Good afternoon. Welcome back from lunch. To introduce myself, my name is Richard Wagner. I work with Jason Gerberry on the U.S. large cap pharma names. I am based in London. On behalf of my colleagues, Chi Fong and Dina Ramadane, covering analysts for Roivant and Immunovant respectively, I am pleased to welcome Matthew Gline, CEO of Roivant, for a 40-minute fireside chat. Thank you.
Thanks for having me. It is a pleasure.
Thank you for coming. Roivant has achieved several key milestones this year, including positive phase II readout of your once daily inhaled sGC, mosliciguat in PH-ILD, and approval of your TYK2 JAK inhibitor, brepocitinib in 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 12 months?
Yeah, perfect. Look, it has been a period of a lot of progress for us. It has been a great 12 months behind. We just, as you mentioned, got brepocitinib, now LISRAYA, approved, and we are making some real progress on the sGC on the pulmonary hypertension franchise. Look, coming up the next 12 months, very busy 12 months ahead. Obviously, one of the most important things for us is, with brepocitinib now on the market, we are in the early innings of that launch, but we want it to go as well as we possibly can have it, and so there is a lot of work going into making that successful.
We have some major clinical data coming in brepocitinib, including between now and the end of the year in non-infectious uveitis, where we have not given specific guidance on when, but relatively soon, we will have data from that phase III program.
If that's successful, we then file for registration there, that would be a second potential registered indication for LISRAYA, for brepocitinib. After that or in addition to that, we have a bunch of data and sort of goings on, as it were, for our FcRn programs at Immunovant, including later this year, updates on both the CLE program as well as probably more importantly, the D2T RA, the late line rheumatoid arthritis program, where we will talk about our development plan there and our path forward after putting out some good early data earlier this year. Next year for Immunovant is a huge year, with registration data, less importantly in myasthenia gravis and much more importantly in Graves' disease, which are major indications for us. Those are sort of upcoming data.
Other than that, I'd say major priorities here are getting everything else up and running, continuing to start new studies with pulmonary hypertension program and to initiate new indications for all the other drugs as well.
Thank you. That's a great introduction. I'd like to start with brepocitinib, or brepo. You mentioned one month into the launch in 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 are three weeks in, so there's really very little to say that's productive. I will 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, that has certainly translated into our early experience. What that means in terms of scripts and coverage and everything else, it's just too early to know. We feel great about what we are doing and optimistic that we are going to have a good outcome there. Slow and steady remains the guidance. Look, first time there has been a novel therapy launched in dermatomyositis in a very long time or ever, so it's just hard to know the unknown unknowns.
You mentioned scripts. 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. I think mostly we're focused on having the launch itself go well, having the patient experience be positive, having the reimbursements be positive, and letting the sales speak for itself over the medium term.
Good. Thank you. Do you see any read-through from the evolving competitive landscape for the commercial opportunity for brepo and DM?
Mostly, no. I guess the most obvious version of that question is, argenx put out their myositis data, whenever it was, late in the summer. 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 dermatomyositis subset. That said, I think their data in DM probably exceeded their own internal expectations. 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.
I think a reasonable expectation is they will have to run a study in dermatomyositis, potentially some sort of small bridging study similar to what they did seronegative MG. We will have to see. Our view commercially all along has been, look, this is an orphan indication with very high morbidity, with reasonable mortality, a lot of unmet need. I think a rising tide is going to lift all boats here in the sense of my hope is that they get approved. I think their approval will be good for us. I think brepo remains in DM specifically, excuse me, the drug in pole position. I think it would be good if they got approved as well over time. I think their data was reasonably impressive for what they clearly view as a secondary indication of myositis.
Okay, good. So turning to non-infectious uveitis, what outcome would you define as a good outcome for brepocitinib?
