Roivant Sciences Ltd. (ROIV) Earnings Call Transcript & Summary

Good afternoon, everybody, and thanks for being here powering through towards the end of the day. There are 2 more days of this, so keep up the energy. My name is Albert Wong. I'm a Managing Director in Investment Banking at Morgan Stanley. I'm going to read a disclosure here. For important disclosures, please see the Morgan Stanley research disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. So let me get started. Matt, I think most people know who you are, but if you can just give a quick intro, and I will then get into the questions.

Thanks. Thanks for having me. It's great to be here. Thanks for having us at the conference. We only have to do this for one day, so you all have the marathon. We have the sprint version, which is great. I'm Matt. I'm the CEO of Roivant, which is a biopharma company that -- the truth is it's mostly trying to do what everybody else is trying to do, which is develop medicines that matter. We have some data coming real soon in dermatomyositis, among other things, and excited to talk about all that today.

Okay. Great. Why don't we just jump right into brepocitinib. It's data you said second half of '25.

We did. We are in the second half of '25. What we said about the timing there is the last patient, last visit in the study happened in July, which should be imminent. So brepocitinib, maybe just take a 2 second step back, is a dual inhibitor of JAK1 and TYK2. So these are relatively well understood, very powerful anti-inflammatory mechanisms. It's a drug that we in-licensed from Pfizer a number of years ago, and it's really the only late-stage drug of this kind and certainly one of the only late-stage JAK inhibitors to be going into kind of rare and orphan inflammatory disease. And dermatomyositis is a terrible disease, an inflammatory disease that presents with both a really bad skin rash as well as a muscle wasting that's secondary to inflammation. And we are really excited to be developing a drug there for a patient population with very high unmet need. And this is a registrational program. So if this data is successful, we think it should be sufficient for approval.

Right. And this is the -- it's called VALOR, right?

The VALOR study. That's right.

Yes. It's Phase III registrational. And dermatomyositis is an interesting indication. Can you talk about the mechanism and why you chose dermatomyositis as the first...

Yes, perfect. It's a great question. So DM, as I said, is an inflammatory condition marked by this rash and this muscle wasting. It's a sort of down the fairway inflammatory disease. We know from the pathophysiology that it's got a lot of interferon activity. And obviously, both JAK1 and TYK2 and in combination are interferon signalers. We know from other studies, there's a Pfizer drug called dazukibart. That's an interferon-targeted antibody that has shown reasonable data in Phase II. There's also some data from STELARA and IL-12/23 that shows activity from that mechanism. And we know that TYK2 is involved in IL-12 and 23 signaling. So it's a disease where we really had good reason to believe that both JAK1 and TYK2 are active components of the sort of -- are both active signalers that can mediate the disease. And so we thought it was a good choice from that perspective, having a JAK1/TYK2 targeted drug. It's an orphan disease. There's really not a lot approved. The only sort of current generation therapy, if you will, is IVIg. There's a Pfizer IVIg called OCTAGAM, that's an approved drug. But other than that, these patients are mostly treated with steroids and immunosuppressants, steroids and methotrexate and things like that. It's got a lot of comorbidities, a lot of bad sort of life effects. It affects people's ability to move, it affects their ability to go out in public. It's a really tough disease. It seemed like there was high unmet need. These patients are sick enough that even when we started the study back in 2021, 2022, it didn't feel like the black box class warning associated with JAK inhibitors were going to matter at all to the patient and physician population. That continues to feel true both based on our conversations with docs as well bluntly as there's lots of patients in somewhat less severe and more common diseases who are obviously using JAK inhibitors at this point. And so it feels like we're happy with that. And yes, it just feels like a high unmet need disease where there's also quite a lot of evidence that JAK inhibition as a mechanism specifically works, I should have led with that. There's been no large placebo-controlled studies, but there are now four investigator-sponsored studies, mostly with tofacitinib, but one with baricitinib as well and hundreds of -- literally hundreds, about 600 case reports of the use of JAK inhibition as a mechanism to treat DM patients, all of which show some combination of skin and muscle benefit for these patients. So it feels like a like a mechanism that the doc community is excited about and familiar with, but there's good preclinical rationale that there's some good clinical data and there's some good clinical data by proxy from some downstream anti-inflammatories. And so it feels like a really good place for us.

Okay. And are there others out there that are doing JAK and TYK at the same time because it seems like you mentioned a lot of JAKs that are...

