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

Good morning. My name is Terrence Obreski, and I'm your conference call operator. As a reminder, this call is being recorded. Before we begin, I would like to remind everyone that today's conference call will include certain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements include, for example, statements regarding the potential efficacy and safety of Immunovant's product candidates and Immunovant's expectations regarding the timing, design and results of its clinical trials, including the timing of future data readouts and the announcement of future indications. These forward-looking statements are not guarantees of future performance and are subject to various risk events and uncertainties and assumptions, known or unknown, which could cause the actual results to vary materially from those indicated or anticipated. For more information, investors are encouraged to review Immunovant's most recent quarterly report on Form 10-Q filed with the SEC on February 6, 2025. Joining me on the call this morning are Dr. Pete Salzmann, Chief Executive Officer at Immunovant; and Matt Gline, Chief Executive Officer at Roivant. Following their prepared remarks, we will open the call up for questions. With that, I would like to turn the call over to Matt Gline.

Thank you, everybody. Good morning. Thanks for joining this morning's call. We appreciate it. Obviously, this is principally an Immunovant show, and I'll be handing it over to Pete in a second to take you through all the details associated with this data. We are, in short, incredibly excited of what we're putting out today. We think it demonstrates, frankly, a new bar for the treatment of MG patients by an FcRn. Obviously, we showed seriously significant and clinical meaningful outcomes across multiple end points. We had a clear dose response, which is something that was important to us with 340 milligrams, consistent with other FcRn programs with mid-60s IgG reduction and 680 showing across the board, across a whole range of measures, greater improvements, including on MG-ADL, including on a variety of other responder rate endpoints. Pete will go through all the details. Obviously, one of the talk tracks today is going to be about placebo publicly. Placebo MG-ADL improvements were greater than an earlier generation of studies, but consistent with, for example, what we saw last year with nipocalimab. The truth is that because bato 340 behaved so similar to the competitive programs, we were mostly focused on that arm of the study from a comparison perspective. But obviously, there will be a broader discussion in the world about that. And we're in the middle of Period 2 maintenance data, which we'll talk a little bit less about today, was in line with our expectations and safety and tolerability, also consistent with earlier bato and other FcRn studies. CIDP, again, best-in-class efficacy as we see it and a clear link between IgG suppression and clinical benefit, which is something that we hope to show in CIDP and we've seen here. So look, overall, incredibly exciting data and a big opportunity. The only thing I wanted to do, and I know Pete is going to do a little bit on this, too, is just remind people who are maybe at a tiny bit of arm's length to the story, one of the reasons all of this matters, which is we have IMVT-1402, our second generation. So the data today is with batoclimab. Our second-generation anti-FcRn antibody, we think is incredibly well teed up as of this morning to be a true best-in-class program across all attributes. It has robust IgG lowering, the same as batoclimab at the top of what everybody in the FcRn field can do. It has a clean, simple subcu form factor with a 2 cc auto-injector at launch. And multiple now ongoing clinical programs, including an MG study that Pete will talk about later, that will be ongoing in a matter of weeks. And look, I think at this point, I'm sure people will find ways to quibble around it, but our view is the deeper is better thesis has been adjudicated. At this point, we have not run a large clinical program that has not shown the deeper IgG expression yields better clinical benefit. And again, I think we've set a new bar for absolute treatment magnitude in the 2 diseases we're announcing data in today. So I'm going to stop talking now. I'm going to hand it over to Pete, who will go through this data in detail and then I will jointly do some Q&A at the end. But again, we appreciate everyone joining and excited to talk more about this data. Pete, over to you.