Yeah. So this is another indication where there has not been a lot of medical innovation, and so there is a lot of unmet need. This is the third leading cause of blindness in the U.S. It is a pretty devastating disease, and tolerance among the ophthalmology community around clinical information is very low because it can lead to blindness and permanent damage. The only sort of approved "novel" or next generation therapy is HUMIRA. There are about 50,000, a little bit less than 50,000 NIU patients currently on TNFs. Our phase II data was very, very good in cross-trial comparison. The primary endpoint in these studies is time to treatment failure, which is what it sounds like. In the HUMIRA studies, placebo was three months and change, and HUMIRA itself had, I think, 5.6 months time to treatment failure.
In our phase II study, we did not 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 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 III program sort of "better than HUMIRA" in cross-trial comparisons, it may not matter that much in the sense that HUMIRA has a pretty high treatment failure rate, and these patients are generally looking for new options relatively early into treatment. So I think we are going to have, as long as we are statistically significant, we should have a drug and a good commercial opportunity.
Within that envelope, 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 would you see it positioned commercially given that the TNF biosimilars are available?
Yeah, look, I think you got to assume that the default expectation here is that we live in a HUMIRA refractory or TNF refractory population, both from an access perspective and frankly, the FDA's general stance on JAK inhibitor and JAK inhibitor-related mechanisms in TNF-approved indications is that a TNF 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. I think because this indication can lead to blindness, because tolerance throughout the information is very low, I think it's possible if our data is good enough that docs would push aggressively for earlier line uses, and that may help both with the FDA, ultimately, and with payers.
I think as a reminder, with biosimilar TNFs available, et cetera, in a world where docs feel like they need to get patients through a TNF in order to get them onto an effective therapy, if our data is very good, I think you could just see TNF use increase as docs are trying to cycle patients onto brepocitinib 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. Again, there's 50,000 NIU patients on TNFs. Many of them have inflammatory comorbidities like an RA or an IBD or something like that.
If you are on a TNF for any of those indications and you develop an NIU, by definition on a TNF, there is nowhere to go but to move patients onto something else.
Okay. You mentioned soon, having the phase III 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. That puts us squarely in the second half of the year, the second half now.
Okay.
I have not seen any data.
Okay. No data in-house. Turning to IMVT-1402, the FcRn you mentioned, and you set up the different readouts very nicely. Starting with difficult to treat RA, expecting the randomized phase II data.
Yeah.
In the second half of 2026, you've guided to sharing a comprehensive update. Also cautioned that phase II may not look as great as the open label phase I data. Can you speak about the potential data scenarios if you hit or not in phase II, and what would be the implications for—
Sure.
—path forward?
As a reminder, this is sort of an interesting study. This was a study of our anti-FcRn antibody, IMVT-1402, in late-line treatment refractory RA. These are patients who have failed at least two biologics classes in RA. Think IL-6 inhibitors, TNFs, JAK inhibitors, et cetera. Many of them, I think 60%, had failed a JAK inhibitor, for example. These patients have few other therapeutic options, and are quite sick. The study we ran was a randomized withdrawal trial with an open label run-in period, followed by, for those who had achieved an ACR20 response in period one, they were then re-randomized, either a lower dose or they either stayed on drug, went to a lower dose, or dropped off altogether onto 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. 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%, the ACR20 responders, that means 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 ACR20. You've got all these patients who have achieved an ACR70 or an ACR50, who, in order to meet primary endpoint responders, have to drop down below ACR20. It just feels like a pretty high bar to imagine hitting statistical significance in period two, given the depth of response in period one.
What that means is what we said at the time about the period one data. I think period two from a data perspective is probably less informative than it could be because the period one data was so good. Now, the good thing is the likelihood that we're even an open-label study, spontaneous ACR70 responses don't occur in this RA population very often. Then we looked at period one data and we're like, "Okay, we have a drug. This is very likely some signal here." I think we'd like to see some amount of separation in the period two data that the patients who went 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's only 12 weeks long, so it's hard to know exactly. We'd like to see some separation in order to just make us confident about phase III. 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. I think success here looks like no red flags that would stop us from running a phase III study. 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 T-cell engager or CAR T kind of therapies, or 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? There's a pretty wide envelope from relatively small, hundreds of patients, a few hundred-patient studies, to the typical thing in RA development would be multiple 1,500+ patient RA studies. It would be surprising to me if FDA in this late-line population want us to run something more like that program, but we won't know until we talk to them. I think the big update later this year is going to be 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 III?
