All right. Good day, everyone. Welcome to day one of Cantor's Global Healthcare Conference. For the next session, we are very excited to host the Roivant team. Representing Roivant, we have CEO Matt Gline. Matt, coming off the back of a very strong data set, happy to host you here.
Yeah, great. Thanks for having me. It's always easier to do these after putting out good data.
Great. Why don't we start there? First of all, congrats to your clinical operations team.
Oh, yeah. They've.
As well as your BD team who got this asset from Bayer for, what, $15 million?
About that, yeah, a little less.
What's the secret sauce?
I don't know the answer. If I did, I couldn't tell you.
Anyways, maybe focusing on mosliciguat first, given it's hot off the press, what were some of the more surprising aspects of the data set now that you've had some time to digest?
I've had like 36 whole hours. So look, for those that don't know, mosliciguat is a drug that we've had in development. It is an inhaled sGC activator that we are developing in pulmonary hypertension. It's a drug we got, as you mentioned, from Bayer a few years ago. I think what I said about this data set all along was if it worked, it was going to be obvious in hindsight that it was a good idea. If it failed, it was going to be obvious in hindsight that it was a bad idea. Because the truth is we know that inhaled vasodilators are generally effective in pulmonary hypertension. Also the only other sGC-targeted therapy ever tested in PH-ILD, riociguat, had a death imbalance against the drug and was harmful to patients.
That was obviously not a great setup, but our hope was that by delivering the drug in an inhaled format, we were going to have good efficacy. So we put out data yesterday morning, and the data was phenomenal. We had the deepest-ever PVR reduction shown in any pulmonary hypertension study. The study was very much not powered to show placebo-adjusted benefit in six-minute walk and very much did get a P value on that endpoint. So there's a lot to love in this data set, and overall, just the consistency of it, the hemodynamics working so nicely in concordance with the clinical endpoints. You just look at this, you're like, this drug was effective in this study. By the way, I don't know how familiar people are with PH-ILD as an indication.
These patients are really, really sick, so to be able to deliver this kind of benefit, I think it is going to change the field in many ways. Overall, the data was phenomenal. I would say the depth of hemodynamic responses in particular are probably the thing that has changed the most for me, in that they opened my mind to a much broader set of indications across pulmonary hypertension. Whereas I think if we had seen a narrower benefit, PH-ILD is still a phenomenal indication. We were thinking about IPF even before, but I think with data this good, you want to go broad.
Got it. The conversation has shifted from the clinical data to what is the size of the market and how big this product be in PH-ILD and maybe other indications as well. But maybe focusing on PH-ILD, what is the current market right now, and how many patients could be addressable with a drug like this? Yep.
Yeah. There is a range of estimates for the PH-ILD market. Our competitors have numbers out there that range from probably 30,000 patients in the U.S. on the low end to 100,000 patients on the high end. We probably think the market is on the higher end of that range, and we have not put out our own research yet. Could even be bigger if you really push me on it. PH-ILD has a lot of patients that are really sick, and the thing that you see in PAH, which is the much more developed pulmonary hypertension market, people have been treating PAH patients with novel therapeutics for decades, is the more drugs enter the market, the better every drug does. The patients are living longer, they are healthier for longer, they use drugs stacked on top of each other.
I think the idea that we can be a new class in the PH-ILD market, it should further expand upon the really good work now done by United Therapeutics and Liquidia and others who have got products on the market in PH-ILD.
Okay. You talked about the indication expansion. Given the strong efficacy here, clean safety, how are you thinking about the indication expansions, PAH, PH-COPD, IPF?
Yeah.
How do you prioritize the opportunities where you maximize the value for this asset?
Yeah, the first thing I'll say,
Aggressively.
