Welcome, everybody, and thanks for joining us here at the BofA Global Healthcare Conference in London. My name is Jason Gerberry. I'm one of the SMID-cap biotech analysts. Pleased to be introducing our next company presenter, Roivant, and CEO, Matt Gline. Matt, thanks for joining us. Thanks for having me. We're your first fireside since the brepo data. I think that's right. Yep, thank you for having me here. Imagine you're sleeping a little bit better. I know you're a little nervous about placebo effects and things like that going into the data. Now that everything's sorted out and you've got the result that you wanted, maybe that's a good place to start, talking about that data. If you want to maybe just contextualize that data, what it means for patients, how doctors you think will interpret the data, and what that means for the practice to ultimately DM. Yeah, thank you. I was sleeping better, and then I was like, this doesn't feel right. I decided to do a day trip to London instead, which will mess up my sleep, but good. Look, this was a big moment for us, obviously, but I think even more than a big moment for us, to be honest, it was a huge moment for the DM community. We have a slide in our data presentation. DM is just a graveyard of drug development. We went out to physicians, and we were like, hey, the study worked. This is what the data looked like. We literally had physicians choking up on some of these calls because they've been through decades of everything: rituximab and Stelara and all these other things, like RAND studies. We're not able to get across the line. You know, IVIG, there was a positive Octagam study, but I feel like that's viewed as an old medicine by the DM treatment community largely because they've been using it for a very long time. I think this is really the first time a novel targeted therapy has been successful in a registration of late-stage study for DM. I think that in and of itself is a major moment for patients. It's a sick patient population without a lot of good options. You think about IVIG, I think among the popular treatment regimens for IVIG in DM is a one week, a month, five hours a day regimen. If you think about what that means, like hold a job or whatever, it's very difficult to make work with most people's lives. Now there's a one pill once a day sort of compelling alternative. I think that's going to be important. Remember, the majority, the 75% of the patient population that is treated is treated on steroids and immunosuppressants. What we were able to show is a meaningful benefit against a backdrop of steroids and immunosuppressants while getting patients down significantly on their dose of background therapy. I think important in the sense that it's a novel option for the first time in a long time, important in the sense that the data was clinically meaningful, important in a field without a lot of other options. I think all around, just a really exciting package. Yeah. How do you see brepo getting adopted by clinicians? Do you anticipate they'll still usually start with steroids and ISTs, and then at some point look to down-titrate the steroids and onboard brepo, and that IVIG is kind of this last-line thing? You said it's really cumbersome. It's hard to give somebody IVIG on the schedules and in the IV infusion dynamics. Yeah. Look, practically speaking, for a variety of reasons, including that it's the right place to start, these patients will go on steroids and ISTs first. They'll do that for however long. I think in general, the answer is any patient who's pushing 10 mg or more of steroids on a relatively regular basis is going to be thinking, how do I stop doing this? It's an unpleasant experience. Frankly, it means at some level that treatment is not working the way they want. I think that entire patient population is sort of brepo eligible. People who are on IVIG are probably looking in some cases for a path off, just given the sort of regimen they're on. I think patients who are contemplating IVIG will want an alternative. There are a handful of patients on other things, off-label JAKs or off-label rituximab or something like that. Those docs, in addition to the fact that each of those drugs has own individual issues and the JAKs that are currently used are not particularly good compared to what I think brepo should have done here, I think the docs are doing a ton of work to keep patients on those therapies. The fact that a sponsor is going to come in with an on-label drug that has really compelling clinical data, I think, is going to create a positive opportunity for those. I think, you know, we track, call it, 35,000- 40,000 treated patients with dermatomyositis. Much of that universe, to be honest, is like eligible for treatment with brepo. I think docs will be thinking about it for a huge portion of that population. OK. You kind of see it playing in both segments of the world, the IVIG segment, as well as those who are on high-dose steroids and in need of an alternative. Is there an