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

Good morning, good afternoon. Welcome to the Jefferies Healthcare Conference in London. My name is Dennis Ding, Biotech Analyst at Jefferies. I have pleasure of having Roivant, CEO, Matt Gline here with us. Welcome. Matt, so there's obviously been a lot of things going on with Roivant, right? You guys had a great deal last year around the TL1A sale by Roche. Congratulations.

Thank you.

And this year, you still have a lot going on yet. There's a perception out there that pipeline may not be worth as much as you'd like it to be. Still a lot of nice developments in NIU, Graves', et cetera. Those are all good. But -- just help us understand, I guess, what's been going on in the last year and your comments on some of the narrative that's been out there.

Yes, thanks. Thanks, everybody, for having me. Thanks, Dennis, for having me. It's great to be here again. We say we've been doing this for a number of years running. I appreciate the question. I'm trying to decide how to react because I feel like the bar for me is not pipeline worth as much as I'd like it to be. Pipeline worth anything would be a good place to be. So look, I -- first of all, I'll say, I continue to feel just unbelievably pleased with where we are as a business. We have a collection of really great late-stage programs between the FcRn franchise, obviously, brepocitinib, which has pivotal data coming next year in dermatomyositis. The LNP litigation, obviously, with a trial next year and a number of other programs, including the recently announced mosliciguat. So I think in terms of where we are from a late-stage pipeline perspective, I feel great, obviously, a lot of attention on our potential future BD activities. That pipeline is where the sort of collection of things we might do in the future is as robust as it has ever been, and we see some really tremendous opportunity. So on the fundamentals, I can't -- couldn't feel better than I do. It was the totally honest answer. And also -- and it's a complicated capital market right now. We have all the cash we could ever need to fund everything we have our eyes on, which is a great place to be. I think from an investor narrative perspective, it's hard to say in the sense that I think there's been a lot of attention on sort of waiting for the next deal and thinking, that's going to be a revitalization of the story. I think that's probably true in the sense that when we do deals, I think they will be attention grabbing. And I think we have some really great things on our racket. But mostly, we're just trying to execute every day and run the clinical trials that we think are good studies. And the thing that's great for us now is we're heading into just a totally stacked 18 months with data coming in multiple programs and a whole bunch of key catalysts over the next year or so I'm excited to play that out.

Yes. And I think like you said, BD is a big part of the story, I think, that people are focused on, given the massive amount of cash that you guys are sitting on. So talk a little bit about your BD, I guess, philosophy. You guys did unveil Pulmovant a few months ago. That deal was done, I believe, last year. Are there any changes in how you're thinking about in-licensing assets or multiple assets or therapeutic areas or anything like that?

Mostly, no. Look, I think -- this is Roivant's 10-year anniversary this year. We've been playing versions of this sport for the entire decade. And I think we've gotten better and better at it every time. And I think what we are good at is finding opportunities that we think are worthwhile for patients hiding in corners that many people aren't looking, often by partnering in we hope productive ways with big pharma companies, but not only. And to do that well, we're therapeutic area agnostic. I'd like to say we live in the the cookie dough that is outside of everybody else's cookie cutters. We live in the interstitial space between the Christmas tree and the snowman. And there's just been a lot of value for us in that configuration. Obviously, the most extreme version of that was with the TL1A that you mentioned. But we see lots of other opportunities that look and smell pretty similar, to be honest. And I expect we will do that again and again and again, if not exactly, then close in the years to come. And I think the reason that's possible is because we have this sort of no dogma go anywhere strategy that is not bound to a specific therapeutic area. And I think it's because we are very patient and looking for the right opportunities. So again, I think roughly the same as it's been before. I think we're looking for especially late-stage programs, especially things where we can design and run Phase II and especially Phase III clinical trials. I think part of our bread and butter is trials that have a higher cost associated with them where we can really be alone in -- or unusual in being able to take those programs on. And I think there's a tremendous amount of need in big pharma right now, for partners on late-stage programs as many of our larger -- many of the larger companies in our space are trying to manage earnings. So I think we're here for it.

And historically, you have been pretty transparent in terms of therapeutic areas and things like that. I think before you mentioned cardiopulmonary, rare diseases, and things like that. Can you remind us if that's -- if that's kind of still valid or any updated?