I'm sure later in this conversation, we'll talk about brepocitinib and we'll talk about FcRN. I think a month ago, I would've said, okay, Roivant is a three-legged stool where two legs are bigger than the third. mosliciguat was kind of coming up from behind. I think this data catapults mosliciguat into approximately equal standing with the other two programs in terms of what I think it could be long term. It makes you want to think broadly, as I said. IPF was certainly something that we would've been thinking about even prior to this data set, just given what Tyvaso was shown and the nature of that market. I think what we would've said about PAH prior to seeing this data is PAH is competitive, and it's hard to know exactly where we would play.
Now that we have seen this data, I think the answer is clear. I think we should be an early line therapy for PAH patients if we decide to go there. I think we're evaluating that. We're evaluating other forms of pulmonary hypertension. PH-COPD, based on our subgroup data, is a little less scary, although many drugs have failed in PH-COPD. Then there's Group 2, Group 4, and Group 5 of pulmonary hypertension, which are more or less completely white space therapeutic areas that are now. We're rapidly working to come up to speed on those areas this week as we try and figure out where else we can go because it's phenomenal to be in this situation, but it's not like we anticipated the data would be this good.
Okay. What's the constraint? Is it capital, or is it just resources, or?
We're very blessed that it's never really been capital for us. We've just always run with a strong balance sheet, thanks to some deals we've done and so on. At the moment, I think in terms of getting these trials started, I don't mean to be trite, but it takes a lot of manpower to figure out what you want to do and run a phase III study. We have a lot of manpower, but we don't have enough manpower to start eight studies all at once tomorrow. I think that we've got to scale up, we've got to prioritize a little bit just to get things up and running, and we've got to figure out how to get the right people in fast so that we can grow the opportunity quickly.
Now, the other good thing about mosliciguat is we have IP into the mid-2040s, and so this is a long game, not a short game. But you really want to, whatever. Once you know you've got something you want to work on, the right day to start it is yesterday.
Yep.
In fact, one of the things that we did, which was going to look stupid in hindsight in a bad data scenario, and looks good in hindsight in a good data scenario, is we started the phase III study six months ago, so we are now enrolling patients. That is all up and running. We have got the protocol in place. The fact that we are underway there is a huge benefit, in part because it means we can probably be faster to start the next study because we are not starting at a standing start already.
Got it. So phase III, six months back, you said?
Well, yeah. I started with the planning process.
Okay.
Getting the protocol running. We are really just starting to enroll patients now.
Okay. Got it. Well, maybe we can move to the next leg of the stool, brepocitinib.
Sure.
Realize it's only.
Lisraya.
Sorry?
Lisraya.
Yeah.
I don't know. I'm trying to get you to call it by the brand name.
Yeah. I'm still getting used to it.
Yeah, me too.
Let's stick with brepocitinib.
Yeah.
Realize it's only been a few weeks, but any early feedback on the launch from the physician community and yeah.
We called all our physicians, and we asked them what they thought of the launch, and they all said the same thing. They said they thought the launch was going to be slow and steady.
Sticking with it.
That's right. No. Look, I think it's two weeks in. It's much too early to have anything useful to say other than even before the drug was approved, the receptivity from the DM community was extraordinary because of the high level of unmet need here. It's just exciting to be able to get out there with the drug after all of this time getting ready. I do think the DM doc and patient community are prime. Frankly, one of the reasons we've been so consistent with our slow and steady messaging is the docs have been doing a great job of getting everybody else onto a more aggressive message.
Yeah.
We've had to talk people back to the realities of okay, they say that, but they're going to take time to get their patients in the office, and they're going to take time to get their patients through the process. We've got to work with what we've got. But the doc community is very enthusiastic.
What about access? How quickly would you expect access to come in? Because it's a rare disease, high unmet need. Nothing is approved.
Yeah, look, at least initially, this is a patient-by-patient process, right? Each patient is sick. Each patient has a need. We have a patient support hub and a co-pay assistance program that are designed together to get patients on drug seamlessly. Initially, it's too early for me to know what the normal timeline is, but what I know is that we have a team that is committed to helping each patient that wants to be on this drug get on it in an economical and efficient way. I think as long as we're working together, we're going to be able to get them on drug quickly, and we're going to be able to get them covered, I hope, quickly as well.