analog you can look to, to sort of a steroid-sparing benefit in the INI world? Like Tepezza is one example I could think of, of a drug that docs hated steroids, right? They went to Tepezza for TED. Yeah. Look, I think Tepezza is a great example because it's been so successful in TED, and the docs don't like steroids. Frankly, the steroids don't work as well. I think that's also sort of what we saw in our clinical data. I think we will see something similar in NIU, actually, those are both anti-inflammatory diseases. I also think like lupus is a good example of a condition where steroids are aggressively used as background therapy. You've got things like Benlysta. One of the labeled benefits of Benlysta is steroid reduction. I think a lot of what people are trying to accomplish with novel therapies for lupus now is getting patients off heavy steroid regimens. I think this is true for other conditions. I mean, I think it's true for patients with big systemic skin disease like psoriasis or whatever. I think it's like other conditions where patients have sort of systemic inflammatory disease where the name of the game has been getting patients off steroids. Yeah. OK. Maybe just how do you think about the prescriber base? Because you have derms, you have rheumatologists, you have a dermatologic aspect of the disease, right? You have a muscle aspect of the disease. Rheums have historically been much more liberal about using JAKs in RA and comfortable with the risk profile. Derms historically biologics and immune agents. I'm just kind of wondering, do you see this more as a drug for rheum's or both? I just want to have that. Yes. The first thing is DM as an indication is treated in a pretty concentrated fashion in the U.S. There's about 200 referral centers, some derms, some rheums, that wind up treating more than half of the patient population. The first thing is we just know all of those docs at this point. We've engaged with them. They've engaged with us. Whether they are derms or rheums, they are familiar with JAK inhibitors. There are JAK inhibitors used in derm too, obviously abrocitinib and some of the others that are approved in AD. There are analogs. I do think it's trivial for rheums, obviously. They, as you said, use it all over the place. I think are sort of itching for it. I think in DM specifically, both derms and rheums are excited for JAK inhibitors as a mechanism. I think it is helpful that the safety table for this specific study sort of showed the picture in a useful way, which is, look, the truth is this is a JAK inhibitor. It will have JAK class labeling. It will have, over the fullness of time, across the fullness of patients, it will have many of the JAK class sort of issues that those things will present in this patient population. What I think the safety analysis of this data set showed is this is just a sick patient population. Frankly, many of the sequelae either of dermatomyositis itself or of the use of heavy steroids are similar to the sequelae of the safety and tolerability concerns for JAK inhibitors. You look at our safety data for this trial and, bluntly, placebos or background steroids looked worse than the drug arm in the study. I think part of what that is a reminder of is these patients have a lot of these issues anyway. Treating their underlying disease and getting them off steroids will improve their profile on many of the same axes that we worry about with JAKs. I think that is a message that has already resonated with derms that we've talked to about the data set. I'm just not that worried about it. I guess the other thing is it's not like derms are otherwise reaching for Skyrizi for dermatomyositis patients. It's not available. It doesn't work. I think derms are just itching for things that will treat these patients well. I think the magnitude of effect on CDASI, for example, will just be the thing that matters most. Fast forward, you know, a year, a year plus, you're back to being a commercial company again. This is, I would assume, a pretty capital-efficient sort of call panel reach, if you will, in terms of promotion and promotional outlay. How do you see this? Maybe, you know, VTAMA had its own challenges, right, because of gross tenets and payer access dynamics and challenges, right? I imagine here, you know, how you kind of see the go-to-market outlook. This could not be more different than VTAMA in terms of the way the business is built. I think Organon is going to do a nice job with VTAMA. I think there's a real market there, but that's a low-priced ground game where you're shooting for high volumes and you're trying to get people. This is a rare disease launch. What do I think matters for this launch? I think the sort of physician relationships matter. The patient relationships matter. I think we've invested very heavily through the clinical trial in making sure that we're building those relationships. They're familiar with the drug. They're familiar with the medical literature. They're familiar with what we're