Thanks, Matt. I really appreciate that, and good morning, everyone. I'm really excited today to share the top line results from our batoclimab trial in MG and the initial results from Period 1 of our batoclimab trial in CIDP. And I'm going to start where Matt left off with a really important so what and remind everyone that Immunovant's go-forward strategy revolves around our second-generation asset, IMVT-1402. I know we have a lot of 1402 experts joining us today. And I also know that we have some great investors joining the call who are newer to the Immunovant story. So very briefly, why is 1402 so exciting? As Matt said, basically because it shares the same very positive feature of batoclimab, which is the ability to provide uniquely deep IgG reduction in the subcu preparation, but it does not have the analyte abnormalities of batoclimab. Both batoclimab and 1402 bind tightly to the Fc receptor. However, the binding orientation is different such that batoclimab inhibits albumin binding and 1402 does not inhibit albumin binding. This advantage of 1402 was confirmed in the 1402 healthy volunteer Phase I trial. So with that, let's turn to batoclimab data we're discussing today. You can here -- see here that we set out to achieve several very important goals with these studies. First, of course, was to establish potential best-in-class efficacy in both MG and CIDP. The second goal really relates to the current unmet need in MG. And specifically, although FcRn inhibition has been a major breakthrough with 2 approved products, the reality is that many patients have residual symptoms or breakthrough symptoms or both. We set out to demonstrate the ability to deliver deep and durable clinical responses, which I think will be the new bar, and we'll get more into that later. Our third goal applies beyond MG and CIDP, and it's really to settle the lower is better to me, which I completely agree with Matt is settled. We're going to show a lot of data demonstrating that deeper IgG reductions drive better clinical improvement and believe that there will be a read-through to many other indications because of the consistency of that correlation that we observed. And lastly, back to MG and CIDP, the batoclimab programs give us the opportunity to accelerate our programs in MG and CIDP with our lead asset, 1402. These were bold goals, and I'm very excited to share with you today how we achieved them all. Starting with MG. I'm going to focus today on the primary analysis. In other words, how did batoclimab perform in Period 1 in AChR-positive participants. AChR+ patients made up about 70% of all enrolled patients, similar to other pivotal trials in MG. Period 1 has the broadest generalizability, and I believe you will find the results very compelling. We also have Period 2 data in hand, and I'll make a few comments about it towards the end. The results from Period 2 also support our goals. As a brief reminder, the primary endpoint for this trial occurred at the end of the 12-week Period 1 and assessed MG-ADL change from baseline for AChR antibody positive. Baseline characteristics across the 3 arms of the study were well balanced and consistent with other anti-FcRn Phase III studies in MG. In particular, our trial and others generally enrolled patients with a baseline MG-ADL around 8.5% and a QMG around 16. The primary endpoint of mean change in MG-ADL from baseline in AChR-positive patients was achieved and statistically significant for both batoclimab arms. What I find most exciting about these data is the result of the 680-milligram dose, which has set a new benchmark with a magnitude of treatment effect observed with FcRn inhibition during the placebo-controlled portion of a clinical trial. As you can see on the right side, the 680 dose achieved a mean IgG reduction of 74% and a median change from baseline in MG-ADL of 5.6 points at the primary endpoint. The 340-milligram dose of batoclimab achieved a mean IgG reduction of 65% -- sorry, 64% and a mean change from baseline of MG-ADL at 4.7. Both doses separation from placebo was statistically significant with 680 milligrams demonstrating a p-value less than 0.001. The placebo arm observed a 3.6 point mean change in MG-ADL, higher than earlier studies, but similar to more recent studies in the class. Expectation bias often increases the placebo rate after a class has been validated in particular, that's true what patient reported outcomes. As you'll see those throughout the presentation, the placebo responses were much lower than looking at durable deep response. Here, we see that 340 milligrams of batoclimab delivered MG-ADL reductions in line with other FcRns at their Phase III doses where IgG lowering was also seen. Of course, it's important to note that these data are not generated from the same study, but there were differences in study design. So that comparison should be made with [indiscernible]. From left to right, VYVGART, nipocalimab and batoclimab 340 milligrams all delivered 4.6 or 4.7 point reductions in MG-ADL with IgG reductions in the mid-60s. With 680 milligrams of batoclimab, a greater benefit was observed with a 5.6 point reduction and a 74% mean IgG reduction at 12 weeks. One of the takeaways for me from this slide is that the 340-milligram dose of batoclimab basically serves as an internal reference arm. Period 1 of this trial is essentially a head-to-head study of high-dose versus standard dose batoclimab with the standard dose of batoclimab similar to other FcRn inhibitors. In this view, we evaluated response rates across the publicly available data, Phase III data for VYVGART and nipocalimab. 340-milligram of batoclimab once again looks pretty similar, reinforcing its utility as a reference arm. 680-milligram batoclimab once again separates from the pack, beating low dose batoclimab by more than 10% in absolute percentage terms. Taking a similar approach, but focusing on super responders, we see the same pattern. In each graph, batoclimab 340-milligram super responder rates at the primary endpoint are similar to those reported by VYVGART and nipocalimab at their primary endpoint. Across multiple thresholds, higher response rates are observed in the 680-milligram of batoclimab arm compared to the internal reference arm of 340 milligrams of batoclimab. Here, we're looking at deep responders at week 2, what we are calling early super responders. We aren't aware of these cuts being publicly available for competitors. So these graphs take advantage of the internal comparison between batoclimab doses. You can see I'm looking from left to right at the graphs on this slide that at week 2, there are already large differences between the dose arms and placebo when it comes to early super responders. For the 5-point or greater early super responders, the high dose is 15% better in absolute percentages than the standard dose. For the 7 points or greater super responders, the absolute difference between the dose arms is 9%, and the relative difference is nearly 100%. Minimum symptom expression or MSE is an important concept for neurologists and their patients. It is defined as dropping MG-ADL to 1 or 0. At week 12, 42% of patients on 680 milligrams of batoclimab achieved MSE. And this is 11 absolute percentage points higher than the internal standard dose -- internal reference arm of batoclimab at the lower dose. Placebo, of course, was very low. It's also important to note that we are using a more stringent definition of MSE than competitors, requiring MSE at the primary endpoint versus at any point during blinded therapy. Okay. And now we come to perhaps the most important slide in the deck with a new and very patient-focused concept. We've done market research for both patients and neurologists to understand the unmet need now that FcRn inhibitors have been approved and launched. Neurologists and patients really appreciate the innovation and treatment that approved FcRn inhibitors have delivered. At the same time, they are also very clear about what they want now. They want consistent resolution of symptoms. They want to feel normal all the time. They want a deep, durable response. This graph shows that potent FcRn inhibition with 680 milligrams of batoclimab nearly doubled the number of patients who experienced a deep and durable response on the internal reference arm of 340 of batoclimab. Placebo doesn't really have a chance on this very strict response criteria. In this analysis, we looked at everyone who had a chance to achieve 6 or more straight weeks of MSE by accessing everyone who first achieved MSE prior to or at week 6 and then measuring how they were able to maintain it through week 12 of the primary endpoint. 