Okay. Are there specific segments of the DM market that may need some more work to get on brepocitinib? For example, some of the feedback that we have got is some severe phenotypes that have just polypharmacy may be a little bit slower to adapt because it's a JAK. You have to make sure that the safety profile is fine. Based on your work, any specific subsegments of the DM market that you feel will need some work?
The first thing, and I appreciate this has been a consistently unsatisfying answer, is in terms of how different docs tell us they intend to use brepocitinib, there is actually, in a pleasing way, a fair amount of heterogeneity. There are docs who are big users of off-label JAK inhibitors and want to move all of their off-label JAK inhibitor patients over. There are docs who are big IVIG users, and their patients don't like the infusion burden of IVIG. There are docs that use neither of those things and have a lot of patients running around on very high-dose prednisone and are trying to get their patients to lower doses of steroids, and they really like the steroid-sparing aspect of our data. So I do think it varies a little bit practice by practice, patient by patient, in terms of who's going to get on drug early.
Look, I think one of the slightly complex dynamics here is some of the sickest patients are also the ones who are on things already. They're on IVIG. They're on an off-label rituximab or something like that. On the one hand, there are a lot of really good reasons that the docs and the patients have available to them as to why they might want to make a change. But on the other hand, if you're this sick, there's also a if it ain't broke, don't fix it kind of thing going on. So you're balancing those two considerations. That said, I don't think there's any one patient or group of patients that are going to be particularly hard to get on.
Look, obviously it will be easier to get more severe patients covered versus a patient who is reasonably well-controlled on low-dose prednisone or just methotrexate or whatever may wish to switch to brepocitinib for better disease control, but it may be a little bit harder to push those patients through from an access perspective. But in general, these patients are sick, and I think we won't have a lot of trouble.
Okay. One lingering, I think, investor debate in the DM market, and maybe relevant for some of the other markets where you are testing brepocitinib is these docs are all already using off-label JAKs, so why wouldn't they continue using off-label JAKs? Some of those are generics right now or will go generic in the future. Why would they prescribe.
Yeah.
A $400,000 drug?
I think you've got two things. First of all, as a reminder, and I think this is a really important point, brepocitinib is not a JAK inhibitor. It is a dual inhibitor of JAK1 and TYK2. These are largely interferon-driven diseases, certainly dermatomyositis is, and while JAK1 is relevant in signaling interferons, we do think there is likely a meaningful effect that comes from hitting both of these targets. And I think the doc community, by and large, believes that as well. They believe that this drug is as effective as it is in part because of that dual mechanism. I think against the backdrop of any JAK inhibitor, off-label tofacitinib that is basically generic or off-label RINVOQ that is definitely not generic, I think there's a general belief that we have a reasonable likelihood of being more effective.
There is an enormous amount of clinical data now generated by us around the use of brepocitinib, whereas all of those other drugs, you are just speculating on how well it is going to work. I think that is a driver of people moving over. As far as the practical realities of the world, look, putting a patient on off-label generic tofacitinib is not very hard in the sense that you can write the script and get it filled. It is not that expensive for the patient to fill it, although there is no co-pay assistance and no support program generally for those patients. Tofacitinib among JAK inhibitors is not like. Even if you think of brepocitinib as in the same pantheon, tofacitinib is a very minor deity by comparison.
I think you just have to understand that docs are not like, "Oh, I am so excited to get patients off label Tofa. I am not looking to consider new options." I think they want to put their patient on the most effective thing. I think in general, there is a belief that RINVOQ is, again, probably not as good as brepocitinib because of the fact that it is a single inhibitor versus the dual inhibitor of JAK1 and TYK2, but may be an effective drug. Getting a patient on off-label RINVOQ is extremely difficult. Payers are not there to help. In fact, it is basically medically challenging for payers to get patients on off-label drugs. Certainly they can never push an off-label drug over an on-label one. Docs and patients want the on-label therapy. They want the therapy that has been properly studied.