doing. I think that's one piece of this. We've had medical professionals engaging with the doc community since we started the study. The other thing that clearly matters in these launches is patient support, right? I'd say the lesson, if the lesson from argenx and MG has been that doc engagement matters, I think the lesson that Horizon taught the world is that the way these launches go best is you see from day one, you're building a patient support organization that is helping these docs do the work to get patients covered. We've built a phenomenal team already to begin that process. We've got people who ran that effort for Horizon working for us now. I think that will be the other built-up piece of this. In terms of traditional sales reps or whatever, the truth is that you don't need very many. It's a concentrated prescriber base. It's more of a medical engagement conversation than a promotional conversation. A focus on those 200 referral centers primarily. First and foremost, I think there'll be a long tail of docs excited to use the product. OK. As we think about the pipeline and the drug aspect of brepo, what does de-risking DM do in terms of your thought process, in terms of other areas to go, and just remind us your IP runway on the drug. Do you feel like this affords you now an opportunity to interrogate some other indications and go more broadly with brepo? We have competition with extensions through 2039, so we've got plenty of room to run here. We are studying brepo already in two other publicly disclosed indications. We have a registrational package currently under study for non-infectious uveitis, and we have a phase II study running in cutaneous sarcoidosis. What I'm supposed to say is obviously the DM data is massively de-risking. The truth is that brepo was an active agent before. It has positive data in six or seven other indications under Pfizer's ownership in IBD, ulcerative colitis, Crohn's, psoriasis, psoriatic arthritis, and vitiligo. We knew that it was an active drug irrespective of the outcome here, so medically, I'm not sure this makes a huge scientific difference. I think it gives us confidence in what we're going to be able to deliver in rare disease settings, which is really where we have decided to take the product. I have a ton of confidence now in the Priovant team that ran the study. I think they enrolled fast and they did great work with the docs, and obviously, the data speaks for itself. I think we feel really good now looking down the barrel at the NIU data, which should come first half of 2027. As currently guided, that study's enrolled really well. I'm excited to see what comes out of this cutaneous sarcoid proof of concept study that we're running, and we have other indications in mind already where we're excited to get going. OK. I think one of the cool things about brepo is in 2021, when we partnered with Pfizer on the drug, it was just this sort of tumultuous moment for JAK inhibitors where the EMERALD study had recently come out and everyone was worried about the black box warning. Rinvoq was a $3 billion drug at the time. I think people kind of thought it was going to sort of flatline. Now Rinvoq is an $8 billion drug on a path to $15 billion or more. I think the market's kind of spoken about JAK inhibitors, but a ton of baby got thrown out with the bathwater the first time around. We not like literally 100% uniquely, but almost uniquely are occupying this sort of rare and orphan disease. I think we're the only JAK1/TYK2 combination that's focused on that, or generally JAK1/TYK2 dual inhibitor that's focused on that sort of portion of the world. That just feels like a really privileged position to be right now. I mean, imagine how different the DM conversation would be if rheumatologists were gun-shy about writing JAK inhibitors. They still might write it here. It would be a totally different conversation than what we're having now where they're bluntly giving Rinvoq out like candy. To your point on sort of the landscape of JAK1/TYK2 combination, I think Galapagos might be the only other company in the field. Is there anyone you're aware of competitively that's at your heels? Biohaven has a JAK1/TYK2 that's CNS penetrant that they're doing something totally different with. Galapagos has a JAK1/TYK2 that I don't think they're studying in any of the overlapping indications. They have an allosteric TYK2 that I think they're running a dermatomyositis study in, although it's hard to tell exactly how committed they are to that program. I think the truth is we don't really have competitors in the dual mechanism that are late stage. OK. With NIU, can you just remind us how you arrived at the 45 mg dose? What discussions you had with FDA, getting them comfortable? You're going up in dose and not wanting you to maybe interrogate a lower effective dose. Yeah, remember, we did run a phase II study in NIU where we interrogated 15 mg and 45 mg on a blinded base. I think that was helpful for understanding what the full picture