Yes. So there are very few -- there are no other late-stage JAK1/TYK2s in development for any indication. There's some earlier-stage programs, but I think basically no other sort of Phase III JAK1/TYK2s. And I think there may be an earlier stage study from a Galapagos molecule in DM that targets both. But other than that, I think there really aren't any other DM studies in a comparable mechanism. Yes, so I think it's really just us there.

Okay. And I want to go back to some of the things you said about the clinical presentation and the use of steroids. So two separate questions. First one, maybe describe the Phase III, how big it is? What are your endpoints and what you're really looking for to try to solve part of the clinical presentation that you're seeing?

Yes, perfect. So the Phase III is a 240-ish patient study. It's got three arms, placebo, 15 milligrams of brepo and 30 milligrams of brepo. Our main focus is on the 30-milligram arm in terms of the drug arms. It is a 52-week study. That's basically what FDA requires at this point for studies in dermatomyositis. The regulatory endpoint in DM, not our choice, is an endpoint called TIS or total improvement score, which is one of these composite indications in immunology. It is itself a collection of a whole bunch of different scores on different components, some of which are individually multicomponent tests. It measures both skin activity and muscle activity. And some of the endpoints are very objective, things like muscle enzyme testing. Some of them are like sort of muscle activity testing where like the doc puts his hand out and the patient has to push up on the hand. So some of that's more subjective. Some of them are skin assessments and things like that. But that's the endpoint. TIS is not a great regulatory endpoint in the sense that it is, a, not particularly clinically relevant in the sense that no patient is invited, it's a change from baseline. So no patient is walking around thinking about their TIS on any given day. And then also because the change from baseline, it can only go up, it can never go down. It's an improvement score. And so I think, therefore, just in a normal distribution of patient outcomes, you're going to get some placebo response. But it is something that the end physicians are familiar with. And our primary endpoint is mean TIS, delta on mean TIS from placebo is really what we're solving for. And I think we measure a bunch of other secondaries, including some skin-specific measures like CDASI and other subsets of the DM TIS endpoints that are more specific to dermatomyositis. TIS is used across different versions of myositis or flavors of myositis. And we have an endpoint called DMOMS that is sort of a different cut of the roughly same data that's more DM focused. So we're looking to see improvement across those measures. That would include improvement across muscle symptoms, improvement across skin symptoms, really just things that make these patients' quality of life better.

Yes. Okay. And given the score has some subjective and objective endpoints, are you worried about high placebo rate or just some variability among the three arms? This is a powering question.

Yes, I am worried about that. Look, I think given all the supportive evidence, I'm hopeful the drug works. There has been some variability in placebo performance in DM studies. Placebo TISs have ranged from 20 to high 30s basically, which are pretty high rates of improvement. And so I think there is some reason to be worried about that. We've taken a lot of steps to try and mitigate placebo in the study. Probably there's a lot of sort of operational things, investigator training, standardization, just like spending a lot of time on trial sites, making sure they're doing things the same way as each other. But also, we have probably the most important thing is a mandatory steroid taper in the protocol that starts at week 12 and requires that all patients be below 5 milligrams of oral daily steroids by week 36. We have basically every -- 98% of patients successfully adhered to that taper. And so I think that should be helpful. It should mitigate some of the placebo risk and give us a little bit more of a chance to separate. We are the first late-stage DM study with a steroid taper in it. And so we don't know for sure how much it's going to help, but I think it should be a potentially significant benefit in the study. But I do think placebo response risk is the single biggest risk we're facing at this point until we see the data.

Right. And this steroid taper that you're having patients go through, have you seen this in other studies or previous studies in the past where you can, I want to say, predict what a patient will look like?

So in dermatomyositis, the answer to that question is no. There has not been a large study in dermatomyositis with a mandatory steroid taper. So there's like natural history studies, there's physician interviews you can do. There's like things you can do to sort of figure it out. But we don't have a lot of like placebo-controlled data to point to for steroid taper. This is obviously a mechanism used in a lot of other places in immunology to mitigate placebo response risk. So it's incredibly important to lupus studies, for example. It's been used in some other places. I think one of the reasons I get some of the investor questions about this is, there was a pemphigus study from an FcRn run that had a steroid taper that was maybe insufficiently strict and resulted in not being able to show a static difference. So I do think this is a mechanism that people use in other places.

Okay. And dermatomyositis is an indication that has very few drugs.

That's right. Yes.

So therefore, there have probably have been some failures. How do you look at your drug? And what have you learned, I guess, from the previous failures? Or how do you think you're different?