I think that is a question we will have to discuss with FDA. The Rheum Division is historically relatively conservative on that point, but again, this is a patient population with few options, and the data from the open-label one period, at least here, was impressive enough that it's certainly a conversation worth having, but I'm not sure what's the honest 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 Ts and T-cell engagers, where there will just be a preference to expose as few patients as possible in clinical settings without an obvious risk-benefit discussion to that kind of risk. I think we have that going for us as we go in front of the agency, where 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 IMVT-1402 need to demonstrate for the company to commit capital behind a phase III program?
Yeah, it's a good question. We've always described, and frankly, we described RVT-3101 the same way as well before we had the data. CLE really is an option bet. That is, it was never intended to be a heart 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 TLR7/8s included from Merck KGaA. There's a bunch of other mechanisms. A lot of those mechanisms have the advantage of being less frequently dosed than an FcRn. I think we have to not just think about what a successful study looks like, but how do we convince ourselves that we'll be commercially viable in a world where all those programs are coming?
There's a little bit of we'll know it when we see it on the answer to that question, but I think it's got to be pretty good data. 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've spent 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 a few of those bets.
Mm-hmm. You mentioned, I think clearing a lane was your analogy.
Yeah
Would you see this then as a broader validation of FcRn inhibition across the lupus spectrum?
Bluntly, no, in the following senses. One is specifically within lupus. Look, we know that FcRns can deliver some benefit in lupus now. Nipocalimab, for example, has generated positive data in a properly powered, much larger study in SLE. I think there isn't really a need to, quote unquote, "validate the idea" in lupus spectrum diseases. I think it's more of a specific referendum on CLE. Again, this study is fundamentally underpowered at some level in a way that makes it hard to treat it as validation in either direction, either affirmatively or negatively. I think the answer to that question is it's not that relevant.
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, Sjögren'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. Look, we picked CLE over SLE because SLE is tough, and CLE should be slightly less tough, but it's tough. I just think it's hard to overread 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, in itself, a relatively risky registrational program, just given the nature of lupus.
In 2027, you have the phase III Graves' disease readout.
Yeah.
What keeps you up at night operationally about the phase III 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. There's a lot of things that keep me up. 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 FcRn has ever been studied, none has clearer biology than Graves' disease, or more straightforward endpoints than Graves' disease, at least in terms of thyroid hormone levels." Graves' disease is the disease where anti-thyroid antibodies affect the TSH receptor and lead to an overactive thyroid. It's a relatively straightforward thing, and the disease is clinically managed on T3, T4, and to some degree, TSH, and that's sort of the focus of the study.
If you want to feel good, the biology is very clear, and our phase II data was unequivocal. If you want to feel less good, our phase II 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 conducted. We have very little information going into this study about the variability of these patients, et cetera. Among the things in the endpoint is an anti-thyroid 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. Look, I think there are real and meaningful risks associated with that study.
Biologically, the rationale for the phase II data was quite good, so I am pretty optimistic, and I think it is a less risky study than something like CLE or than D2T RA was before we got into it. I think of the major studies we are running, Graves' was definitely the riskiest.
Okay. Where would you see IMVT-1402 positioned in the current treatment landscape, assuming success in the phase III?
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 and you model Graves' disease as a commercial indication, there truly are, call it 350,000 uncontrolled Graves' patients in the U.S. who have exhausted every treatment option available to them. The truth is, for an FcRn, if you can get 5% or 10% share of that kind of market, you have a huge drug. I think, against that backdrop, these numbers just get unimaginably large very quickly. What do I think in terms of where we could be used? I think some of this is what we are trying to learn in the clinical setting.