looked like there and what the sort of range of dose benefit was going to look like. I think the view for NIU, so NIU, it's an eye inflammatory disease. There's about 400,000 NIU patients in the U.S., of which about 70,000 have back of the eye inflammation that can really only be addressed with systemic therapy. About 40,000 of those patients wind up on some kind of biologic or advanced therapy, and that's kind of the population that we see as eligible. I think our view was more so that, in DM, you said it yourself, we're sort of brushing up against the dermatology community that you sort of think about this from their angle. In the ophthalmology community, the tolerance among ophthalmologists for eye inflammation is very low. I think they're just looking for the biggest guns to get these things under control. I think NIU is one of the leading causes of blindness in America. If these patients don't get under control, they lose their sight. I think there's a lot of willingness to try aggressive therapies for these kinds of patients. I think you see this with Tepezza as well, where Tepezza is not a walk in the park, but people are using it all over the place because it's effective. Ultimately, they want to get this disease under control. I think our view was it was a good opportunity for that. I think our view was from a pricing perspective, from a patient severity perspective. Especially Humira is approved in NIU, and so there's a chance we wind up kind of living in a Humira refractory setting. We just felt like it was going to sustain the sort of bigger gun dose. Obviously, the phase II study showed 45 mg worked extremely well. It sounds like probably a comparable size market opportunity to DM, ballpark. Yeah, that's about right. Yep. OK. Maybe we'll pivot to Graves'. You guys had a recent update on Graves'. As we think about the primary endpoint selection in Graves', euthyroid and ATD free, I'd imagine that these patients in a clinical trial setting are unlikely to show any response at getting a placebo. Yeah, I think placebo response will be very low is the answer. I mean, the truth is that given that these are all patients who were selected for being uncontrollable on ATDs, they're just like not going to spontaneously remit and be able to get off ATDs. That ATD free prong is going to dramatically reduce the placebo response, right? Was the decision to go with that endpoint versus a lower dose of ATD or just euthyroid, T3-T4 normalization, like was it this is the most impactful endpoint for providers, or is it a regulatory discussion? How did you arrive at that as the primary endpoint selection? We're measuring all of the above. We're measuring sort of reductions in ATD dose. We're measuring, you know, people who are not fully euthyroid but have T3 and T4 control. We're measuring a lot of things. I think the combination of them is going to be relevant to different patients and different prescribers. I think it was a relatively easy choice to pick the big gun endpoint as the primary because it's just going to hit. I'm sorry. It's likely to hit. I think it felt like a reasonable place to sort of drive the study. Obviously, FDA is not going to have any issue with an endpoint. It's obviously clinically meaningful to these patients. I think it was a reasonably straightforward decision. Some of the early data, if we could go back to phase II, I think half the subjects on the 600 mg through 12 weeks were, I think half the subjects had gotten to this endpoint response. The definitions were a little bit different, but we had, I think at 600 mg, about 56% of patients at week 12 who had T3 and T4 below the upper limit of normal and were off ATDs. Is that because I know that when they dosed down after that, because of the design of that study, they went down to like mid-30s or something like that, right? Would you expect that rate to just hold based on what you've learned through the evaluation period, the open-label extension? Is that kind of 50% what you internally think is a likely 26-week response rate? I think apples to apples on the sort of endpoint measured in the phase II, which didn't include TSH, I think the answer is, if anything, I would expect that number to get larger the longer the duration of therapy. As we look at these patients, the longer they're on deep IgG suppressing data, the more of them get controlled. My expectation would be, if anything, longer duration therapy at higher doses shows a better outcome is what I would expect to see. Yeah. I guess talk a little bit about how you think this study will inform how doctors will use this if the trial is successful and it gets out in the field, right? Is it going to be a 26-week treatment course, a year, and then, you know, hey, the patients should be in remission? Do you think some doctors will use it longer term because they still haven't gotten into remission? I'm just kind of wondering how you see the 26-week data and then the remission data sort of informing the ultimate long-term use