So we're generally agnostic. That said, certain things are easier for us historically than others. We historically have not connected the bat that much in oncology. I think the main reason for that other than every big pharma company has an oncology shaped cookie cutter, is that a lot of those portfolios are built in combination, and it's hard to build a proper combo portfolio out of the sort of deal here, deal there business that we're in. We -- generally -- there's some other things that are also sort of concentration businesses that sort of gene therapy, gene editing, cell therapy space where you can be absolutely right on biology, absolutely right on indication and still get run over by manufacturing steam roller, is something that we have struggled with historically and probably not top of mind for us, although definitely never say never. But other than that, we like a lot of things across a lot of therapeutic areas. We like -- you mentioned cardiometabolic and pulmonary. Obviously, we've done one deal in pulmonary already. We still continue like immunology and see things in immunology that we like. We continue to like rare disease. There's -- I think I said cardiometabolic, but especially cardiometabolic kind of outside of obesity, although there's even some things in the obesity world. But -- and then there's still parts of dermatology, we like, parts of inflam we like, just a whole bunch of stuff that we're interested in. We like -- and we're part of with Immunovant, but we like the emergent field, the sort of IgG and B-cell immunology and think there's a lot to do there as well.

Okay. And then how should we think about the timing of your next BD announcement as we go into 2025?

Yes. In general, I'd say we're hoping to do what I would call one small and one big deal a year. And a big deal for us is something that we're putting into like a late-stage pivotal study and a smaller deal is maybe something where we're making a smaller kind of a proof of concept bet. I think we are not yet through 2024 and have not quite hit that objective for 2024. I don't know if we'll hit it for this year or not, but that's kind of the pace that we're looking for. And I'd say we have a robust set of late-stage opportunities on our racket that we're excited about. So we're just trying to connect those and get them done.

Got it. Very helpful. So flipping over to Immunovant, and we're -- as we look into 2025, obviously, some MG data coming in early '25 that could be interesting as well as CIDP and TED. Can you explain to investors why that should be something that they should be excited about?

Yes. Look, first of all, I think the setup for Immunovant is pretty exciting because FcRn just continues over and over again to prove that it is an efficacious mechanism that it works in a variety of indications. Obviously, commercially, the doc enthusiasm for VYVGART and MG has been very high. And I think we would like to be in the front of the back in expanding that to a wide variety of prescriber bases. Look, I think in terms of indications for our commercial future, we're tremendously excited about Graves' disease where we generated data earlier this fall that we think -- look, we think it's impeccable, to be honest. We think it will make a huge difference for these patients in a field where there's basically nothing else and Graves' disease that has millions of patients of which probably 350,000 are like truly uncontrolled with every possible therapeutic option exhausted. And we showed in that kind of patient population that we can get close to 80% of those patients controlled and almost 2/3 of those patients, close to 60% of those patients off other background medications, which is -- it's -- in our view, it's field changing data that will change the paradigm here. So we're really excited about pushing that forward into pivotal studies. Against that backdrop, it's clear that one of the questions about FcRns is sort of how are they going to differentiate and what role is 1402 going to play in the space and the position that we've staked out very strongly is that we think deeper IgG suppression is always going to matter in delivering clinical benefit to patients, that it's going to matter to at least all patients in some indications and some patients in all indications is how I framed it. I think the thing that's interesting about the MG data, look, that thesis is, in my view, mostly not that controversial at this point. We've shown it in Graves' disease in our own data set. It has been shown by us in TED, it's been shown by J&J in Sjogrens, it's been shown by J&J in RA. It's been shown by UCB in ITP. It's been shown in a variety of settings. But to be fair, it has never been shown in MG. And MG is the indication for which FcRns are best known. It's the indication of requiring the least commercial imagination. And it will be the first indication where there is like a ready numerical comparison to do between Immunovant and efgart and the Argenx drug. And so I think for all of those reasons, there is real attention being paid to the quality of the dose response data in MG. Commercially, I don't think it's the most important data set in the world. It is a Phase III data for the first generation molecule while we're going to wind up progressing 1402 in the vast majority of indications. And MG is the most competitive indication we will ever be in an FcRn because it is the only indication where we are several years behind, but I think there was a proxy for the hypothesis and as a focal point for people to sort of draw their attention to where we can differentiate, it is certainly the biggest stage in which we've had a chance to show that. So I think that's why there's focus on MG. CIDP has similar dynamics. It's an indication for which Argenx is approved and on the market. It's an indication for which there is a high level of unmet need and where we have an opportunity to show a dose response. And so I think those are both important readouts, both coming in the first calendar quarter of next year.