Look, it is an indication that has had some failures. It's not like lupus or something where the ground is littered with dead bodies. It's an indication that has been understudied, to be honest. So there's a handful of drugs in history. IVIg, as I said, is approved, but there are some other IVIgs that have failed. One of the things that I think we believe is some other people have used responder endpoints, especially TIS 20. Given the high placebo response rate, we find TIS 20 of a more challenging endpoint. And so I think we were happy to use the continuous variable to use TIS as primarily in the study and to put some of those other things in the secondaries. I think the steroid taper is another thing that we implemented after looking at those other protocols to try and keep placebo response rate more well managed. I think we thought a lot about the mechanics of that taper. One of the things that's different about our study than basically all of the precedent studies is that we have a 52-week endpoint. There was one other study that was intended to be a 52-week study that got cut off sort of midway through due to corporate issues for the company that was running it. But in general, these have been shorter studies. That's less a sort of intentional decision on our part and more it's just the way FDA has decided to go in studies for dermatomyositis. But I think it has some puts and takes associated with it and some facts about using the 52-week endpoint could be helpful.

Okay. Great. And...

Sorry, one other thing. We enrolled patients who both have active skin and active muscle disease. And that was an intentional choice to try and make sure we had sick enough patients to really get a full picture of them.

So the patient has to have both?

Both, that's right. Every patient is both skin and muscle presenting.

Got it. Okay. So we're looking forward to that data in second half. And let's just look into the future and assuming that's successful, what are next steps?

Yes. So DM is a great indication for us. It's successful, it's a good-sized opportunity. There's probably somewhere between 40,000 and 70,000 patients in the U.S. with DM. Like I said, not well controlled on the existing therapies. About 20% of those patients on IVIg and the rest are sort of floating around on other things. And so it's a challenged patient population, high mortality, a lot of comorbidities. So I think it's well set up from that perspective. It's a very concentrated sort of treatment paradigm landscape. There's about 200 DM referral centers that together treat more than half of the patients. So I think in terms of like field force kind of dynamics for a commercial product relatively straightforward. And the doc community likes this mechanism. They've been very happy with the study. JAK inhibitors are used to varying degrees off-label. There are some docs who use them very widely. Obviously, you see all these case reports in IIT that's sort of more evidence of it. So I think we have tailwinds for doc familiarity and enthusiasm, tailwinds from a concerted prescriber base. It's an open market without a lot of other competing therapies. There's some things like an FcRn efgartigimod that is coming later with the study that reads out maybe next year. But in general, I think it's sort of an open playing field. And we get to follow the playbook that other orphan therapies have now shown us, which involves a lot of patient support to make sure access is provided, lessons learned from Horizon and from Madrigal and from Verona and from others that I think we're going to take the heart and pay close attention to. So I think commercially, the picture looks good. If this data are good, we'll file -- I think we said that the NDA filing would go in sort of early next year. We hope for an approval in '27. So I think that's kind of what the path looks like from here.

Okay. And given the 40,000 to 70,000 patient population, how do people think about pricing for this?

Yes. Obviously, it's premature for us to give any specific pricing guidance, but IVIgs in DM are priced at $250,000 or something. And if an FcRn enters, obviously, FcRn is $500,000, $600,000 a year drug. So I think that probably sets some bookends from other mechanisms, and we would look closely at our data and think about where we want it to be.

Okay. And the FcRn one from argenx, do you know when that data is reading out?

I think it should be next year. They had a Phase II study that read out in June. That study is in a different patient population. It's sort of a pyomyositis study. So it's not just the end patients, but that data will come next year. They're maybe 18 months behind us or something like that.

Okay. Got it. Well, speaking of myositis and other indications, what are the other indications you're going after following dermatomyositis?

Yes. So for brepocitinib specifically, we have an ongoing pivotal program in non-infectious uveitis, which is an eye inflammatory disease, quite prevalent. There's about 400,000 patients with it, about 70,000 of which have the particularly difficult to treat back of the eye form, poorly controlled. The only other sort of novel approved therapy right now is HUMIRA, which bluntly looks okay, not great. So I think there's opportunity. And we ran our own Phase II study in NIU that read out last year and it was truly exceptional. The data was really, really, really strong. We were very happy with it. And so we're now running a pivotal program with two Phase III studies that are enrolling very well, and we'll read out. Our current guidance is the first half of '27 for that readout. And so right around the time, we should be getting an approval in DM, we should also be stacking on data in the Phase III program for NIU. We also have an ongoing proof-of-concept study that reads out next year in cutaneous sarcoidosis and other very severe skin disease that if that data are positive, would pivot into a pivotal program thereafter. And we have a bunch of other ideas for places to go from here with additional indications for brepo, which has IP out to 2038, 2039.