case. Yeah. In practice, there are patients treated for a full year in the phase III. There are patients treated for half a year and then off therapy for half a year. The second phase II study is just a six-month study. What I think we will see in practice is that the sort of algorithm will look a little bit like the methimazole algorithm. That is, you'll put patients on drug, you'll monitor T3, T4, and TSH. I think some patients, just as some patients are sick enough that methimazole just doesn't get them there and so they stay on methimazole for life, I think there will be some subset of patients who are sick enough that we are not able to get them fully controlled with this therapy. I think those patients will be on it chronically. They'll stay on this drug. When I say controlled, maybe they'll get T3 and T4 under control, but TSH will still be elevated or whatever. I think it's just going to be different depending on the patient. I think what docs will look for is they'll look for thyroid normalization. If they see thyroid normalization, I think they will start to have a conversation with their patient about whether they want to try a holiday based on the data that we've seen here. I think some patients will say, I've lived through uncontrolled thyroid hormone levels for many years, and no, I just want to stay on a drug that's working for me. I think some patients will say, yeah, I'm happy to stop taking a weekly shot if I can. I think that's how it will get used in practice. I think after six months, docs will start to track thyroid hormone levels. Some patients will need to stay on, and some patients will choose to stay on, and some patients will choose to take holidays. What you said reminded me of something I've heard from some doctors about methimazole or ATDs, which is that they're keeping patients on longer than they should be on, basically like in the hope, and hope is never a good strategy, but in the hope that like they maybe have a response after a year or two. When I think about your patient numbers, right, and how you characterize, I wonder how you, you know, estimate that dynamic, right? Because if 1402 is approved, I imagine this is a paradigm change, right, for these doctors. Perhaps some of that practice stops, right, where doctors are like, you know what, I'm not going to keep somebody on an ATD beyond a certain time point. Oh, yeah. How does that paradigm shift? What I think is definitely, in my opinion, going to happen is right now, if you're a patient on methimazole and you're not controlled, your thyroid hormone levels are still moving around, you're just on methimazole, to be honest. What I think happens to a lot of patients is they're not controlled. They go up and up and up in dose on methimazole, and they get to 20 mg or 25 mg or whatever. They're unhappy on the methimazole and still not perfectly controlled, so they go back down to 10 mg or 15 mg, and they just like live with it. The ones who are really unhappy then go get thyroidectomies and things like that. Otherwise, they're just sort of living, bouncing around, and you know, whatever. Some six-month periods, they decide to go back to trying higher methimazole dose, and they deal with those consequences. Sometimes they take a break, and they deal with the consequences of the thyroid hormone levels being out of whack. What I think will happen after we're approved, knock wood, is after whatever, after six months of methimazole not working for a patient, the doc will say, hey, I've got another option for you, and it may work better. I think we will see instead of patients being on these sort of long duration bouncing around methimazole kind of regimens, they will transition to 1402 as a last line therapy. OK. You have these two buckets. You have an incident kind of bucket, right? Those patients may get determined to be candidates in a more expeditious manner. You have the prevalent pool of patients, and perhaps they're lingering on methimazole for. are 330,000 of those who are just walking around effectively on methimazole and uncontrolled all the time. There is a huge patient population in that prevalent bucket. Who’s taking care of these patients right now? How do you kind of understand where these patients are at in the treatment system? Is this all generally a primary care kind of setting? It's not. It's endocrinologists is the answer. It is a range from academic endocrinology practices to, you know, community endocrinologists do treat Graves’ disease, including chronic patients, and so it's a mix. Interestingly, the academic docs tend to believe they can control any patient. The patients don't always feel that way. That is, like, some of the patients are like, my doc put me on 25 mg methimazole, and he or she thought it was going to work, and I hated it. The academic docs tend to feel like they can, whereas the community endocrinologists, who often I think live with more of the chronic patients, they live with the more standard chronic patients, right? Patients who are