75% of patients achieving MSE in the 680-milligram arm maintains their MSE response consistently for 6 or more weeks. When looking at the internal reference arm of 340 milligrams of batoclimab, you see that only about half as many patients maintained MSE consistently in this arm. Prior to FcRn inhibitors arriving on the scene, MSE wasn't even so much of a concept in MG. Now it is a concept, but most of the marketing materials focus on MSE at a single point in time. Now with deeper IgG suppression given continuously in a simple subcu, I expect the new high bar to be maintenance of MSE, and it certainly looks like deeper IgG suppression have been really big advantage. In terms of safety, batoclimab was generally well tolerated with low discontinuation rates and treatment-related adverse events that were consistent with other batoclimab. As we've seen previously, analyte abnormalities of hypoalbuminemia and hypercholesterolemia did occur in both batoclimab arms and to a greater degree in the high dose. There was 1 death in the placebo arm. Before transitioning to CIDP, I have this slide and to remind everyone that the study did have a Period 2. We're not covering Period 2 data in any detail today. It's very interesting as it really would require a whole separate call. I do want to emphasize though that the treatment benefit was maintained with continuous dosing. So for example, patients who received 340 milligrams of batoclimab in Period 1, when they were re-randomized to continue taking 340 milligrams of batoclimab in Period 2, they maintained their benefit. When these same patients were re-randomized to a dose reduction of 340 milligrams every other week, they lost that benefit. So consistent with other studies, it appears that in order to maintain a therapeutic effect, patients will need to stay on the dose that is working for them. No real surprise. Okay. We'll switch now to the initial results from our batoclimab study in CIDP, where you'll see similarly impressive results. The CIDP trial design includes an open label, meaning on drug run-in period, followed by a randomized withdrawal period, which is Period 2. I won't be reviewing any Period 2 data today. Recall that participants entered Period 1, following a washout period in which they were required to worsen once their standard of care was stopped. In Period 1, participants were randomized to either 340 milligrams or 680 milligrams of batoclimab delivered weekly 12 weeks. For a combination of regulatory and competitive reasons, we chose not to unblind the study by dose, and we are instead reporting pooled batoclimab data as well as data separated by IgG response using our standard greater than, less than 70% IgG lowering. Hope you're able to [Technical Difficulty]. In terms of baseline characteristics, these are the baseline characteristics for all 73 patients who entered Period 1 after worsening during wash. The baseline disease severity characteristics are pretty similar to VYVGART's published Period A baseline characteristics as is the mean time since diagnosis. Almost half of our patients were treated with IVIG, with others having been treated with steroids and a third group that wasn't on any current treatment, though most had previously been treated with IVIG or steroids. Here, you see the blended results for all batoclimab patients entering Period 1. By week 12, the mean change from baseline in adjusted INCAT score for the batoclimab participants was double that observed and reported in Stage A of the VYVGART Phase III ADHERE study. These are, of course, cross trial comparisons and not head-to-head studies, so the comparison should be done [indiscernible]. At the same time, the 1.8 adjusted INCAT improvement I believe to be a very good result. In order to assess the relationship between IgG lowering and INCAT response, we separated the participants in Period 1 into 2 groups. Those who achieved at least a 70% IgG reduction and those who did not achieve a 70% IgG reduction. We've shared these types of analysis before, for example, in our Graves disclosure, and I want to remind everyone why we chose a cut point at 70%. The reason for choosing this cut point is that patients on 600 milligrams of IMVT-1402 will have an IgG reduction above 70%. This is also true for the large majority of patients on 680 milligrams of batoclimab. On the other hand, other FcRn inhibitors generally reduce IgG by less than 70%. This is also true for batoclimab at 340 milligrams. So the 70% cut point provides a nice division between what the high dose of 1402, what the high dose of batoclimab generally does and what the rest of the pack will do. Turning back to the CIDP data, the relationship between depth of IgG reduction and INCAT response is strong, with an 84% response rate in the deeply reduced IgG participants versus a 44% response rate in the other. I should note that this is a different responder definition than VYVGART used. They used ECI or evidence of clinical improvement, which incorporated INCAT, I-RODS and grip strength. Our study used just INCAT response, which is stricter since that's just 1 part of the ECI composite. Let's look at some other efficacy scales in CIDP. I-RODS is a patient-reported outcome, whereas MRC-SS and grip strength are physician assessments. In the blended batoclimab period 1 data, we observed larger improvements across all 3 scales, likely driven primarily by the higher dose. Okay, let's settle the debate. I'm not going to read all the points on this slide, but instead, I want to remind everyone again why this is so important, why it matters. The key positive differentiator of batoclimab is its ability to deliver the deepest IgG lowering in a simple subcu. Unfortunately, batoclimab also lowers albumin and it turns out that this lowering of albumin rates is less strong. But then there is the good news that our second-generation asset preserves the ability to deliver the deepest IgG lowering in simple subcu. However, the reduction in albumin and raising of LDL has been eliminated by engineering a different binding orientation to the Fc receptor for 1402. So the lower is better reads through to our second-generation assets that achieves lower without analyte abnormalities. Let me just show 1 or 2 additional data cuts to support this point that lower is better. Here, we're looking at multiple different scales used for MG efficacy assessment and you see a consistent dose response here across all 3 skins. When we look at MG-ADL, mean change from baseline at week 12 by greater than or less than 70% IgG cut, we see that for those patients who achieved greater than 70% IgG reduction, their mean improvement was 6.1% versus 4.9% of those who achieved less than a 70% reduction. Here, we're showing MSE for patients who achieved greater than 70% IgG reduction, which was 53%. And again, deeper IgG reduction led to greater MSE rates. Putting in all together here, when we look at the totality of our data across graves, MG, CIDP studies, we consistently see meaningfully improved response rates for participants achieving 70% or more IgG reduction, which, by the way, is the IgG reduction that we expect for the vast majority of patients treated with 600 milligrams of 1402. We believe that a 10-point improvement in response rates between 2 active agents represents a meaningful differentiation in a commercial setting based on a wide variety of prior immunology precedence. These differences are all greater or much greater. Okay. So what's our path forward in myasthenia gravis? The IND is approved, as we've previously discussed, for 1402 and MG, and we are in the process of initiating the trial I'm about to show you. We're going to focus on 1402 going forward in MG, given its superior tolerability profile without albumin and cholesterol changes, and we do not plan to seek regulatory approval for batoclimab in MG or CIDP. One question I sometimes get is, how much unmet need remains in MG? And it turns out that there's a lot. Neurologists and patients are very excited, as I said earlier, about the first-generation FcRn inhibitors, but they are also clearly seeking stronger FcRn inhibitors that can deliver deeper and more durable responses. It used to be that achieving a solid percent of patients who achieved a 2-point MG-ADL response was a win. Now with FcRns approved, the borrower has shifted to achieving MSE, achieving MSE at a single point in time is now seen as a win. Going forward, I believe the bar is moving to maintenance of MSE. Bar will no longer be achieving MSE at some point during therapy, but rather maintaining MSE consistently for weeks. When it comes to maintenance of MSE, 1402 is well positioned to deliver on this new and higher expectations. How will we show this with our 1402 trial? Well, here's the schematic of our pivotal trial in MG, and it's actually very straightforward. We're studying a similarly severe group of MG patients as we enroll them in our batoclimab trial and as other Phase III trials have enrolled. We're including AChR+ patients as well as MuSK+ and LRP+ patients in the primary analysis pool. And this reminds me to mention that the results for MUSK+ and LRP4+ patients in the batoclimab trial were consistent with those seen with the AChR+ patients. So we're confident to include all 3 groups in our primary 1402. Patients will be randomized to 600 milligrams or 300 milligrams of 1402, which are similarly or slightly more potent than our batoclimab doses, 1/3 of patients will then go into placebo. The primary endpoint is at 12 weeks, after which all patients will continue on blinded therapy with those patients on 600 and 300 remaining on the dose that they were randomized to initially and placebo patients switching to 600 milligrams in a blinded fashion. We're also very close to finalizing our CIDP design, and that will be unveiled soon. Great. Before I get to a summary of key points for 1402, I want to make a point around translatability. A big, big thing for today is translatability, translatability from batoclimab to 1402 in terms of deeper IgG reduction, driving greater clinical improvement. As I said, we expect 600 milligrams of 1402 to behave like the deeper than 70% IgG reduction cuts. As I already mentioned, batoclimab has an on-target analyte side effect of lowering albumin that's well characterized and can lead to dose interruptions. In other words, holding a dose or missing a dose due to hypoalbuminemia. 1402 will not have this problem. Here, we show the results when we only include patients who didn't miss any of their last 4 doses. On the left-hand side of the graph, you see the chart you're already familiar with from earlier in the presentation with all randomized patients. On the right-hand side, you see a cohort where that includes only those patients that did not miss any of their last 4 doses prior to the primary endpoint at week 12. And here, you see an even bigger reduction in MG-ADL 680, nicely clearing a 6-point reduction in MG-ADL bar that previously seemed unattainable in the controlled version of the trial. I'll conclude here with a high-level summary of why 1402 is so exciting. It's exciting based on the compelling results we shared today showing that lower is better and based on 1402's profile, which can deliver deeper IgG reduction without analyte abnormalities. And based on the composition of matter patent until 2043 for 1402. And based on having 6 INDs cleared with many other exciting indications to come. Based on all of these reasons and more, I believe that 1402 has an exceptionally bright future. With that, I'll turn it over to questions for me and Matt.