They want the therapy that has been characterized. I think that is why when you talk to some of these physicians and they have patients on off-label drugs, they want to switch them over. It is because they like the mechanism writ large, and now they want help getting their patients onto the most effective version of that mechanism that has been shown to work in this disease, and that is brepocitinib at the moment.
Right. There is also the medical liabilities of prescribing off-label.
For sure. Yeah.
Got it. I guess, how big do you think brepocitinib could be in DM? I know you are not going to put out guidance or anything or peak sales numbers, but street estimates are anywhere from $2 billion- $4 billion. Do you think they are at a reasonable ballpark compared to how are you thinking about it internally?
Yeah, look, my first comment on this is in terms of what I think needs to happen for brepocitinib as a drug to be a big and important franchise. I think there are plenty of numbers even below the lower end of that range, which if you think about the size of the wall and the number of bricks we are trying to put in it, even just already underway pivotal programs. We have DM, we have the NIU program that is going to read out shortly, we have CS, we have LPP. I want to add a bunch of indications beyond that. Whatever, if we wind up in seven or eight indications and all of them are only $1.5 billion, that is a really big drug.
I think it is not. It is much more important to my mind that we set up the drug well for the long run, that we get all these other indications up and running, that we get the patient support piece right, that we do not mess up access, that we get the pricing dynamics right, so that we can build the bigger thing as opposed to over-indexing on DM. I think DM has the potential to be a very large indication. I think people's enthusiasm is well-founded. There are at least tens of thousands and potentially many tens of thousands of DM patients. The unmet need is high. There has been a graveyard of therapeutic development, and even sort of on the come, we are a little ways away from the next entrant at all.
I think there's a lot of reasons to believe that DM rhymes with some of the other great opportunities that have come to biotech, where you can make a big difference for patients and generate a lot of value doing it. I think the upper end of the range that you described, above the upper end of the range you described, all plausible outcomes.
Okay.
The truth sitting where we are right now is that the error bars are wide because you're talking two weeks into the launch, not a single whatever. You're really early, so it's hard to know. You could tell me brepocitinib is going to be a $2 billion drug in DM, and you're going to be thrilled. You could tell me it's going to be a $6 billion drug, and you're going to be thrilled. You could tell me it's going to be a $1.5 billion drug, but it's going to be a giant drug in LPP, and I'm going to be thrilled. I think there's a lot of different good ways for it to go.
But I think the upper end of the range and beyond are certainly on the table given the quality of the data and the quality of the opportunity and the unmet need.
Great. That's a good segue to the other indication for brepocitinib, NIU. You have data coming hopefully soon. That's a big catalyst for Roivant as well. What are you hoping to see there in terms of is it just stat sig enough in NIU and.
Yeah.
Yeah, maybe we can start there.
I am knocking on a metal table, which is the wrong thing to knock on. The truth is that is probably wood. There we go. The data is coming. Hopefully, it will be good. NIU is another indication. First of all, today has been fun in part because we put out this great PH-ILD data yesterday. Yesterday it was a different investor conference, and most of the questions were about PH-ILD. Then I walked in today and I sat down and in my first meeting, there were 12 people in the room, and all of them were just grilling me about NIU because it turns out that is just the way this works. What have you done for me lately? That was interesting. I think NIU is a market where, first of all, the commercial potential is likely underappreciated at this point.
There are a lot of NIU patients. They are at a high risk of blindness and long-term complications, and the stuff that is out there by and large does not work very well. HUMIRA is the only really approved modern agent, and it has very high treatment failure rates. In fact, the time to treatment failure on HUMIRA in the study on average was 5.6 or 5.6 months, I think. Less than six months, and these patients are failing off therapy. So there is a huge amount of need. Bluntly, in order for us to succeed in a post-HUMIRA setting, I think all we need is simply to be successful. If we get a label for NIU in the post-HUMIRA setting where your choices are risk blindness or try brepocitinib, even pretty middling data would result in a commercial success.