just like dealing with this for many, many years are not like always going to an academic center. I think those docs are obviously receptive to new options for those patients. Anyway, they're treated endocrinologists. It's a bigger prescriber base than in something like a dermatomyositis because these community endos, there's just like a lot of them. That's who treats it. I think they're okay. The data that we showed earlier this month, the like sort of disease modification data, has clearly been an eye opener for docs in terms of value proposition. Because a doc who previously was like, yeah, I can drive response from high dose methimazole, I think those docs were like, so why would I try something new? I think the answer is, if you do this for six months or a year, you may get your patients off methimazole, is a very compelling answer. Yeah. OK. So you'll have some data for the previous generation FcRn, 1401, and TED. Yeah. I think toward the end of this year. Yep, that's right. Let's just say you see fabulous data, right? I think you've shown some data through five weeks, I think was what I recall. A little bit more than that, yeah. It looked directionally similar to IGF1R approaches. Yeah, directionally is a good word for it. Look, I think the IGF1R is. Small sample, right? That's right. As someone who would cover Horizon, I remember looking at that and handicapping that as a competitive threat. If that data are encouraging and support the FcRn hypothesis inTED, how do you think about maybe would you adjust your Graves' study to include a stratified sub-segment of TED? would you want to elucidate the benefit for 1402 to get some label language around treating specific thyroid eye disease manifestations? We thought a lot about this over time. I think initially we had contemplated stratifying in the phase III to make sure TED patients. What is immediately clear even from the phase II study that we ran is we do not need to stratify. There will be TED patients in the study no matter what. We absolutely, you know, TBD on exactly which, but we absolutely will have key secondaries on proptosis and the development TED that will allow us to make hopefully label claims if successful about the development of TED. I think that is first and foremost as far as Graves’ is concerned. One of the things we'd like to do is be able to tell endocrinologists if you put patients on this drug, it will forestall the development of TED. It will slow the development TED. if they have early signs of proptosis, it will help them. I think one of the things Graves’ patients worry most about TED and having either, you know, risks to vision or it's just like a tough aesthetic thing. It's uncomfortable. I think being able to say this will help there is good. Obviously, TED data is extraordinary, if it looks like every bit as good as an IGF1R but without some of the side effects, there's certainly an option to launch batoclimab or an option to add either a stratification that allows us to get a TED or a separate TED study. That's certainly an option if that data is extraordinary. I think we prefer in some ways the angle of going after the endocrinologists and helping keep these patients out of the ophthalmologist's office. OK. Maybe just a few other topics within the FcRn realm. RA, what underpins the confidence here? I think J&J was supposed to have some phase II data for nipo here in the ACPA+ population. I don't think we've seen it yet. We have. You've seen it? Yeah. J&J put out the data from the combo study this summer, I think. They didn't show separation from the, as you remember. J&J showed data in the monotherapy setting like two years ago. It showed activity. It was clearly an active drug. It was clearly even more active in the ACT4 positive population than in the general population. It was also clearly more active in patients with deeper IgG suppression. What J&J then went and did with that data is they ran a combo study with Cimzia to ideally show adjunctive benefit on top of TNF therapy in a relatively early line of patients. They didn't see what they were hoping for. I think our view is, first of all, and that was enriched for the ACT4 positive population to your point. I think our view was, first of all, J&J has dosed nipo in a way that does not suppress IgG as deeply as we do. Second of all, showing performance on top of a TNF was always going to be a little bit tricky, just given how well TNFs work in this patient population, which was why we went later line and why we always believe that deeper matters. It would have been nicer if they had seen more separation, I think it's the data you're referring to, it would have been nicer if they had seen more separation from the TNF only group. I don't think it materially changes what we're trying to do. You ask about confidence. Look, I think this is the bar for enthusiasm, the bar for excitement is relatively high for us in that it's an open-label portion, it's a run-in portion of a randomized withdrawal study. I think you