[Operator Instructions] So our first question comes from Brian Cheng at JPMorgan.

Maybe just first, Pete, can you walk through the super responder at week 2 and also the MG-ADL impact at week 12. When we look at other FcRns historically, the data there had historically anchored after the first cycle between week 4 to week 8. Can you here talk about how the MG-ADL response looks here at week 4, specifically tied towards your high dose and the placebo arm? And from week 4 and on, how does that look over the course of the 12 weeks? And I have a quick follow-up.

Right, Brian. I think there's -- I think a couple of important points there. There's a lot of different ways that you could cut the data. So we were trying to focus on what's going to be most important for patients when we introduced the concept of durability. And what's most important for them is being able to just consistently achieve a deep response. Achieving it early is also really nice, which is why we showed the early super responders. But if we want to get a sense for the maintenance of a deep response, I think the maintenance of MSE chart is the best one to look at. And the 340-milligram arm serves as a really good internal reference arm. I think it's the more important comparator when you're looking at deep responders at any time point or the maintenance of deep response you're trying to compare what can high dose IgG suppression do versus lower dose and the 680 to 340 is a good way to do that. So whenever we looked at that, when we looked at a single point in time, when we looked at durability, the 680 is consistently outperforming the 340, which again, we see the 340 is essentially showing us what any other FcRn inhibitor would do if it were dosed consistently.

Brian, just one other comment from me. Look, I think obviously, the sort of underlying question about this data overall, and I think probably embedded in your 4-week question, is just -- this is a competitive field, and we have an existing product on the market in VYVGART that's really popular and has 4-week data. And I think the reframing that's important to me is to take a step back and say, okay, why is the field looking at forward data? The field is looking for 4-week data because that was how the early trials in MG were run, not because that's how MG patients live their lives. MG patients want the same thing that patients in every indication want. They want fast control of symptoms, and they want it to last once it kicks in. And the reason we've shown 2 weeks and the reason we're focused on the durable MSEs that Pete talked about is because those are things we -- the reason we don't think the field is looking at those things right now is because bluntly, we don't think those are things the field is able to deliver, either based on the way those programs have been run or based on the level of IgG suppression they have. And so I think it's important to us that we focus on the unique attributes that 1402 is going to have in MG, and we'll talk more about other indications, obviously, over the course of this call. But specifically in MG, we're clearly going to be able to do better based on this data set is get deeper, faster and hold those responses for longer. And that is that's the impact of the deeper IgG expression that we deliver. So that's what we're focused on.

Okay. And just a really quick one. To win in MG and CIDP today, do you think -- I mean just given what we saw in the Phase II -- the Phase III trial design for 1402, do you think you will ultimately need to run at that trial against [indiscernible]?

No, I don't think that's going to be required. I think there's -- we have a big advantage in having 2 doses. I focus today primarily on the additional benefit can be achieved with a higher dose. But having 2 doses is also a big advantage just in and of itself in MG. Neurologists appreciate the ability to have dosing flexibility. So that is why we're including both doses in our 1402 pivotal trial. And again, that standard dose, the lower dose of 1402 will serve as essentially an internal reference arm and internal head-to-head. So we'll generate the data that physicians will need to understand how deep IgG suppression compares to standard IgG suppression with the design that we shared.

Brian, one of the things that's nice about Pete and I both think on this call is Pete is a naturally more conservative person than I am. So what I'll say is first of all, I feel like we already did run the head-to-head. It's in this trial with bato 340 performing as we think any agent that suppresses IgG by mid-60s would. And the truth is, if we get the sense after this data that what docs and patients really want to see is a true head to head, look, I think we'll talk about it. This data supports the fact that we should be able to deliver on such a study. And I think the market would be forced to pay attention if we were running one. And by the way, just 1 last point on the 4-week thing. Just with the -- all the time points were completely consistent with the data we've shown here for avoidance of doubt, the curves looked exactly the way that you would expect, connecting the dots between 2 and 12. Thanks.

Our next question comes from Derek Archila at Wells Fargo.

Congrats on the data. Just 1 in the follow-up from us. So obviously, there's a lot of focus here on the absolute rates versus placebo-adjusted rate. So obviously, you got to ask the question, why you think these are more relevant for comparison? And then just a quick 1 on -- so it looks like in the 1402 trial, I guess, you're going to look at 600 mg weekly in Period 2, I guess, was the driving factor of that from the beta switch to 340 from 680. Did you see kind of those patients worsened kind of confirming the dose response? Is that the driving factor?

Yes. Thanks, Derek, for those 2 questions. So I think the emphasis on the absolute treatment response is based on a couple of things. First of all, placebo-correct is important. It's important for getting approval. So you need to be a placebo to get approved. But when comparing different agents, our discussions with clinical neurologists who treat a lot of MG patients consistently says that they prefer treatment effect because it gives them a better sense for how the patient is going to respond versus his or her baseline. It's easier to explain. The other thing is we see a consistent treatment effect across the various FcRn programs, the ADAPT-SC trial, which didn't even have a placebo. So everybody knew they were getting efgartigimod essentially reported a very similar treatment effect in terms of MG-ADL than as compared to the placebo-controlled Phase III trial. So the treatment effects are really consistent across different agents and therefore, gives us the ability, I think, to compare it the way we did. In terms of why we designed the trial to include -- essentially you have a 600 per -- for 6 months versus 300 for 6 months, and we're just doing the primary endpoint at week 12. And the reason for that, it gets a little bit back to Brian's question about providing comparability. The 600 arm will be compared to the 300 arm and I expect it to show deeper and more durable responses, and that provides an internal head-to-head up to 6 months. That is going to be very compelling data eventually for prescribing those.

Got it. And just 1 clarification on the consistency that you're seeing. Does that consistency on MG-ADL also allude to consistency on QMG for the data that you saw across the doses?

Yes, right. We -- there's so much data to present. We chose to focus primarily on MG-ADL because then we could show a lot of different cuts at different time points, different depth of responders without having an inordinate amount of slides. But whether you looked at MD-ADL, QMG or MGC, you saw the same thing, same trends.

Our next question comes from Tom Smith at Leerink.

Congrats on the data. Just 1 question, 1 follow-up, please. Just on the Phase II MG data, I thought the super responder and the durable MSE looked really compelling. It looks like you're seeing absolute MG-ADL improvements in the ballpark of what we've seen with some of the cell therapy data sets. I'm just wondering whether there are any changes you can incorporate into the 1402 Phase III study design that would maybe mitigate some of the placebo response that we've seen recently, not just in this study, but across the last few pivotal readouts in the space.

Yes. We looked at the placebo response in the batoclimab trial obviously to determine whether there was anything special that seemed to be driving it, and there wasn't anything. So that leaves you with just expectation bias that when you're enrolling a principal investigator discusses an FcRn trial with you today, versus 5, 6 years ago. Now they're doing so very, very enthusiastically. So that expectation bias is hard to engineer out. And in a lot of ways, it's actually a good thing that people are so excited about FcRn inhibition. I think as the primary endpoints will remain pretty similar, mean change from baseline and MG-ADL or some are using a 2-point or 3-point responder. It's a little bit like ACR20 in rheumatoid arthritis. But the most important endpoints are going to shift to these deeper and more durable responses, which will be secondary endpoints. And on those responses, placebo just does much, much, much worse. The placebo-corrected deltas when you look at deep responders and durable deep responders become a lot larger. So because the expectation bias is mostly getting a little bit of intermittent response and more modest response. So that's maybe the best thing that helps us from not worrying about placebo standpoint is the performance we're seeing on the steep and durable endpoints.