The better the data is, the faster patients will want to get off other drugs and onto our agent. If our data is blow-it-out-of-the-water good, I have no doubt that docs will try and push for earlier line use. So there is a range of goodness in the outcome, but I think in order to be a commercially interesting drug, we just need to hit a P value.
Okay, got it. The third leg of the stool in the interest of time, immuno eng.
Sure.
The FcRN IMVT-1402. Two catalysts that are very important. I will touch on the first one, the difficult to treat RA part two. I feel like this readout has been talked about and debated a lot, maybe because in hindsight, part one was so good. Most scenarios, in my view, tend to be a positive outcome in part two. What would be a disappointing result in your view in the part two two of this difficult-to-treat RA?
I will say what I have said before, which is bluntly, I do not think we are going to learn very much from part two of this study at this point, because the part one data was quite good in a way that to me suggests we have an effective medicine that is doing something in these patients. We are going to run another study, and that study is probably going to have a more conventional placebo-controlled design, and we are going to see what it does in that setting and try to get it approved. We would do that almost regardless of what we see in period two of this data.
So I am not exactly sure how we will change the design of our next study, anything about the future of the program based on what happens in the randomized withdrawal period, given the quality of the data in period one of the study. The only thing I can think of that would be a truly disappointing outcome is if placebo and drug patient degradation of response looked identical in period two, and you are like, "Okay, how do I know the drug is actually working and this was not all some weird placebo fever dream?" I think that is extremely unlikely, because the truth is ACR70s just do not spontaneously happen.
So the depth of responses we saw in period one, which is what makes it potentially harder to hit stat sig in period two, is also the kind of thing that makes you feel like, okay, this is a quote, unquote, "real data set." But I think if we saw just parallel degradation with no separation of those curves, I would be like, okay, that is a little bit nerve-wracking for the next study. Other than that, if you see some separation, if the inflammatory markers confirm it, if the drug is clearly doing something relative to a placebo, then I think you are going to run the next study.
Actually, the major interesting question is not what happens in period two of the study, it is what can we agree on with FDA in terms of the right treatment paradigm in a population for which a registrational study has never been conducted before, which is to say, a population specifically restricted to multi-mechanism failure, where you would want to run a smaller study, potentially with a more stringent endpoint, and where the unmet need is high, so FDA might be comfortable with those sort of things. We would have to have that conversation. There is a pretty wide range of regulatory outcomes. That, to me, in some ways is the more, quote, unquote, "interesting question" than what happens mechanically in period two of the study.
Right. On that regulatory pathway forward, one study versus two study, does that make a lot of difference? Except maybe some capital and some resources.
Yeah. Look, I think the short answer is all else held equal, we would rather run one study than two, probably, and we would rather run a medium to smallest study than a very large study. If we had blow it out of the water stats on every endpoint in the randomized withdrawal trial, we would probably think for 15 minutes about whether to ask FDA if we could just run another randomized withdrawal trial, given the first one. Now, the FDA dislikes randomized withdrawal trials, so I think they would probably just say no. Anyway, that is a question that someone could ask. Other than that, I think one study versus two, big study versus small is mostly a question of time and cost.
I think barring something truly extraordinary in those interactions, we'll probably choose to run a study of some kind regardless, with more or less sponsor risk, depending on what FDA thinks we should be doing. We'll see. I think multi-mechanism failure RA has the potential to be among the largest FcRN indications. I don't know. I'm not going to sit here and choose between that and Graves' disease or whatever, but I think it's certainly one of the most exciting things we are working on. I think the opportunity to be there first in a big way for a population that's probably 75,000-100,000 patients with high need and a high willingness to try pharmacotherapy is great.
Yep. We agree it's a big market as well. You talked about Graves' disease. The readout is coming next year. Probably one of the bigger catalysts in the biotech world next year.
I agree with that.
You're creating a new category.
Yeah.
With this indication. Maybe one first question on the competition. Lilly bought Merida recently for their TSHR. Seems like there is pharma interest in Graves' as well. I think the one thing that we have talked about TSHR as a mechanism, as we think about FcRNs as well, it is more selective, but probably makes you hyperthyroid. But the argument that the TSHR companies would make is, all right, you can take SYNTHROID.