have to sort of discount it from that perspective. I think it's a tough patient population. If we're successful, it's obviously a big opportunity. Yeah, this is probably in the higher risk of your portfolio of indications. Absolutely, yes. What would you just need to see in this open label trial? We haven't set up, this is the open-label run into the randomized withdrawal study. We haven't given a number. I think you'd want to see response rates that look, you know, obviously highly compelling for a fourth-line setting is what I would say. I think unambiguous is what we'd want to see. Yeah, with MG and CIDP, there's great validation commercially now, right? Yeah. The lead. I know that there was some data that you guys had with your first generation. It's obviously difficult for the comparisons to be made cross-trial because there's some different metrics that are out there around super responders. Ultimately, as we kind of fast forward, where do you see that fitting within the broader portfolio? I imagine Graves' is the anchor. Yeah. You know, something like RA is, I don't want to call it a moonshot, but it's the higher risk, you know, big opportunity. MG and CIDP feel like low risk and maybe don't have the upside opportunity unless maybe you ultimately end up differentiating on the form factor and/or the IgG suppression gives you some directional unique data points to market. I don't think I get much benefit from disagreeing with that point of view now. Look, what do I actually believe? I really liked the data we showed in March. I think it did show that deeper IgG suppression matters. I know there was debate over the point. I know not everyone agrees. I think if we can move the field, as every other immunology field has moved, towards remission endpoints, towards MSE endpoints, towards sort of deep responders, I think we will be better able to deliver those kinds of endpoints than our competitors because of the depth of IgG suppression. I think it will matter. I think that is correctly viewed as an upside scenario commercially in that, look, the truth is argenx has done an amazing job building support and understanding in the doc community. I think kudos to them. I think that efgart is an enormously popular therapy. It will be difficult to unseat in any meaningful sense. The truth is with the size of MG as a market now, even if we take relatively little share, the drug is going to work in MG. It's got a nice form factor. Maybe some people will find the extra benefit of deep IgG suppression compelling, even if others don't. It does not take a lot of share for it to make lots of economic sense to run the study. I feel really good about it as an indication. You know, in terms of like what I think is going to capture the hearts and minds of investors at this stage, I think MG is just going to be a whatever. It will be in people's models. I think it will be NPV positive in people's models. It's not like the thing that's going to drive the story. I think that's fine. Yep. I think CIDP is a little bit different in that I think it's clear. I think argenx is also doing a nice job in CIDP. I think it is clear there is more room left on the table in CIDP than in MG, right? You see some of these articles that suggest that docs are washing patients off IVIG and are not happy with sort of the lull in the middle. I think our early CIDP data looked pretty good, and if that continues, I think we have an opportunity to be a bigger sort of obvious player in that market. Yep. I think we've got to hit that bar. OK. Maybe I'll come back to some early pipeline, but I wanted to hit on LMP litigation because it seems like we're in a very actionable phase here in 4Q with the Section 1498 government contractor defense and whether that's applicable. I guess the consequence of it, if it could sort of fragment the litigation pathway a little bit if it was deemed applicable. I guess will we get clarity on 1498 applicability? I know that we have to size that applicability in trial, right, as I understand. What Moderna in their own frame has said is their view is that 1498 in the U.S. trial, they believe it should cover a little bit less than half the sales. Obviously, we believe it shouldn't be applicable. That's sort of the dispute, as it were. The most important parts of that dispute will be settled by the judge in summary judgment in all likelihood. We will know the answer to that question. Now, half of what is still a question that will be decided at trial. We've asked for $5 billion in damages before enhancement for willfulness. Moderna has said about $2.4 billion would be covered by 1498. The denominator there, whether it's $5 billion or $4 billion or $6 billion or whatever, will be decided by a jury. Yep. Whether 1498 applies will mostly be determined by a judge in this summary judgment phase. I say mostly because there are some corner cases in which parts of that question go to a jury. I think the most likely thing is mostly decided by the judge here. Is it tied to a specific