I think there are, first of all, there's about 20,000 patients a year who have their thyroid surgically removed and confined to a lifetime of synthetic thyroid hormones. I think those are pretty good candidates for therapy, and at least before they have that surgical procedure, they might consider trying something like an FcRn. Then there's just a lot of patients who are either uncontrolled, meaning even at quite high doses of methimazole or other anti-thyroid drugs, they can't get thyroid hormone levels controlled, or who can get control on methimazole, 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 reasonable places for us to think about, and we're studying versions of them both in phase III.
When we talk with KOLs, they speak about the threshold of patients, focusing on patients who achieve thyroid hormone normalization. You had mentioned tapering—
Yeah.
—that may not go off of the anti-thyroid 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 Graves' disease. First of all, there are millions of patients with Graves' disease, and many of them can get adequately controlled pretty quickly on a reasonable dose of methimazole, and we're not even trying with those patients. We're not enrolling them in the study, we're not focused on them, et cetera. I think the real question is, in the 350,000 patients for whom methimazole is just descriptively not sufficient in one way or another, and I think the answer is, at that point, the threshold is not "displacing" methimazole. The threshold is just clinical meaningfulness. The threshold is just what level of normalization of thyroid hormones is going to be sufficient to keep 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 II study, I think close to 60% of patients were able to get off ATDs, or to reduce their ATD dose meaningfully while getting normalized from a thyroid hormone perspective. I think anything like our phase II data would be a grand slam lights out outcome for us.
Are you looking at drug-free remission as a value driver?
We studied it in the phase II, and we are studying it again in the phase III. There are reasons to believe in Graves' disease, taking a step back, that, well, biologically, part of what happens in Graves' is you get these negative feedback loops where the anti-thyroid hormones, the anti-thyroid antibodies attack the thyroid, the thyroid becomes enlarged and inflamed, and then that seems to beget a negative cycle of more autoantibodies. Methimazole, in many patients, can lead to remission because these patients are just not that, some of them, not our patients, but some Graves' patients wind up being not that sick with Graves' disease in a way where you use methimazole, the thyroid re-regulates, it shrinks down in size, and the body stops producing enough of these autoantibodies to have a problem.
It stands to reason then that for sicker patients, okay, you cannot treat them successfully with methimazole 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. I think that is encouraging. In our phase II study, we were able to get a pretty significant portion of patients under control in an off-drug remission. Remember, all of the patients in the phase II came in uncontrolled, and 17 out of 25 of them, I think, were still controlled months after the end, more than that maybe, were still controlled months—
17 of 21.
—17 of 21 were still controlled six months after discontinuation of therapy. I think we do have a possibility of some durable off-drug remission.
I assume that there is an open label extension that you would be able to—
In fact, one of our two phase III 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. It is not just an open label. We will generate placebo-adjusted remission data in the study.
Just a general question about FcRn. As we 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 indications, 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 can dig. But to be honest, first of all, FcRn biology is not actually that complicated. You are reducing the level of pathogenic autoantibodies in diseases where pathogenic autoantibodies are some level of disease driver. I think the burden is on the poser as far as arguing that there should be a threshold effect, and we have not found 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.
My honest view is there will not be a threshold effect, that in any disease, deeper IgG suppression will matter. The curve of how much it matters versus other things may vary from indication to indication. And bluntly, there is a commercial question, which is like, whatever, take myasthenia gravis. I think if you ran a head-to-head study versus VYVGART, we have a reasonable chance of winning just given the depth of IgG suppression.
Does that mean we would then win commercially? I am not sure. argenx is very well established, and VYVGART is a well-loved drug, and it helps control these patients. And, if our data is only marginally better, which who knows what our data will be, our MG study is coming out next year, it is just not obvious whether we can take a majority share commercially. I think we get some share commercially, but take majority is hard to know.
But in general, the answer is I think deeper IgG suppression appears to yield 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 autoantibody-driven disease. One learning of ours, as I said, is deeper IgG suppression seems to do 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 have really narrowed it down to patients who are still sick, who cannot be treated with anti-inflammatories, which I think is suggestive that a driver of disease for them is autoantibodies, and you are obviously also assessing the 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 brepo or IMVT-1402? Then, transitioning to mostly I actually did have one just on—
Oh, you did? Sorry.
