RKJAA, like a bunch of other mechanisms. A lot of those mechanisms have the advantage of being less frequently dosed than an FCRN. And so, you know, I think we have to not just think about what a successful study looks like, but like, how do we convince ourselves that will be commercially viable in the world where all those programs are coming there's a little bit of like we'll know it when we see it on the answer to that question but it's got to be like pretty good data and bluntly i think it's not very likely we're going to clear that bar but that was the point all along if we clear the bar we've opened up a new swim lane for fcrn and that would be really exciting if we don't clear the bar we spend very little money on a small study and it didn't work out and that's sort of fine that's part of the portfolio that we're taking forward with FCRN is to have to deal with those benefits.

Yeah, you mentioned, I think, clearing a lane was her analogy. So would you see this then as a broader validation of FCRN inhibition across the spectrum?

Bluntly, no, in the following senses. One is specifically within lupus. Look, we know that FCRNs can deliver some benefit in lupus now. Nupacalumab, for example, has generated positive data in a properly powered, much larger study in SLE. And so I think, like, there isn't really a need to, quote, unquote, validate the idea in lupus spectrum diseases. And so I think it's more of a specific referendum on CLE. And again, this study is fundamentally underpowered at some level in a way that makes it, like, hard to treat it as validation in either direction, either affirmatively or negatively. So I think the answer to that question is, like, it's not that relevant. And then the other thing that I'll say is, insofar as an important question about FCRNs is how do they work more broadly in sort of multifactorial immune complex kind of diseases that involve, for example, RA fits in this bucket, Sjogren's fits in this bucket, CLE fits in this bucket, SLE fits in this bucket. I think the amount of data that has now been generated across these diseases is supportive of the idea that FCRNs can play a role in their treatment in a way where, again, I think whether this trial has failed or successful, it's not going to radically alter at least our view of what FCRNs can do with those kinds of diseases. And look, we picked CLE over SLE because SLE is tough and CLE should be slightly less tough, but it's tough. And I just think it's hard to over a single small CLE study. Again, I think the main question is just, do we see enough signal in this study to want to run? What will be itself a relatively risky registrational program? just given the nature of lupus.

In 2027, you have the phase three graves disease readout. So what keeps you up at night operationally about the phase three graves study?

Biotech is an industry that everything keeps me up at night all the time. I guess that's where I'm going with that comment. It's just biotech is a wood chipper designed to shred souls. So, you know, there's a lot of things that keep me up. But with Graves specifically, if you want to feel comfort about our Graves study, you would stand back and you'd say, okay, of every indication in which an Epstein has ever been studied, none has clearer biology than Graves' disease or more straightforward impacts than Graves' disease, at least in terms of thyroid hormone levels. Graves' disease is the disease where antithyroid antibodies affect the TSH receptor and lead to an overactive thyroid. It's like a relatively straightforward thing. and the disease is clinically managed on T3, T4 and to some degree TSH. And so that's sort of the focus of the study. So if you want to feel good, the biology is very clear and our phase two data was unequivocal. If you want to feel less good, our phase two data was a single site, roughly open label study run by one investigator in Germany. And that is plus or minus some TED studies, which aren't really the same patient population. The only modern study of Graves' disease ever were conducted. So we have very little information going into this study about the variability of patients, et cetera. And among the things in the endpoint is an antithyroid drug titration criteria, which rhymes with all of the challenges people have always had in immunology trials, titrating people down on steroids and other things. So look, I think there are real and meaningful risks associated with that study. Biologically, the rationale of phase 2 was quite good. So I'm pretty optimistic. And I think it's a less risk study than something like CLE or than DGTRA was before we got into it. But I think of the major studies we're running, Graves was definitely the risk test. Okay.

And where would you see 1402 positioned in the current treatment landscape, assuming it's exhausting like phase 3?