And 1 -- just 1 or 2 comments on that. One is, just as a reminder, I don't -- we didn't call this out specifically. On those stringent measures where there are head-to-head comparisons possible across trial, we are better on a placebo-adjusted basis than the competitors. For example, on MSE, our placebo-adjusted delta is we think the best ever seen, certainly in a late-stage study. And I think that just gets to the point that placebo kind of is what it is here. But when you start doing the things that push placebo down in the obvious ways, like look at the really deep responses, we actually win on a placebo-adjusted basis. Obviously, the discussion we just had on the prior call about whether we would run a head to head, that is certainly 1 change we can make to mitigate placebo adjusted impact. I guess the other point I'll make, just as a reminder, is MG is unique, actually, among all the indications we're going after, maybe MG and CIDP, in that we have to "worry" about a difference in time point or study conditions for placebo purposes. In graves, to be honest, if anything, our competitors, although those endpoints are going to be less sensitive to placebo than these, should be worried about the fact that we're ahead of them. And in most indications, the answer is we're going to be running our Phase III study under the same conditions as our peers are running them. And so whatever this headwind looks to be in this specific study, it's something that is really specific to like MG to this point in time, et cetera. So I think most of the answers on the breadth of indications, I at least am not that worried about it.

Got it. That makes sense. And just a quick follow-up. Maybe just talk a little bit about the learnings from these 2 studies and how you plan to accelerate development of 1402 in these registrational studies and drive enrollment in these increasingly competitive indications?

Yes. Thanks, Tom. So obviously, we've designed our -- both of these trials, the MG and the CIDP trial, 1402 [indiscernible] at risk because we wanted to be in a position to start them very rapidly once the batoclimab data was available. And in the case of MG, we designed this trial that I shared today for the best case data, for the case where the deep IgG suppression was consistently associated with deeper and durable responses. And so in that sense, there really aren't any adjustments that need to be made. The data hadn't been as strong, we might have had to make some adjustments. But given how strong that data is, we don't need to make any adjustments in our best case scenario [ applying to 1402 ]. The CIDP trial, that one is still being finalized, but largely just the same idea it applies, which is we've got really strong dose response. I think because there was less data in CIDP available at MG, I think the uncertainty around showing a dose response in CIDP was a little bit higher. But the dose response we saw on the INCAT responder was really, really strong. So that gives us a lot of confidence in emphasizing the higher dose for the CIDP trial.

Our next question comes from Yaron Werber at Cowen.

Great. Kind of 2 questions that are interrelated. The first one for the CIDP study, I know you did a nice job breaking it up for us by IgG lower than 70% and above 70%. Do you have a sense to give us a sense kind of how did the data look all across the board, just so we have a sense kind of how that study did? And then secondly, as I think you very nicely highlighted, the challenge here is we're trying to compare sort of 4-week data with VYVGART, the way they do their cycles and then they're off and they're on again to your kind of on 12 weeks. So is there -- you showed us the 2-week data. What does the 4-week data look like? And is there like a correlation between -- the MSE was like 40% at week 2, and I think 65% or 70% at week 12, what was it like at week 4? I'm just trying to even kind of get to an apples-to-apples comparison.

Yes. So I think for the first -- thanks for those questions, Yaron. For the first question around CIDP, the responder rates are measured in a different way between the different trials. Ours is a more stringent INCAT only responder rate. And I think when you look at the group that got a deeper than 70% IgG reduction, which was a little bit more in that half of the group, those response rates are just outstanding. In order to kind of compare across the whole group, as you asked, there, I think you can look at the mean INCAT, I-RODS, MRC-SS change from baseline. Those are maybe talked about quite as much as the response rate is, but they're publicly available, and you can go look them up and we have them on our slides. And what we saw there was across just a wide range of scales used to assess efficacy in CIDP, we saw improvement that was better than anything else that's been shown from the blended batoclimab data. I don't have the 4-week -- but to your MG question, I don't have the 4-week data at my fingertips, but it looked very good. I mean you see an improvement from week 2 to week 4 to week 6. And -- but then at that point, you sort of peaked. In those patients who are on the higher dose therapy, as we showed with the maintenance of MSE, they mostly maintain it through week 12 and not just from week 6 and then again, at week 12, but every single week. That's a very, very high bar that maintenance of MSE. If you miss even a single week, you went to an MG-ADL 2, then you're not counted in [Technical Difficulty]. So we're seeing early responses. We're seeing durable responses. And to the point Matt made, placebo corrected and absolute differences in the deep durable responses, we think is past [ 2 ] months.

We'll eventually get all of this data, probably including time point curves and everything in the medical meetings and presentations. My request of you all because you have better access than we do is ask our competitors to put out their 2-week data and their durable response data as well, so that we can compare across all the fields.

Our next question comes from Sam Slutsky of LifeSci Capital.

Great work on today's update. Just assuming a dose response is also shown in Phase III with 1402, could you just talk about how that data could potentially be marketed in the real world as it relates to selecting between the 300 and 600 mg doses as well as just switching patients from other FcRns who might have some optimal responses?

Yes, absolutely. And that's a great question, Sam. It's such a tremendous setup to have both doses available because you get an internal head-to-head, and that allows you to compare between the benefits seen with higher dose, deeper IgG suppression and standard lower dose normal suppression. On the head-to-head topic, I think Matt and I are as far apart as we'd like to do. There's no question that we could be, I think, any other FcRn. And at some point, we may do that. But it's very, very cost and time-efficient to just use our own standard dose, which is 300 milligrams 1402 as a comparison. And the beauty of that then is you have comparative data you can show physicians. I imagine a [ DHLA ] that will have a wide variety of efficacy endpoints and depth and durability of response, and they will show it at 300 or show it at 600. And you might say, well, why bother with 300, why not just use your higher dose versus placebo. Well, there are some patients who do -- there are some patients who do well on the standard dose and physicians really like the ability to titrate between the 2 doses. So there are many drivers to studying both doses in our -- at least in MG. This won't be necessarily true in every indication in our 1402 pivotal trial. And that's just going to give us a wealth of head-to-head data -- head-to-head high dose versus low dose that I think will then get to your next question, which is, okay, who's going to get the high dose? Well, it will be those people who aren't getting a deep durable response on an existing FcRn inhibitor. I think at the time that we launched 1402, most patients who are on a modern therapy for MG would be on an FcRn inhibitor because that class is preferred or strongly referred to other classes by neurologists. And some of those patients are going to be doing great, but many of them are going to be doing okay, they are great 1 week and less great the next week. They have residual symptoms, they have breakthrough symptoms. And without 1402, there's nothing really they can do. They can add prednisone, they can add some other recombinant medications, but they don't have a product to upgrade to. With the launch of 1402, that group of patients who is having breakthrough symptoms, who is having residual symptoms on a first-generation FcRn is a really, really, really nice patient for physicians to gain experience with a high dose of 1402 by upgrading them to [indiscernible] medication, and it's going to be available on the super form factor, which will be a nice icing on the [indiscernible].