Yeah.
It is probably one of the most widely prescribed medications out there. It is not a big deal. We are way more selective. So what is your take on that?
First of all, I do not want to pitch for a competitor too hard. Merida is not a TSHR-directed therapy. Merida is a TSHR autoantibody-directed therapy, so it is effectively an antibody degrader for TSHR mAbs. I say that because I think the anti-TSHR, the ones you are referring to, like the Kineta small molecule or the, I forget, there is a couple other companies that have TSHR-directed mAbs. Look, I think those are going to work, obviously. To your point, I think my prediction is the way most of those drugs will be developed is they will be dosed to saturation, they will send people hypo on purpose, and then they will replenish with SYNTHROID. I think the answer is, does that have a role to play?
Look, if there is a patient who comes into an FcRN study with 100 times the upper limit of normal on TRAbs, and then we degrade their TRAbs by 80%, they will have 20 times the upper limit of normal on TRAbs. They will still be sick with Graves' disease, and we will not be able to cure them. It is possible that a TSHR mAb could shut down their thyroid, allow it to re-regulate, and actually, with SYNTHROID and enough dosing, they could potentially get re-regulated and maybe even off drug. I think for certain patients, the ability to go after it with a TSHR mAb could be helpful. I think right now we know most patients would prefer to be hypothyroid and on SYNTHROID relative to having the worst forms of hyperthyroidism and Graves' disease.
But mostly, they would prefer not to be hypothyroid and on SYNTHROID, which is why they choose to suffer through the side effects of methimazole and all these other things to avoid having a thyroidectomy and stuff like that. So I think in general, the TSHR mAbs will find a place, but it is just the direct targeting of TSH receptors, like a less elegant mechanism than targeting the autoantibodies, because it can send the patients hypo. On the autoantibody-directed degraders like Merida or some of the other approaches, that is also an elegant mechanism, and in theory, if you could selectively degrade 100% of the anti-TSHR autoantibodies, you would be better than us. But I think there is a whole bunch of scientific questions that nobody has answered yet around the heterogeneity of those antibodies, the side effect profile of these drugs.
So look, I think it is an interesting potential competitor. It is in the pretty distant future. Lilly must have seen something constructive in the data they were allowed to look at to do it. But it is just hard to know until we have actually seen what these drugs can do.
Right. And maybe coming to the phase III for Graves' disease, the mechanism makes a ton of sense. Ultimately, you are reducing the autoantibodies that are causing the disease, so it should work. But maybe some of the pushbacks on the prior data from investors could be that small sample, few sites, some of the sustained reduction in the thyroid receptor antibodies even after batoclimab was discontinued, but your IgG level comes up. So what is your take on some of these pushbacks?
Yeah, look, first of all, I am trying to think if the following statement is true. In Roivant's history, I think we have never run a study that is less biologically complicated than what we are trying to do in Graves' disease. Mechanistically, this is down the fairway. We are reducing autoantibodies in a disease that is like, look, every disease is more complicated when you scratch the surface, but pretty well understood to be caused by anti-TSH autoantibodies. So great. So I think the biology is actually pretty straightforward. I think there are reasons to be nervous about Graves' disease in the same way there are reasons to be nervous of anything, and I think idiosyncratically in Graves' disease or whatever, as is so often the case, our greatest strength is also our greatest weakness.
Simply the fact that we are first in this indication, which is an indication that's managed heterogeneously with varying levels of background with methimazole and other things, and we just don't have a lot of data with which to characterize these endpoints. I think that sort of dearth of information makes Graves' scary, and in fact, if we fail in Graves' disease, I suspect the reason will be, I hate to say this, but it's going to be a study design point. It's going to be just like there was something we missed in the characterization and study of these patients that the many people behind us as well as maybe we in a subsequent study would then get right again. We just had to take some bets based on our phase II data.