Yeah, this is the crazy thing about Graves' disease, which I think we have struggled with a little bit, to be honest, is if you sit down any model graves use as a commercial indication i mean there truly are call it 350 000 uncontrolled graves patients in the u.s who have exhausted every treatment option available to them and the truth is for an fcrn if you can get five or ten percent share of that kind of market you have a huge huge huge drug and so i think uh against that backdrop these numbers just like unimaginably large very quickly what do i think in terms of where we could be used i think some of this is like what we're trying to learn in the clinical setting but you know i think there are first of all there's about 20 000 patients here who have their thyroid surgically renewed to a lifetime of synthetic thyroid hormones i think like those are pretty good candidates for therapy and at least before they have that surgical procedure they might consider trying something like NFCRN. But then there's just a lot of patients who are either uncontrolled, meaning even at quite high doses of methimazole or other antithyroid drugs, they can't get thyroid hormone levels controlled, or who can get control on methimazole, but who deal with, but can't get off methimazole and deal with a lot of negative side effects associated with methimazole. I think both of those populations are like reasonable places for us to think about, and we're studying versions of them both in the phase three.

When we talk with KOLs, they speak about the threshold of patients, focusing on patients who achieve thyroid hormone normalization, and you had mentioned tapering, that they go off of the antithyroid drug. What threshold do you think would be needed to displace methimazole in first-line?

I don't think we will displace methimazole in first-line treatment of grave disease. First of all, there are millions of patients with Graves' disease, and many of them can get adequately controlled very quickly. I don't know a little bit of a reason to put those with them as well. We're not even trying for those. We're not really studying. We're not focused on them, et cetera. I think the real question is, in the 350,000 patients for whom with them as well, it's just like descriptively not sufficient in one way or another. And I think the answer is like, at that point, the threshold is not, quote unquote, displacing with them as all. The threshold is just like clinical meaningfulness. threshold is just like what level of normalization of thyroid hormones is going to be sufficient to get people on drug and how successfully do we need to get patients off ATDs for them to want to be on another agent. In our phase two study, I think close to 60% of patients were able to get off ATDs or reduce their ATD dose meaningfully while getting normalized from that hormone perspective i think anything like our phase two data would be a grand grand slam lights out outcome for us are you looking at a drug-free remission as a value driver we studied it in the phase two and we're studying it again in the phase three there's reasons to believe in graves disease taking a step back that well biologically part of what happened to graves you get these negative feedback loops for the antithyroid hormones but the antithyroid antibodies attack the thyroid the thyroid becomes enlarged and inflamed and then that seems to beget a negative cycle of more autoantibodies and methimazole in many patients can lead to remission because these patients are just like not that some of them not our patients but like some graves patients wind up being not that sick with graves disease in a way we're like you use methimazole the thyroid re-regulates it shrinks down in size and the body stops producing enough these autoantibodies to problem. It stands to reason then that for sicker patients, okay, you can't treat them successfully with Mimazol and get them into remission now. But if you could add on a layer of treatment on top of that, you might be able to actually regulate. And so I think that's encouraging. In our phase two study, we were able to get a pretty significant portion of patients under control in an off-drug remission there were all the patients in the face who came in uncontrolled and like 17 out of 25 of them i think were still controlled months after the end more than that maybe we're still controlled 17 of 21 17 of 21 we're still controlled six months after discontinuation of therapy and so you know it's uh i think we we do have a possibility of some dermal off drug remission And I assume that there's an open-label extension for you to be able to. In fact, one of our two-phase-three trials has a 12-month study with a six-month primary where there is a proper responder re-randomization to measure remission built into the study. So it's not just an open-label. We will generate placebo-adjusted remission data inside. side.

So just a general question about FCRN. As they move into increasingly heterogeneous diseases, what have you learned about which diseases for which deeper IgG lowering actually matters versus where you may be constrained by a ceiling?

We have studied this question ourselves in many and I appreciate that it is convenient for our competitors to talk about the existence of possible ceiling effects because they have limitations as to how deeply they but to be honest first of all FCR biology is not actually that complicated you are reducing the level of pathogenic autoantibodies in diseases where pathogenic autoantibodies are some level of disease drive I think the burden is on the poser as far as arguing that there should be a threshold effect.