And one -- just one point on switching. Look, I don't expect us to live in like a competitor refractory, VYVGART refractory patient population at all. But if you just look at like the overall MG-ADL2-point responders, for example, so I think the VYVGART -- there's like a million different ways to cut this, but the VYVGART number was, call it, 78% and our number was 93%. Just a reminder, what that means is you were basically 3x as likely to fail to generate a response on VYVGART as you are on bato. And so I think like one point about switching is there actually are a bunch of patients who will be underwhelmed by performance of some of the competitor agents. And I love the phrase Pete just used first-generation FcRn, and we want to switch off a first-generation FcRn onto a next-generation compound, of which, by the way, I'm only currently [ aware of ] one in late-stage development.

Our next question comes from Dave Risinger at Leerink.

And congrats, Matt and Pete, on the data. So I just wanted to step back to a couple of high-level questions. So first, looking ahead to future commercialization of 1402, and Pete, you addressed this a little bit, but how do real-world physicians generally consider absolute efficacy versus placebo adjusted efficacy when selecting a drug? And then second, with respect to the timing for key indications beyond MG and CIDP, could you please group them and highlight which indications 1402 will be ahead of competitors, which ones -- and which ones will be roughly in line from a timing standpoint, just to frame out the long-term commercialization opportunities in other indications beyond what you discussed today?

Thanks, Dave. Look, on the first question, and Pete's done a lot of the doc calls, so you should chime in at the end here. But I think just repeating what Pete said, I think -- look, I think docs have made it clear, they're going to look at the fatality of data, but also patients don't care how placebo does. They care about how the drug they're on does. Patients are people too, when they look at the overall data, and they care about things like a 93% response rate. So I think the answer we get from docs is they're going to look at the data and they're going to figure out the easiest way to talk about these drugs in their comparative efficacy. By the way, we've talked basically not at all on this call about form factor, but there's not even going to be a trade-off at some level. These patients -- the docs are going to tell you, this drug is easier to take because of the auto-injector and has a higher response rate, better MG-ADL improvements, et cetera. So I believe the absolute efficacy is how most docs will think about this on a practical basis. And on the timing point, Pete can give you a more specific answer or not, but look, obviously, in indications like Grave's, where we've announced the Phase III program that no one else has begun, we're definitely ahead. I would say there's 1 or 2 others of that category that we're yet to announce or maybe even more than that. Every other indication other than that handful in MG and CIDP, we will be neck and neck. So if you're looking at an indication, and it's not Grave's and it's not MG and CIDP, you could assume that we will be aligned from a timing perspective with our competitors.

Our next question comes from Alex Thomson at Stifel.

Congrats on the data. I guess to follow up a little bit on time lines here, I guess now that 1402 is officially green lit on the path forward, could you give us a sense of really what the catalyst path can look like here over the next 12 to 18 months in terms of some of the initial 1402 readouts? And then with that, curious what path is the batoclimab moving forward? Is there a path forward here for maybe some more rare indications that others aren't going after given sort of the FcRn pricing dynamics? How should we think about where batoclimab might go?

Yes. Thanks, Alex. In terms of the catalyst path, that's going to be rich as it unfolds. So we have 6 INDs approved. We've only unveiled 4 of those, the Grave's program, the difficult-to-treat positive RA, MG and CIDP. The other 2 will be unveiled very shortly here. The difficult-to-treat RA study includes an open-label run-in with just a high dose and then a randomized withdrawal. So that gives us an opportunity to generate data earlier. And then some of the new indications that we're launching that we'll be unveiling also incorporates designs that will enable us to get some data a little bit earlier. The Grave's and the MG programs are optimized for fast to approval. So those are -- they won't have the data in 2026, for example, but they will get faster to approval. So -- and then finally, with our indications, 7 through 10, some of those will also be POCs that can generate data sooner. Essentially over the next little bit, you'll see a portfolio of studies across a variety of indications. That's going to just generate a drumbeat of data in '26 and '27. And obviously, in the second half of this year, we've got the thyroid eye disease data in batoclimab. In terms of whether we would study batoclimab in some specialized indications, I don't know. I mean, it has a patent until a composition of matter patent until 2035. So we have plenty of time to make that decision. But in the short term, we're really going to be focused on launching a wide variety of trials for 1402 across indications, and that's our main effort.

Our next question comes from Yatin Suneja at Guggenheim.

Congrats on the data. Just a clarification question on the MSE data. So there are 2 sets of data you presented. One was on Slide 14, the other one was on Slide 27. Can you just talk about how are you calculating this MSE at week 6, the 75% number that you report? And then on Slide 27, there seem to be a bunch of patients that don't qualify for week 12 analysis. Like how do you get to that number? And what's going on in those patients? So that's a question on MSE. And then I think in the past, you've talked about indication priority. Can you just now, again, now that you've seen the data, where does gMG fall on your indication priority list?

Yes. Thanks, Yatin, for those questions. So in terms of the maintenance of MSE, the way that, that analysis works, what we're really trying to understand is for those patients who achieve MSE, how well can they maintain it. And the idea is that with deeper IgG suppression, you're going to be more consistently at the MSE if you achieve it, meaning your week after week after week after week, you stay with an MG-ADL of 0 or 1; whereas with lesser IgG suppression, you may have some weeks you're at MSE and some weeks you're not. So if you look at the individual patient curves, they're kind of bouncing up and down, MG-ADL 0, 1 and they go up to 2, 3 and maybe they come back. So in order to generate those percentages, we used our Period 1 data, so that's 12 weeks of placebo-controlled data. So that way, we were able to show 680 performance, 340 performance and placebo performance. And we wanted to have 6 weeks of MSE to count as durable MSE, which means that you need to achieve minimum symptom expression prior to or at week 6. Otherwise, there's not 6 weeks left in the 12-week period. So for everybody who achieved MSE regardless of which arm they were randomized to in weeks 0 through 6, they're part of that analysis. For everyone who achieved MSE in the 680 arm, 75% of them maintained it consistently until the end of the period, whereas nobody maintained it on that kind of disease. So that's kind of how that work goes. The -- I think you're referring to the -- your second question about the MSE when we looked at the performance in 2 groups, those who achieved a greater than 70% IgG reduction and those that achieved less than 70% IgG reduction. And that was defined as at the end of week 12. And we didn't have -- there was a few patients who didn't have an IgG for. So that sample set is slightly different, and that's the reason that those arms are different, but not a big difference. In terms of indication prioritization, I think we've consistently said that we're really, really excited about Grave's. That's an inordinately large potential indication for Immunovant because we're first-in-class, because we see a strong dose response, a strong IgG correlation to clinical benefits, which gives us an opportunity to be best in class. And if you can be first-in-class and best in class, that's very, very hard to catch up to for competitors. And then on top of all that, it's among rare diseases, this is a population of patients who are -- have Grave's disease and are not responding to an antithyroid drug, which is the group we're going after. That's a large group that's on the high end of a rare disease in terms of size. And then there's a final really nice dynamic, which is because there hasn't been any innovation for a while, there's a sort of a pool of patients who kind of stacked up waiting for something new. So at the time of launch, in addition to having just a regular pool of incident patients who have this big group of prevalent patients. So everything has really lined up well to make Grave's disease an inordinately large opportunity for Immunovant. Across the rest of the indications, they're all sort of similarly sized. And this data, I think that we -- to answer your question on MG, this data, it's such a strong correlation between IgG lowering and deep durable responses puts us on our higher case in terms of what we expect to achieve with 1402 in MG, but it's still not as large an opportunity as Grave's.