I think our studies are going to work for the reason that the biology is very clear, and I think we're running good studies, but that's the scary thing about Graves'. I think the fact that we are the first to run a late-stage placebo-controlled study ever in Graves' creates a measure of irreducible risk, no matter how well we think we've designed the study.
Okay. You're running two studies, so will there be ways to modify one if something goes.
Sure, yeah. Look, we'll get to watch both, and we can make changes potentially, and we can always run more studies. The first one, the short study, will almost certainly read out meaningfully before the second one. So yeah, absolutely, we've got choices. I think this is a real risk. I've gotten myself in trouble previously for pointing out that biotech's a risky business, but I think mostly I feel pretty good about these studies. We have a good track record of successful clinical development, and I think that track record is mostly that we're not cowboys and we don't take a lot of risk. So I think for us, the Graves' study is a risky study, but I think it's against a backdrop of most of our studies are in relatively well-categorized territory.
Got it. The timeline is still 2027.
Yep.
Should investors expect that you will narrow down the timelines at some point in the future?
Once these studies are fully enrolled and we are ready to announce that, we will announce that they are fully enrolled, and I think at that point, the timelines will become clearer.
Okay. Got it.
I have a question.
Go ahead.
As Immunovant becomes more mature, how do you think about it in terms of the somewhat unusual structure and for how much longer do you think it will continue to make sense?
Maybe I can repeat the question for the audience. As Immunovant continues to mature, how do you think about standalone versus maybe consolidating some of that?
Do you ask Sanofi that question about Regeneron?
No.
Regeneron's a big company. They're successful. They have a partnership with Sanofi. They've made it work. They've built a big business. I think the answer is if the drug works and it's commercially successful, lots of strange arrangements have persisted in biopharma for a long time on the basis of good medicine. I think one answer to your question is if this stuff works and it produces a successful outcome, then I think a lot will be forgiven. It is what it is. If I had a time machine and could go back and tell 2018 Matt Gline to not take Immunovant public and instead to own the whole thing, I'd also tell him about the complicated rollercoaster of a journey we'd have along the way, but I'd probably make that decision.
If there were a way for us to own all of Immunovant efficiently tomorrow in a way that made sense, look, we love the story. That's something we would always be thinking about at some level, but practically, the status quo is working well for us right now. Most importantly, I think it's working well for the drug right now. That is IMVT-1402 is being well developed. It is properly capitalized. We have the ability to capitalize it together with outside market participants, and I think the most important thing right now is to maximize the value of IMVT-1402 by running the right studies, running them well, and generating the best possible data.
Maybe if I can ask a follow-up on that, what would be the, I guess, obvious attributes to consolidate? There are synergies in terms of the markets that you both are competing in with even DM and IM where FcRNs have value.
I think those are all mechanically solvable problems if we need to solve them mechanically. The truth is from Roivant's perspective, you talk about myositis, we own 75% of Priovant, Pfizer owns the other 25%. We own 60% of Immunovant, the public markets own the other 40%. These things are different, but they're not so different that from Roivant, the trading as between them is a big economic delta that drives our incentives. Our incentive is to make the pie bigger, to make both of these programs as important as we can, and that is, I think, how we will act in every instance. Look, hindsight is 2020. We should've bought Immunovant when it was a $5 stock, and if Immunovant were ever a $5 stock while Roivant was a $42 stock, I think it would be a pretty easy decision from a concentration perspective.
The gosh darn it problem is that Immunovant is now also a $40 stock, and so the values are sort of moving up in parallel, and that means that every moment we just have to keep making that decision in a value-oriented way.
Oh, it's a good problem to have for both companies.
It is a good problem to have. By the way, they're both cheap, so.
All right. That's all the time we have today.
Subject to all of the appropriate securities disclaimers that I'm supposed to make when I say that.
Thanks, Matt, as always. Really appreciate the time. We couldn't get through all of these, all of the different pipeline indications as well, but there's a lot going on at Roivant right now.
Great.
So maybe in the future. Thank you so much.
Thanks so much. That was fun.