And we have not found the one anywhere.

That is, in every indication we have ever studied, we have found, at least at the individual patient level, that patients with deeper IgG suppression had better responses than patients with lesser IgG suppression, which I think is what you would biologically expect. And so my honest view is there will not be a threshold impact that in any disease, deeper AIDS depression will matter. The curve of how much it matters versus other things may vary from indication to indication. And bluntly, there's a commercial question, which is like, whatever, take Myasthenia Grappis. I think if you ran a head-to-head study versus VivGuard, we have a reasonable chance of winning just given the depth of AIDS depression. Does that mean we would then win commercially? I'm not sure. Argenix is very well established. and VivGuard's a well-loved drug and it helps control these patients. And if our data is only marginally better, which who knows where our data will be, our DMD studies coming out next year, it's just not obvious whether we can sort of take a majority share of commercial that we'll get some share of commercial. If you take a majority, it's hard to know. But in general, the answer is that a deeper energy suppression appears to do a better benefit. You started out this question by talking about the complexity of some of these diseases in terms of being multifactorial, like rheumatoid arthritis, for example, which is not cleanly an auto-anibody. driven disease. I think a learning of that, one learning of ours is that deeper expression seems to be better all around. I think a learning specifically from our RA study is that patients who fail anti-inflammatory drugs and have high levels of autoantibodies may be specifically good treatment populations for us. And that you've sort of really narrowed it down to patients who are still sick, who cannot be treated with anti-inflammatories, which I think is sort of suggestive that a driver of disease for them is autoantibodies. They're obviously also assessing antibody level itself. I think that playbook, if it continues to look good in RA, could also apply in some other settings as well.

Any questions from the audience on REPO or 1402? Then transitioning to mostly SIBUAP.

I actually did have one. Oh, you did? Sorry. Yeah. Just on 350,000 patients with great disease, which are poorly controlled. Is there any further way that you segment that market as far as where this drug makes more sense, where patients maybe have come up to the trial quicker or easier?

So I'll say, I think the problem with this indication for a lot of people is you start with 350,000 patient number, and then you try and build a commercial model and it looks sort of silly any way you cut it, if you assume the drug is going to be successful. And I think it's just true. I think like if you assume whatever, 10% share of 350,000 patient market is 35,000 patients at an FCRM price point is a $12 billion indication. So like you could get big numbers very quickly. I think in practice, there's a bunch of different ways that cat will wind up getting skinned to be a little worried about it. I think one is, I've mentioned patients who are having thyroinectomies. I think obviously for that subset of patients, it was a relatively smaller group, I think about 20,000 a year. You can imagine people wanting to try a final therapeutic option before they move to a surgical procedure in a lifetime of Synthroid. But also, I think, you know, patients who are intolerant of methimazole or who need to be on such high doses as to be limited by the side effect profile, I think patients who are living with meaningfully out of whack thyroid hormone levels in a way that leads to real sequelae, I think those are probably like the most obvious first patients versus as the patients who are sort of subclinically hyperthyroid or whatever, or where, you know, their thyroid hormones are out of whack, but on the low-dose methimazole, they're making it work. That's it. There are absolutely patients who are on chronic five milligram dose of methimazole who have been for years and who are incredibly eager to like put that chapter behind them. And I think those patients are absolutely eligible to try something like an FCRN and see where it takes them.

Yes, another question. Just a simple question, looking back, right? Historically, you've had a history of finding attractive buyers for your assets, and now you have a fully developed commercial infrastructure in place. So, you know, have you then decided which assets to keep and which assets to probably sell to others?