Okay. And those indications also are orphan?

Yes. I think once you start thinking about this price point, we're looking for things that kind of fit nicely with one another, and there's lots of opportunity. Bluntly, look, when we in-licensed this drug from Pfizer, I think the general mood on JAK inhibitors was no one knew exactly that RINVOQ was a $3 billion drug. People thought it might flatline with the black box. No one knew where it was going to go. And our view was orphan was, a, a clean swim line. There weren't a lot of other JAK inhibitors looking at orphan and b, an area where people would care less about the black box. Sitting here in 2025, RINVOQ is a $7 billion drug on its way to $15 billion. The market has kind of spoken in terms of comfort with JAK inhibitors. And with maybe one or two exceptions, there's really no one else focusing on orphan disease with JAK inhibitors. We feel like we have just a ton of white space for a mechanism that is widely understood to work on not just a JAK inhibitor, JAK1/TYK2, it's slightly different. But anyway, the bottom line is I think there's a ton of places to go from here in terms of unmet need that will never be fully appropriate markets for the existing sort of broader market JAK inhibitors, but which feel like a great opportunity for brepocitinib.

Okay. Can we cover FcRn? .

Sure, yes. We have 10 minutes, let's do it.

Okay. Lots of indications. I think you're going after at least five, maybe six.

Yes, I think that's right.

Can you maybe go through so that people know?

Yes. So we have a couple of different anti-FcRn inhibitors at Immunovant. The sort of first generation one batoclimab has read out registrational data sets if we wanted to apply for it in MG and there's an ongoing program in CIDP. And then there's data coming in TED later this year. And then the second generation, which I think is probably the more important molecule in our portfolio, IMVT-1402 is currently in registrational development in Graves' disease, which is what I would think of as our lead indication as well as MG and CIDP. It's in a study in difficult-to-treat fourth-line rheumatoid arthritis. It's in a registrational study in Sjogren's. And it's in a proof-of-concept study in CLE, so six indications. Those range from, obviously, MG and CIDP extremely well validated for FcRns. Argenx is killing it commercially where, a, I think there's room for multiple molecules, even RYSTIGGO is like doing pretty well; and b, I think the deeper IgG -- our sort of main differentiator from the other FcRns is that we generally suppress IgG more deeply in practice. We get to close to 80%, whereas efgartigimod, for example, in most studies is sort of closer to mid-60s. And so we think that delta could, should, did in the case of our Phase II data lead to potentially impressively deeper responses. And so in an indication like MG and CIDP, the hope is to be -- we'll obviously be years behind them, but better. But then in an indication like Graves' disease, it's complete white space. We think we have the best drug. We have a great form factor, a simple subcu. And Graves' is just a patient population with an enormous unmet need. So that's -- we are the first of anybody really in Graves' development right now. We have this registrational study ongoing with other programs and other mechanisms kind of behind us at this point, but we think we get to set that stage. And we've generated Phase II data in batoclimab in Graves' disease that we're really, really excited about, up to including some data we put out for the first time last week, showing that the effect persists after discontinuation of therapy and gives a real remittive benefit that a significant number of these patients get to go off all drugs and still benefit from their time on our therapy. So we're really excited about Graves' disease.

Okay. And between you guys and Immunovant, how do you think about which indications are the most important? You have Graves' disease where you're going to be the first one and it's late stage, and you have proof of concept, but you take myasthenia gravis and CIDP where there's a drug on the market clearly doing very well. So how do you balance where your priorities are?

Look, I think there is no question that our top priority is Graves', which is -- first of all, there's millions of Graves' patients. There's probably 330,000 uncontrolled Graves' patients that is fully refractory, have failed every available therapeutic option. The only way for those patients to treat their Graves' disease at this point is either live uncomfortably or surgically remove their thyroid or irradiate their thyroid and then treat an underactive thyroid for life. And so these are sick patients who have no options. It's a huge opportunity, and we get to be truly first and our data is very good. And so there's no question Graves' is sort of the top of our priority list. I think in general, we're most excited about those indications where there's white space. So CLE is another example, at least in FcRn, where we would be the first FcRn and hopefully the best. Then there's a category of indications like a Sjogren's, where we are neck and neck, where we will not be significantly behind from a timing perspective and where we hope we can deliver a more efficacious drug given the IgG suppression. And then sort of the third priority bucket there is indications like an MG or CIDP, where on the one hand, I think there's a chance we deliver really, really great clinical data. I think that gets us real class share. But on the other hand, I think undeniably, argenx has done an amazing job commercially, and I think we will be playing commercially from behind in a category where docs are just like very familiar with and excited about what argenx has done. So I think those are tougher diseases, but where there's an opportunity for better if our clinical data sort of plays out the way that we'd like it to.