So if I can put a finer point on the MG trial. Can you just put that data in perspective and should investors be comparing that to VYVGART. What would be a positive data set for you guys? Is it to be as equally efficacious as VYVGART or given deeper IgG suppression. Are you looking for better efficacy than VYVGART like what would be a positive data set for you?

For me, for all the reasons I just articulated. I think that data set is of intellectual interest in establishing a dose response. The thing that I'm most interested in is can we prove out -- and MG-ADL is a tricky endpoint requires retrospective evaluation. It's very much like I can you lift books over your head kind of thing. There's a lot of subjectivity to it. And so tricky endpoint, but the question for me is, can we prove out in a large enough study that we can generate real dose response there. So what I am looking for is a nice clean step function if we can generate one between placebo 340, which is a dose of ours that is very similar from an IgG suppression perspective to what efgartigimod does and 680, which suppresses IgG by high 70s, low 80s percent, which is more than efgartigimod can deliver. If we see a clear dose response there, that to me is like winning. I think at some level, what the investor community in its wildest hopes and dreams would hope for, is that not only do we see a dose response, but that the numerical placebo-adjusted deltas in MG-ADL response are like numerically greater at the high dose than efgart. I think it's like an interesting question. And obviously, if it's true, it will be very impactful. And unfortunate fact is that placebo response rates in MG-ADL have crept up over the past couple of years. And this is for obvious reasons, right? Everyone knows that FcRns work in MG now. So every investigator and every patient in an MG study with an FcRn expects to get better, and this is definitely an endpoint that has some impact of placebo. So I think you've seen that drift. I think that makes it a pretty high bar to say, hey, we're going to compare the high dose numerically to efgart. But certainly, in a grand slam outcome. It looks numerically better than efgart, and I think that puts a lot of the more as better question to bet.

Okay. And assuming the data is positive, you guys would probably move forward with 1402.

Yes.

And that's going to be a pivotal.

That will be a registrational program for...

Maybe second half of '25. Given that 1402 is still a number of years behind VYVGART. What are some kind of creative ways that you can design the trial so that when it reads out and you guys get approved, there could really be a commercial and marketing leg up over its competitor? Are you using -- would you use like an active competitor? Would you use VYVGART as one of the dosing cohorts?

Yes. These are all great questions on trial design. I don't have specific comments on how we're going to design the MG program I think in general, first of all, I would draw people's attention to the indications where we're not fighting with the competitor who's ahead of us. So I think that's like the first thing is focus on the indications, either like a Graves' disease where we can be first or like whatever, take Sjogren's where we haven't announced program yet, but imagine we were to do one, we could be in front of the pack. We could be sort of neck and neck with Argenx, if we got or J&J, if we got a Sjogren's study up and running. I think in some ways, MG is in the third bucket of indications where like we have to play from behind. So the first thing is like, this is the sort of hardest setting. I think to be clear, even setting efficacy aside, there are some baseline properties of 1402 that make it attractive versus efgart, including notably, we remain the only anti-FcRn antibody that will be a simple subcu auto-injector or at least on the current horizon. 1402 will be an auto-injector at launch of the same kind as DUPIXENT and many other large blockbuster drugs. It will be self-administered at home in all likelihood. I mean, this should be like a very straightforward and patient-friendly route of administration. And then on top of that, look, I think the ultimate hope from that study design, especially if we see a nice clear dose response in the Phase III for bato is that we can replicate that dose response and just show numerically good efficacy. I think it is certainly possible in a world where we show a quite good dose response to imagine ways of drawing the eye to the comparison versus VYVGART. You could imagine small head-to-head studies, you could imagine head-to-head studies and other indications, et cetera. But I think let's wait and see what that data looks like before we -- before I get myself in trouble promising to run a head-to-head study.