Maybe you could repeat the question. Sure. The question was, in the past, on a couple of occasions, we have sold drugs that we have developed to third parties. Probably most notably, we sold the portfolio of drugs to Sumitomo Pharma back in 2019, and we sold an anti-TL1A antibody to Roche in, I want to say, 2023, 2024. I'll start by saying we are in an incredibly privileged position right now. I would hope most companies feel this way, but I would not trade our pipeline for basically any other pipeline in biotech and i think if you drew like a chart of valuation on one axis and i don't know probability of exceeding 20 billion dollars of sales on another axis but we are at a pretty unique corner there right there are other drugs that have some probability of getting there where the companies are less highly valued but they're just like a ton of whatever they're like an obesity company with a ton of complicated compounded commercial clinical risks you have companies like argenics or whatever that have obviously at some level a higher probability of those kinds of sales because they're commercial and already doing many billions of dollars of sales but they're valued much more richly than we are i think we're like at a pretty unique opportunity there is a pretty unique spot on that chart i think it's like a function of the programs that we have and i can't name any other biotech company where i feel like there's three drugs that are as credibly potentially as large as the three that we are focused on right now So I think parting with any of them would be a painful proposition relative to the unique opportunity in front of them. And I think our default case here is let's try and build something big and durable around this pretty unique moment for us. For those who have followed the company, I think you know that Reuven is ruthlessly economic in our decision making and that everything has a price. And that if someone offered us, you know, tens of billions of dollars for Mosley's Ziggoat tomorrow, we would take the call. because it's what we're supposed to do. So I think never say never, but I think our default here is to build something big and durable and not to sell these programs.

Next topic I wanted to touch on was the Cigulat. And you had mentioned that your culture is ruthlessly economic. You're not capital constrained.

How do you balance those dynamics as you build out the development plan? one of the things about how we're structured is in general once you get to executing a trial at least each program's resources don't cannibalize the other programs that is what we can do in pulmonary hypertension is fully distinct from what we can do in orphan inflammatory disease and prebacitinib is fully distinct what we can do in the fcr animal so we have to the extent that we have resource constraints and we do we can't start 10 studies all in the same day. Those resource constraints are sort of by program. And I think the impetus at this point for all these programs, including Mosley, is to get a new study set up as quickly as we possibly can. I think the value for us of indication expansion is extraordinary right now. It's zero upfront, relatively modest capital out the door. I think we're pretty good at choosing indications, pretty good at running studies. And I think that combination is really potent for what we think we can deliver. So look, with Mosley, we made a decision to start the phase three study at risk about six months ago because we wanted to not be sitting around waiting if the data looked good that just would have looked dumb if the study failed and now it looks prescient because the study succeeded and we're all judged in hindsight but that means we probably have the capacity to turn our attention relatively quickly here to like the second indication at mosley and i think we're finalizing our work on that now i think our view of what is optimal for a path perspective has probably changed given the high quality of the data we saw in the phld study and so i think we're just like reassessing that ordering and prioritization i think we've we've definitely you know next year graves and mg will roll off an immune event this year niu is rolling off a prior event you know i think as those indications complete there is absolutely capacity to ramp up new ones and then we continue to hire and grow and build up a clinical team the more we have data that reinforces our views. I think between those things, we should have the capacity to stand up new indications across all these programs in the coming months.

When would you communicate to investors what the next development phase would be?

We, in general, tend to wait until we've started a study before we can indicate the next indication. That's true for a variety of reasons. FCRN is competitive. It would not be surprising to me if our GenX wound up running an RA study. Now that we put out the data, we put out an RA, that they are running a grave study so i think maintaining the lead is helpful and then also just there hasn't been much reason to like get out ahead of our skis on this stuff so we haven't done it uh with the remaining uh time uh just to conclude what what uh excites you in the early pipeline we haven't talked much about anything other than those three programs and i'm probably not going to start doing that now there's bd stuff that we're excited about that we're close to uh And then, you know, there's other other tricks up our sleeves that we haven't discussed very broadly. And then there's, you know, just like I'm personally incredibly focused on and excited about standing up additional indications, starting with RepSynib, but across the whole portfolio. Because, as I said before, look, you look at Argenix added like $12 billion of market cap on their myositis data. The market is rewarding new indications. I think we're pretty good at choosing applications and running clinical trials. And we have three programs for which to choose from, all of which have brought enough biological activity to open up a bunch of doors. So I think there's just a lot of value to that exercise.

Any last questions? Thank you very much.