hearing for summary judgment, or do we just not know more specifically when within this time between now and the March trial that would be? At this point, the issue was briefed. That is, there was a schedule for we both got to submit summary judgment briefs and then motions. There was sort of briefing and counter briefing and counter counter briefing. That's all largely done now. The judge could, in theory, rule tomorrow, although that doesn't seem very likely. The briefs just went in. The original timeline for the case set forth by Judge Goldberg, who was the previous judge on the case, which is the time we're currently on. I think it was clear that Judge Goldberg intended to rule on this issue in October or November. OK. There's a new judge on the case now. He's new to the facts, so he may take a little bit longer. It's sort of at his discretion. I don't think we know specifically, but it could be this fall or it could be early next year. That's kind of where we're at. All right. Any clarity on the O US legal proceedings? I know that that's kind of kicked off. Just like generally, how should investors think about that? I imagine OUS litigation tends to be a little more fragmented. It does. I mean, there are more jurisdictions. It moves faster in a lot of other jurisdictions than it does in the U.S. We started these proceedings this past spring, and I think we will start having real infringement hearings next spring, within a year of launching the proceedings. I think that means there will be a good drumbeat of progress between the U.S. trial in March and the surrounding months where there will be actual infringement determinations made by courts in other jurisdictions next spring. I think that's mostly, look, I think the fastest path to a resolution is that somewhere along the way, we at Moderna have a productive conversation and reach an agreement. Yeah. I think the existence of the ex-US trials gives everyone clarity on what the picture looks like, sooner. It seems like you can't have a conversation until 1498 government contractor defense is decided. I think that's mostly true. You have the Pfizer matter where there's been claim construction. Is 1498 still a similar relevant consideration or not? Pfizer has not asserted 1498 in their case. Remember, their facts are a little bit different in terms of how much government funding Moderna took versus Pfizer. Pfizer just hasn't asserted it. It is still possible they could raise it later, but at the moment, it doesn't appear to us that Pfizer has decided to go down that road. They certainly haven't sought a dismissal on that basis. With respect to the claim construction rulings in the Pfizer matter, do you feel like there are any material differences in outcomes on the interpretations of key claims? We were obviously very happy with the Moderna constructions. My view bluntly is that there was more downside risk than upside for Pfizer just because simply getting the same outcome as Moderna would have been a good outcome. It was probably on the margins better in the Pfizer case in that there were a handful of issues, in which one in particular, most of the issues the Pfizer judge went the same way as the Moderna judge. OK. In one case, he literally just excerpted a piece of Judge Goldberg's opinion and said, I find this compelling. Here it is. There was one specific case, which is probably too technical to go into full detail in a minute and 26 seconds. On the meaning of encapsulation in the 651 patent, the Moderna judge chose a relatively complicated definition for fully encapsulated. The Pfizer judge gave us a much simpler and more straightforward definition for fully encapsulated. I think that will be helpful to us specifically as pertaining to 651. OK. Maybe coming back to pipeline, your SGC. I cover United Therapeutics. Yeah. PH-ILD is a very interesting high-growth market. Yeah, I think so too. Just kind of curious, you know, as you advance the program, I think you'll have some phase II data next year, second half. Yes. Is the focus really concordance of both the hemodynamic aspect of the benefit on PVR as well as six-minute walk? I know six-minute walk can sometimes be considered a little noisy in these trials. PVR is a little bit more of an objective measure. How do you kind of think about those data and informing those steps? Yeah. Look, I think there's really two questions in the phase II-B. I think the first question is just does PVR, we saw very good PVR reductions in the PAH group 1 population. Yep. I think that there's a question of what does that and tolerability look like in the group 3 PH-ILD population? I think it is extremely likely that if PVR translates from group 1 to group 3, the clinical benefit will follow. I would hope that we get a pretty clear picture of what that looks like in terms of six-minute walk and time to clinical worsening in this study as well. OK. We are at time. Matt, appreciate you taking some time to talk on the latest developments. Appreciate it. Thanks, Roivant.