If we can shift over to Graves' because like you said, that's really an area of unmet need, not a lot of novel therapies being developed or approved there. Can you just help us understand the size of that market? How much of that is addressable, et cetera?

So Graves' is one of these indications that when you first try to wrap per head around, I think it's like legitimately hard to believe. Because it is -- and literally, there are millions of Graves' patients in America. I know Graves' patients, I think many people know Graves' patients. It's a relatively prevalent disease. And it's a crappy disease, right? So it's a disease -- it's a very straightforward FcRn disease. It's caused by autoantibodies that attack the thyroid. And when you have that happen, your thyroid hormone levels go out of whack, T3 and T4 and TSH go out of whack and you feel crappy, you feel tired, you can't control your energy, you can't control your food intake. You often gain or lose weight. It's a lousy -- that's a lousy presentation. The good thing about Graves' is for a long time now, a significant portion of the population has been addressable with some pretty old drugs like methimazole. These antithyroid drugs that are effectively designed to block an overactive thyroid and help normalize those levels. And for, call it, 70%, 75% of Graves' patients, they are controllable on and off methimazole and not the market that we're interested in for FcRn. The interesting thing is 25% or 30% of patients wind up effectively either refractory to or uncontrollable on ATDs. They just keep coming back to it, they can't get there. They are walking around with dysregulated thyroid hormone levels. And there are no therapeutic options for them after that. That's it. The opportunity set has been exhausted. The only other treatment available for those patients is to have their thyroid removed either surgically or via a radiation and then be on lifelong Synthroid, synthetic thyroid hormone levels as a sort of lifelong therapy to replace the lost hormones. So it's a crappy disease with relatively poor treatment options. And by the way, having out of whack thyroid hormone levels is not without consequence. These patients have elevated cardiometabolic risk, the elevated risk of certain cancers, it's like not a straightforward proposition. FcRn is perfectly suited to this problem. You can downregulate these IgG autoantibodies, you can restore function of the thyroid. And what we showed in our Phase II study was that for exactly this kind of patient population who is uncontrolled on ATDs that close to 80% of patients on 12 weeks of high-dose FcRn got to normal thyroid hormone levels and close to 60% of patients got to normal thyroid hormone levels while off ATD. So this is a phenomenal response rate for a patient population that literally had no therapeutic option prior to this and sets us up for a really exciting opportunity. And again, there are probably 350,000 of these sort of prevalent Graves' patients who meet this description and 20,000 patients every year having thyroidectomies or radiated thyroid. So you're talking about very large patient populations, especially in the context of where other competitor FcRns are now priced in the marketplace.

Right. And I think what's also interesting with Graves' is that there's not necessarily "bar" out there, right? Because there's not a lot of competition, standard of care is old and not great. So I would argue that as long as you hit stat sig and the data is clinically meaningful that you guys would have a very strong drug.

Yes, I totally agree. Look, this is not a competitive field. This is a field that -- and I'm proud of the fact that Roivant does this, but this is a field that I think like we identified internally and decided that it could be an interim -- obviously, we didn't identify Graves' disease, but we identified it as a treatment option for -- as FcRn as treatment option for it. And we sort of carved it out ourselves. We have had the discussions with FDA and regulatory endpoint. We've been able to define the field and by the way, one of the other great things about Graves' disease. The regulatory endpoint is a biomarker. It's T3 and T4 and TSH. It's a straightforward assessment of the performance of the drug.

Okay. Great. And if you take a step back and look at Roivant and all the various [ Vans ] and deals that you guys have done, you guys have kind of identified second-line plus refractory difficult-to-treat sort of population where there is a lot of need -- high unmet need and pricing power?

Yeah. Absolutely.

Can we shift over to Priovant?

Sure, yes.

A little bit? So you guys had some really promising NIU data. You guys are starting Phase III. Is that -- should people think about that kind of similar as Graves' because we were talking about refractory, no poor standard of care, et cetera?