Sorry, just 2 quick things. One is Pete may have said this, but just because I haven't had the slide in front of me. If your question is about the 20 patients who just aren't included in the plus/minus 70% number on Slide 27, that's just literally they did not have an IgG measure at week 12, and so they couldn't be included in the cut. And why they didn't have one ranges from -- anyway because they didn't get the doctor on the right day basically. It's not a significant thing. And everything else, I totally agree with.

Our next question comes from Sam Semenkow with Citi.

Two for me. Just first on CIDP. Pete, you mentioned a few times how the endpoint for response was INCAT only, which is different than competitor trial. I'm curious on your thoughts if you were to include both I-RODS and grip strength in response analysis, how that could have impacted your responder rate, recognizing that, of course, the difference on INCAT on a comparative level, it looks quite positive. And then just secondly, just following up on the last question, recognizing that there is competition in both MG and CIDP with approved FcRn inhibitors and to your point that you've said a couple of times about how you'll be neck and neck in a lot of other indications, just curious on the market opportunity that you see in terms of maybe peak revenue, any expectations you have for gMG, CIDP versus Grave's RA and some of your other indications you are advancing with 1402?

Yes. Thanks, Sam. So for the -- in terms of CIDP response rates, so for those patients who achieved a deep IgG reduction, they have such a high response rate just with INCAT alone. If you include I-RODS response or [indiscernible] going to be a little bit higher. It probably would impact the other group more because they didn't have quite a -- the lower dose group didn't have quite as high of an INCAT response. So if you added I-RODS or grip strength, it would be a little bit higher. There are some differences also in terms of how patients got into the period 1. So we decided that, that just wasn't the best comparison to try to replicate. And given how strong the INCAT response was, given how strong the mean change from baseline was across all the scales, I think that's the best comparator. In terms of the peak revenue for different indications, as I said earlier, Grave's is an inordinately large opportunity. And difficult-to-treat RA is a little bit technically riskier. It's not sort of a slam dunk like Grave's and MG and now CIDP, although we think the nipocalimab data provides a really, really strong proof of concept. So there's a little bit bigger swing factor there. If the difficult-to-treat RA program hits, which I believe it will based on data generated by nipocalimab, then that's a really large opportunity because although early lines of rheumatoid arthritis are well satisfied with multiple mechanisms for patients who've failed a couple of different anti-cytokines and kind of the [indiscernible] most people who failed a couple of different cytokines do have a high [indiscernible]. So that's a good sized group. And for those patients, there's really not any good options today, and there's not actually much of development in that group, so that difficult-to-treat RA group is really, really good size. And then, of course, we have a couple of other indications that we're about to unveil that I think they're also going to be really exciting. So there's a portfolio of opportunities that I think are really, really, really good. And just to keep saying that, I think Grave's [indiscernible].

Just 2 quick things. One on the CIDP question, just as a reminder, I know we said this and it wasn't specifically your question, but just to reiterate it, the reason we showed the plus/minus 70% cut is because we decided not to unwind the data to dose. And so it's -- I think that is a pretty good proxy in our opinion for what dose response would look like in 1402 or in the study when it is ultimately done, but that's why that data is not available here. In terms of market opportunity, look, this is one of the things, by the way, that on various revenue calls, I've been focused on pointing out is I do think there's a little bit of a myopic perspective around slicing up what I used to call a little slice of pie that is MG. I'll now say it's a big slice of pie that is MG, but still it's only one slice of the pie. Obviously, after today's data, in my opinion, and there will be different views on this until we go into the marketplace and win, my opinion is we will get a bigger slice of that pie than I thought 2 weeks ago just based on the quality of this data. But that's still just one slice for MG. And when I think about things like Grave's disease, for example, there are 300,000 -- more than 300,000 uncontrolled Graves' patients walking around the U.S. right now. If you start trying to come up with peak sales numbers based on that math, you come up with numbers that are embarrassing such that I can't say them out loud in public, but are really large. And so I think the other thing to keep in mind is this is just -- this is not really, in my opinion, about sort of figuring out the sort of competitive like picking up crumbs as between the programs. This is about expanding the field of possible indications. It's about expanding the treatment options in this indication. And it's about unlocking a whole number of new market opportunities, including new patients within MG, but also lots of patients and other indications who don't currently have any options.

Your next question comes from Yasmeen Rahimi at Piper Sandler.

First of all, congratulations. I think listening to the Q&A, I think, in my view, the most important thing that you have proved and that's incredible is the debate on whether deeper matters. And I think this data today this morning really put that to rest. So really want to say congratulations on that and really open up that as you drive greater, deeper responses, you're going to get greater efficacy. So 2 questions. Question number one for me is given the remarkable MSE data, is there an opportunity to power that as a key secondary and therefore, have that as a differentiation on the label? And in relation to MG, question one. And then question two is, given that 1402 has given the better tolerability, it could drive higher therapeutic response. Could you maybe think about how you thought about the powering of the study? And what response you hope to achieve given those nuances and obviously, with the 2 doses? I appreciate that.

Yes, those are really astute questions, Yas. And back to the question around the trial design. So the 1402 trial design, as I said, was kind of done at risk for best case data, which we have. And I don't see any need to alter it. It's a very, very nice design in terms of the dose and duration and that kind of thing. However, the part of the trial that will likely be modified based on what we've learned from batoclimab is the SAP, meaning what do we include as a key secondary and helps the hierarchy there. Luckily, that's not on the critical path to getting the study target because that's kind of you can alter some of the study [indiscernible] database is locked. It's not a problem. And given what we've learned about the potential for deep IgG reduction to drive durable MSE in an unbelievably differentiated way from placebo, that's going to be super easy to power. So this trial will be way, way, way over, I think I just mentioned and I think even between doses. Normally, it's a little challenging to power between those comparisons. But for things like durable MSE or a certain percentage -- or a certain threshold of MG-ADL improvement maintained over time, those kind of things are going to be important to include in the key secondaries so that they're promotable -- easily promotable. That's a change that we'll make.