Okay. Great. And when we look at the broader anti-FcRn landscape, where do you see Immunovant and their role in the overall landscape?

Yes. Look, I think what we believe is there -- so first of all, one nice thing as a clinical developer of an FcRn is FcRn is actually a relatively difficult target to drug. And so as compared with CD19 T-cell engagers or as compared with anti-TL1A antibodies or whatever, where there's like quite a lot of those coming out of China and other places, actually, like there are not very many FcRns in development. And many people have tried and either there's some complicated things about the targeting of specifically the IgG binding domain, and this is the whole issue that [indiscernible] second generation versus the albumin binding is like a lot of this comes down to the specific construct, and then there's other things associated with making FcRn that are difficult. So the competitive landscape is not that broad. Of the other drugs, look, argenx is the undisputed category leader right now and that they are an approved product. They're selling close to $4 billion a year. It's been an amazing success. And I think our main goal is to prove that we can be better basically to prove that we can deliver better efficacy. I think the reason why we believe that's possible, as I said earlier, is we suppress IgG more deeply, and these are autoantibody-driven diseases where you would think the deeper you can reduce the autoantibody level, the better clinical benefit you'll see. How much will vary indication by indication, but we think we've shown across a range of indications at this point that patients with deeper IgG suppression have better clinical outcomes. So I think our hope is that we can deliver a best-in-class molecule. Now the nice thing about FcRn is in indications like Graves', not only do we hope to be best-in-class, but we will be first-in-class in essence, that we will get there first. Whereas indications like MG, we're just sort of necessarily playing from behind from a timing perspective. But I think our role should be we hope we have the best-in-class drug. We hope we are the HUMIRA to argenx and both, as it were. And I think there's a possibility that the world plays out that way, but the data has got to come together. There is another important benefit to our drug that's just worth highlighting, which is both batoclimab and 1402 are formulated into a simple subcu injection. Our sort of low standard dose is a single 2cc auto-injector, and 1402 will be an auto-injector at launch. Whereas efgartigimod is a higher volume Halozyme formulated subcu. And so the injection times are longer. They have a prefilled syringe. It's a longer injection time, and it's got some sequelae associated with being a Halozyme like injection site reaction. So I do hope our form factor will also be a real benefit, especially in an indication like Graves' where these patients are used to oral therapies and things like that. So I think we've got some form factor advantages as well, but I think the main benefit we're hoping to capture is clinical efficacy. Of the other ones, there are really two others that are currently approved products. J&J has nipocalimab approved in MG. Look, I think that's also an interesting drug. It's capable of suppressing IgG quite deeply, but it has the same albumin suppressing effect that our first-generation drug does. And so we believe it has LDL effects and other things. And J&J has responded to that by developing it at lower doses where it does not suppress IgG sort of as deeply as we do in the clinical doses currently being studied. And then UCB has RYSTIGGO, which is also a product, taking decent share in MG for a drug that is not first in market, but has some other -- it is a nice subcu, but it has some other sequelae, including causing headaches. And so those are really the FcRns in development, and we think we have a chance for best-in-class and first-in-class in a bunch of indications.

Right. Okay. We've gone down to the 10-minute mark. So I do want to leave room for questions. Anything more you want to say about brepo or the anti-FcRn?

No, I think we've covered those well, yes.

Okay. And last thing before I turn it open, internal versus external BD. You have a lot of pivotal late-stage data coming out. So do you need to do it? What are you looking for?