Yes. Look, both -- so brepocitinib with Priovant is a very potent inhibitor, TYK2 in JAK1. We are studying it. It's got data in UC and Crohn's, alopecia, psoriasis and HS, I'm missing at least one psoriatic arthritis. It's a very, very powerful drug that we are developing in basically none of those indications. We have carved out a focus on orphan rheumatology and orphan immunology. The sort of lead or first indication there is dermatomyositis, where we have registrational data coming later this year. We can talk about it in a second. NIU is another indication that we sort of found for brepo, where we didn't have a lot of validating data, so we ran a Phase II study. And our hope was that JAK inhibition in particular, in the combination of JAK1 and TYK2 could be a powerful mechanism for improving the health of these patients. NIU is another one of these, yes, it's refractory orphan diseases. There's 400,000 NIU patients a year, of which 70,000 of them have sort of this back-of-the-eye inflammation that is difficult to treat locally. And those patients wind up on extremely high dose treatment of prednisone or of ISTs. And even then, those treatments are not necessarily successful. It is I think the third leading cause of blindness in the U.S. is uveitis. So it's a really high unmet need disease. The only real approved therapy right now is HUMIRA, which has about 30,000 patients treated a year. And HUMIRA bluntly doesn't work that well in NIU, right? The treatment failure rate at sort of 6 months of study in their data, if you measure it the same way that we measure ours is about 2/3, a little bit less than 2/3, compared with about 30% of patients failing therapy with brepo or their primary regulatory endpoint, which was time to treatment failure, half of their patients fail therapy after a little bit more than 5 months, whereas when we finished our study at 12 months, half of our patients were still being successfully treated on brepocitinib. So a real sea change in this refractory patient population. And the kind of price point that we see for other, let's say, rare ocular therapies like TED, even a relatively small percentage of the HUMIRA refractory market makes this a blockbuster opportunity. And these patients really need better options.

And given that HUMIRA is biosimilar, eventually, if this gets commercialized, how do you expect the positioning of brepocitinib relative to HUMIRA?

Look, the data is meaningfully better numerically in our Phase II study than HUMIRA. And [ eyedoc ] tolerance for ocular inflammation is very low. So I think patients and physicians will clamor to use this as early as they can in the treatment paradigm. That having been said, first of all, FDA's general position on JAK inhibitors and indications where TNFs are approved, is that you go through the TNF first. And second of all, with HUMIRA biosimilar, you can imagine payers might like that. But again, it doesn't work that well. And fundamentally, close to 2/3 of patients on HUMIRA fail it. And so even in a HUMIRA refractory setting where we were treated after -- we were used after HUMIRA, I would expect us to have a large patient population relative to the pricing of therapy.

Okay. And in the last minute or 2, maybe we can talk a little bit about DM, which is in Phase III reading out in the second half of 2025. That's obviously a really big late-stage catalyst for you guys, yet I feel like at least based on my conversations with investors, it doesn't seem like people are -- have a strong view around it. I'm just wondering if you can provide some clarity on the Phase III top line, what's good data, what we're hoping to see?

Yes. As with many of these indications, dermatomyositis, 40,000 patients in the U.S., severe inflammatory disease with muscle wasting and a severe skin presentation. And ultimately, many of these patients die within 5 years. It's a very severe disease, very few treatment options. The only approved therapy that's novel is IVIg, Octagam Pfizer's IVIg. And so I think the bar here is success. The bar here is a stat sig study. And if we have a stat sig study, I think this will be an approved and relatively widely used medicine. JAK inhibitors are known to work in DM. There's an open-label study of tofacitinib that showed relatively decent the endpoint in DM is called total improvement score and JAK inhibitors, tofacitinib showed a reasonable total improvement score. They're also sort of widely used in JAK inhibitors, widely using case reports. So I think if we can show data -- it looks like IVIg or even better than IVIg in DM. I think we're both powered for success and also we'll deliver a study that should make a big difference to the many patients with dermatomyositis who are currently without options. And it's the only oral therapy in late-stage development for DM.

Got it. Yes, that's all very cool because you do -- we just went through 3 major events, all of them with pretty much a late-stage development, blockbuster potential yet the stock is trading where it is, and I can understand everybody's frustration there, but...

Well, look, to me, look, we're an $8 billion market cap company with $5.5 billion in cash and $2 billion in Immunovant stock. I think it's an opportunity. I don't know. Just is what it is.

All right. yes.

We are buying.

Great. Well, great. Thank you so much, Matt, for the comments, and hope you have a great conference.

Thank you very much, you too. Thanks for having me.