Yeah. Just on 350,000 patients with Graves' 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 onto the trial quicker or easier?
Yeah. I will say, I think the problem with this indication for a lot of people is you start with 350,000 patient number, 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. I think it is just true, right? I think if you assume, whatever, 10% share of 350,000 patient market is 35,000 patients at an FcRn price point is a $12 billion indication. You could get big numbers very quickly. I think in practice, there is a bunch of different ways that cat will wind up getting skinned, to be a little worried about it. I think one is, I have mentioned patients who are having thyroidectomies.
I think obviously for that subset of patients, which is 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 and a lifetime of SYNTHROID. Also, I think, 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 the most obvious first patients, versus the patients who are sort of subclinically hyperthyroid or whatever, where their thyroid hormone levels are out of whack, but on a relatively low dose of methimazole, they are making it work.
That said, there are absolutely patients who are on chronic 5 mg dose of methimazole, who have been for years, and who are incredibly eager to put that chapter behind them. I think those patients are absolutely eligible to try something like an FcRn and see where it takes them.
Yes, another question.
So just a simple question, looking back, right? Historically, you've had a history of finding effective buyers for your assets, and now you have a fully developed commercial infrastructure in place. How do you then decide which assets to keep and which assets to probably sell to others?
Maybe you could repeat the question.
Sure
Since we're further from the microphone.
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 a 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. Look, I would hope most companies feel this way, but I would not trade our pipeline for basically any other pipeline in biotech. I think if you drew a chart of valuation on one axis and, I don't know, probability of exceeding $20 billion of sales on another axis, that 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 a ton of whatever.
They're like an obesity company with a ton of complicated, compounded commercial and clinical risks. You have companies like argenx 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 at a pretty unique opportunity. I think that is a pretty unique spot on that chart. I think it's 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 most focused on right now.
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 Roivant is ruthlessly economic in our decision-making and that everything has a price. If someone offered us tens of billions of dollars for mosliciguat tomorrow, we would take the call because it's what we're supposed to do. I think never say never, but I think our default here is to build something big and durable and not to sell these programs.
Okay. Next topic I wanted to touch on was mosliciguat, 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 for mosliciguat?
One of the good 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 brepocitinib is fully distinct from what we can do in the FcRn animal. We have, to the extent that we have resource constraints, and we do, we can't start 10 studies all on the same day. Those resource constraints are sort of by program, and I think the impetus at this point for all of these programs, including mosliciguat, 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. 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. Look, with mosliciguat, we made a decision to start the phase III study at risk about six months ago because we wanted to not be sitting around waiting if the data looked good. That decision would've looked dumb if the study had failed, and now it looks prescient because the study succeeded and we're all judged in hindsight. That means we probably have the capacity to turn our attention relatively quickly here to the second indication of mosliciguat. I think we're finalizing our work on that now. I think our view of what is optimal from a path perspective has probably changed given the high quality of the data we saw in the PH-ILD study.
I think we're just reassessing that ordering and prioritization. I think we've definitely next year, Graves' disease and MG will roll off at Immunovant. This year, NIU is rolling off at Priovant. I think as those indications complete, there is absolutely capacity to ramp up new ones, and then we can continue to hire and grow and build out the 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 each of 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 communicate the next indication. That's true for a variety of reasons. FcRn is competitive. It would not be surprising to me if argenx wound up running an RA study now that we put out the data we put out in RA, that they are running a Graves' disease study. I think maintaining the lead is helpful. Also just there hasn't been much reason to get out ahead of our skis on this stuff, so we haven't done it.
With the remaining time, just to conclude, what 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. There's other tricks up our sleeves that we haven't discussed very broadly. There's just like I'm personally incredibly focused on and excited about standing up additional indications, starting with brepocitinib, but across the whole portfolio. As I said before, look, you look at argenx 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 indications and running clinical trials, and we have three programs from which to choose from, all of which have broad enough biological activity to open up a bunch of doors. I think there's just a lot of value to that exercise.
Any last questions? Great. Thank you very much.
Thank you. This was fun. Appreciate it.