Yes. Look, we have always been an active company from a BD perspective. Everything we've talked about today as well as mosliciguat which we did not, our PH-ILD drug and almost everything we've developed in our history has been in-licensed or acquired. We think we're good at that. That is we think we have good relationships with pharma companies. We think we're a good partner. We think we're good at creative deal structuring to solve problems for our partners. And we are cash rich. A number of years ago, as you know, we sold anti-TL1 antibody, and we still have $4.5 billion of cash on our balance sheet today after $1.5 billion of share buybacks. So we have a lot of opportunity to spend on late-stage development and to be a good partner from a capital perspective as well. The environment is awesome. It's a complicated moment for big pharma with a lot of LOEs, a lot of transition, IRA and other, we call it, regulatory and political wins are causing reevaluation of portfolios. So it's been a great environment, frankly, for 1.5 years at this point. We've been pretty choosy given our capital position. So I think we haven't yet done a major deal, but there's some stuff we're very close to that we're excited about. And I think you'll see us active for sure, in interesting areas that we think are worth focusing on. Our pipeline also affords us a wealth of sort of BD opportunities. There's indication expansion possibilities in all of our mechanisms. And I think we are fortunate not to have to choose between our babies, we just have enough cash to do it all. And so it's really just a question of sequencing things out and when BD deals become possible.

Okay. Great. Maybe I'll turn it over to any questions from the audience here. Anyone?

What I've learned internally is that you feel very long awkward positive, eventually someone feels...

So we should keep waiting.

That's up to you.

No, maybe I'll fill it in the meantime, because I did have one last question. Do you think your future BD deals will look like the mosli deal you did last year? Is that a standard type deal that you would be doing?

Our deals have existed historically on a range of spectrums. We paid, in some cases, 9-figure sums for acquisitions of drugs. The mosli deal was of a phenotype where we paid relatively low upfront dollars for something. In that case, it was about, I think, $14 million with some sort of typical back-end royalties and milestones kind of things. We've also done deals like TL1A deal, which were equity splits where we kept 75% -- we got 75% or 80% of the economics or whatever, and our partner got the balance. So I think all of those structures are on the table. I think it is probably not the base case expectation that we would do like large public markets M&A. We have the cash for it. It's just a little naturally stingy, and it's been hard to find things that are interesting, especially in a world where we feel like we can partner with big pharma companies in these creative ways and just do deals that are more our style. But never say never, and there are definitely opportunities in the public markets that we've watched closely. Some of them off the run and some of them on the run. It just sort of depends on the circumstances. So I think we're pretty agnostic in terms of what we do, and there's some great stuff out there. Look, it's been a complicated year in the biotech markets. There are a lot of companies that need capital, some without access. So I think there's just a lot of opportunity around us.

Any questions? Okay. I'm going to ask one more. I don't like the silence. As we're talking about BD, you mentioned that you did $1.5 billion of share repurchase. So capital allocation, are you just seeing more value in your own stock? I mean that's the definition of a share repurchase is you're buying yourself over new BD ideas out there.

Look, we were in an unusual position after the sale of the TL1A. We had over $6 billion in cash on our balance sheet, which is an extraordinary amount for a company of our size and stage. And part of the answer to this question is, and I feel strongly about this, just as a matter of discipline. If we couldn't make it on four, we probably couldn't make it on six. There's just like a certain amount of just like math that says you've got enough cash, this is not going to come down to capital. And look, I think we've got some really -- like we've talked about brepo and DM. We have brepo and NIU. We have all these Immunovant catalyst. We have a litigation with Moderna with that lawsuit. The jury trial is next March, currently scheduled. There's like a lot of opportunity, and I thought it was good for our shareholders to own more of it. So getting the buybacks done leading into those catalysts felt good. But I think there was also, like I said, just a significant capital discipline component to it, which is we sort of had enough. I think we scoped out our existing pipeline. I think at the time that we did this analysis in earnest after the TL1A deal, sort of $2 billion felt like more than enough to develop that pipeline to profitability. We looked at the BD opportunities in front of us and another $2 billion sort of felt like sufficient to do the kinds of things we would want to do, which generally involve, again, relatively lower upfront payments, but potentially for late-stage programs with 9-figure development costs associated with them, and that felt like a healthy sum. And that's still just like left a lot of capital beyond and it felt like a reasonable time to return some of it to shareholders and the buybacks felt like a reasonable format.

Okay. Sounds good. Okay. Last chance. Any questions out there? Okay. Do you want to make any closing comments on that?

No. Just thanks for having us. It's always fun to do this. And look, I think it's conference season happens when conference season happens. I'm excited to actually get my hands on the brepocitinib data in DM and then to get back out and hopefully talk about how great it is, but we'll see what it looks like.

Yes. Well, I wish you luck on that.

Thank you. If you're religious and are looking for something to pray on this weekend, DM patients need to help. I don't know. I'm told it works no matter what you believe.

Okay. So we've been at that interpretation. Anyway, great to see you.

Thanks very much. Likewise. Thank you, everybody.