And if I may ask one last question. Given that a deeper IgG response drives greater efficacy, could you talk about what work could you -- could Immunovant do between now and the MG readout or across all indications to really educate the physician group of proving that deeper matters and that's across a number of indications? Like what type of initiatives will be ongoing before the Phase III's read-out?

That is a very, very good question. And the short answer is a ton of them. So if you go -- some -- or maybe many investors and analysts have asked neurologists over the last 3 months or so kind of a lead up to this data, whether IgG reduction matters in MG. And mostly, they've said, I'm not sure or no because nobody is talking about it. The approved therapies have only a single dose and don't have any real reason to talk about the correlation between IgG lowering and clinical scales. So it's not been a topic. But what has been a topic is there's -- even at a recent neurology conference, there were posters on the -- there were more posters on MSE. And so as you get to MSE and maintenance of MSE, the natural next question is, well, who's -- who are the patients that are achieving durable MSE? And it's going to be the patients who have deeper IgG reductions that we've shown. So we have a lot of data from period 1, from period 2, multiple cuts that you guys asked about that we didn't show today, just because just in the interest of time. That gives us a very, very nice opportunity to share that data at various medical meetings. And I do expect that will generate a lot of conversation with the importance of both deeper IgG reduction and the importance on achieving durable MSE and the link between those 2. So this is a topic that we intend to release a good amount of data on to drive that discussion in the neurology community. And then by the time we're launching, I think there's not going to be a question anymore that it's important to achieve the deepest IgG reductions in order to achieve the best clinical response.

So our final question comes from Jason Gerberry at Bank of America.

So just on CIPD, I was wondering if you can give us a sense of the sample size of the plus 70% threshold or below 70% threshold on IgG, either specifically or directionally. And the reason I'm just curious about this is just wondering if it ultimately makes sense in the Phase III construct to focus on high dose so that you can ensure getting more patients above that 70% threshold and optimizing for efficacy.

Yes. I mean, generally, it's about 50-50 or 55-45 in terms of the percentages. You get slightly more than a majority of patients. When you have patients on 680 and 340 in equal numbers because the vast majority of the 680 patients get there and a few 340 patients get there. So that's -- generally, whenever you're looking at those cut points, they're kind of sort of the group size is about equal. And in terms of focusing on the higher dose, I think for certain indications, we will -- we'll have in some studies where we only use a high dose or we primarily use a high dose. You already see that with Grave's. So with Grave's, we had the same cuts. We showed that the 70% -- those patients who got deeper than a 70% IgG reduction had a 60% ATD-free response versus 23% ATD-free response in those patients who have less than 70% reduction. That's just a spectacular difference in the response rate. And as a consequence, for our Grave's trial, the first one, we only used the high dose. Now many divisions, particularly in the U.S. prefer to see 2 doses. If you have 2 doses that both have efficacy, even at the higher dose is more efficacious. So I imagine that for many indications, we will study both doses, but there's definitely going to be an emphasis on our higher dose.

And just one comment, just literally to repeat something Pete said because I think it's important. The vast -- we expect the vast majority of patients on high-dose batoclimab or high dose 1402 even more importantly, to be above 70%. Our models have a number, I'm not going to give it because it's so high that it will be difficult -- it will be an easier bar to miss than to meet. But the vast, vast, vast majority of patients on high dose will be over 70%. And I think Pete correctly characterized that on low-dose batoclimab, a few patients, right? You look at this data being sort of 50-50 or 55-45 and you sort of do the math, that means if the vast majority of 680 patients are getting there, it's a relatively small percentage of patients on low dose who are getting there. And I call that out just again, to remind people, first of all, that low dose is a proxy for what competitors with mid-60s IgG suppression can deliver. And second of all, that what we believe is that the 70% is a good cut point because above 70% is a territory that we are going to more or less uniquely be able to occupy in terms of the bulk of our patients. And below 70%, it's going to be more densely competitive. And so when we look at these cut points, the right-hand side of all those charts is something that we think we're going to be pretty uniquely able to deliver among FcRns.

So this concludes today's Q&A session. I'll now turn it back over to Pete for closing remarks.

Yes. Thanks, Sarah. This is just an amazing set of data. It's been so fun to look through it over the last few days and prepare for this call. There's a lot of preparation because there's so much data. There's not just 1 or 2 cuts that show this relationship between deep IgG reduction and clinical response, but really every cut. So what we try to do is put together series of cuts that kind of logically and link to what we believe patients are really going to launch, not only in MG, but in other indications, which is a deep durable response. The same is going to be true in Grave's disease. Patients want to get [ new ] thyroid and off their ATD and they want to stay off their ATD. And so this concept of being able to deliver a deep durable response is really the future direction, I think, for many autoantibody conditions. And I think 1402 is just really, really well positioned to differentiate on that, both in terms of comparison to other doses, comparison to other FcRn inhibitors and comparison to placebo. All those differences will be launched.

Can I just make just a couple quickly closing remarks. First of all, something that I can say that Pete can -- I just want to thank Pete and Immunovant team. These things are a lot of work, both to run studies and then to see through. And so thanks to them. Thanks to the patients and the investigators, obviously, you participate in these studies. Thanks to the Roivant team who also works along side the Immunovant team on this. I guess the other 2 comments I want to make. One is, I've said this in a couple of other forums and I struggle to find the right analogy. It does feel a little bit like there's a poker game going on out there and that we're not at the table, we are the tables. And I guess that there's going to be a debate today about placebo-adjusted deltas and there's people who have opinions on these things, and we'll watch it. I think we've proven today the deeper IgG suppression yields better clinical benefit. And I think we've proven it in what is more or less the most difficult setting in myasthenia gravis to demonstrate that. So I feel more confident than I have ever felt that we are going to show that across indications, that we're going to win easily in the commercial settings where we're at or near the front of the pack and that we're going to fight hard in the commercial settings where we're not at or near the front of the pack. And I think the data today 100% supports that profile. The other thing that I want to remind people, and this is easy for me to say, is Roivant is we are fully capitalized to generate this data to launch these programs to compete in the marketplace. And so we're not going to be blind to data. We're going to think really carefully about how we spend money, what we spend it on, what indications we run at, how we compete. But I just want to be clear that like you can think about this however you want to think about it for the next couple of months. But over the next couple of years, we're going to generate a consistent set of data showing that deeper IgG suppression matters. We're going to get out there in the market, and we're going to compete aggressively. And I think that story is going to win the day for patients. So I feel pretty excited about that from here.

Very good. Thank you, everybody.