Good morning. My name is Tara Soboreski, 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, 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 detail associated with this data. We are, in short, incredibly excited about 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 statistically significant and clinically meaningful outcomes across multiple endpoints. We had a clear dose response, which is something that was important to us, with 340 mg 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 in an earlier generation of studies, but consistent with, for example, what we saw last year with Batoclimab. The truth is that because Batoclimab behaved so similar to the competitor programs, we were mostly focused on that arm of the study from a comparison perspective. Obviously, there will be a broader discussion in the world about that, and we're in the middle of it. Period two 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 Batoclimab 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.
Look, overall, incredibly exciting data and a big opportunity. The one thing I wanted to do, and I know Pete's going to do a little bit of 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-IMVT-1402, our second generation. The data today was in 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 anybody in the FcRn field can do.
It has a clean, simple subQ form factor with a 2 cc autoinjector 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. 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 that deeper IgG suppression yields better clinical benefit. Again, I think we've set a new bar for absolute treatment magnitude in the two diseases we're announcing data in today. 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 we'll jointly do some Q&A at the end.
Again, we appreciate everyone joining and excited to talk more about this data. Pete, over to you.
Thanks, Matt. I really appreciate that. 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 one of our Batoclimab trial in CIDP. 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-IMVT-1402. I know we have a lot of IMVT-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. Very briefly, why is IMVT-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 subQ preparation, but it does not have the analyte abnormalities of Batoclimab.
Both Batoclimab and IMVT-1402 bind tightly to the FcRn receptor. However, the binding orientation is different such that Batoclimab inhibits albumin binding and IMVT-1402 does not inhibit albumin binding. This advantage of IMVT-1402 was confirmed in the IMVT-1402 healthy volunteer phase I trial. With that, let's turn to the Batoclimab data we're discussing today. You can 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. Specifically, although FcRn inhibition has been a major breakthrough with two 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.
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 debate, 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 read-through to many other indications because of the consistency of that correlation that we observed. 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, IMVT-IMVT-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 one in AChR-positive participants?
AChR-positive patients made up about 70% of all enrolled patients, similar to other pivotal trials in MG. Period one has the broadest generalizability, and I believe you'll find the results very compelling. We also have period two data in hand, and I'll make a few comments about it towards the end. The results from period two also support our goals. As a brief reminder, the primary endpoint for this trial occurred at the end of the 12-week period one and assessed MG-ADL change from baseline for AChR antibody-positive. Baseline characteristics across the three 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 enroll 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 for the 680 mg dose, which has set a new benchmark for the 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 mean change from baseline in MG-ADL of 5.6 points at the primary endpoint. The 340 mg dose of Batoclimab achieved a mean IgG reduction of 65%, sorry, 64%, and a mean change from baseline of MG-ADL of 4.7. Both doses' separation from placebo was statistically significant, with 680 mg 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, and in particular, that's true with patient-reported outcomes. As you'll see, though, throughout the presentation, the placebo responses were much lower when looking at durable deep response. Here we see that 340 mg of Batoclimab delivered MG-ADL reductions in line with other FcRn inhibitors at their phase III doses, where IgG lowering was also similar. Of course, it's important to note that these data are not generated from the same study, that there were differences in study designs, and that comparison should be made with caution. From left to right, VYVGART, efgartigimod, and Batoclimab 340 mg all delivered 4.6- or 4.7-point reductions in MG-ADL with IgG reductions in the mid-60s.
With 680 mg 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 mg dose of Batoclimab basically serves as an internal reference arm. Period one of this trial is essentially a head-to-head study of high dose versus standard dose Batoclimab, with the standard dose of Batoclimab being similar to other FcRn inhibitors. In this view, we evaluated response rates across the publicly available data, phase III data for VYVGART and Batoclimab. 340 mg of Batoclimab once again looks pretty similar, reinforcing its utility as a reference arm. 680 mg of 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 mg super responder rates at the primary endpoint are similar to those reported by VYVGART and Batoclimab at their primary endpoint. Across multiple thresholds, higher response rates are observed in the 680 mg of Batoclimab arm compared to the internal reference arm of 340 mg. Here we're looking at deep responders at week two, 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 in looking from left to right at the graphs on this slide that at week two, 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 seven-pointer 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 mg of Batoclimab achieved MSE, and this was 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 is 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, 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 with 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 mg 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 criterion.
In this analysis, we looked at everyone who had a chance to achieve six or more straight weeks of MSE by assessing everyone who first achieved MSE prior to or at week six and then measuring how they were able to maintain it through week 12 at the primary endpoint. 75% of patients achieving MSE in the 680 mg arm maintained their MSE response consistently for six or more weeks. When looking at the internal reference arm of 340 mg 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 was not 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 subQ, I expect the new high bar to be maintenance of MSE, and it certainly looks like deeper IgG suppression has a really big advantage here. In terms of safety, Batoclimab was generally well tolerated with low discontinuation rates and treatment-related adverse events that were consistent with other Batoclimab trials. 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 one death in the placebo arm. Before transitioning to CIDP, I have this slide in to remind everyone that the study did have a period two. We're not covering period two data in any detail today. It's very interesting and really would require a whole separate call. I do want to emphasize, though, that the treatment benefit was maintained with continuous dosing.
For example, patients who received 340 mg of Batoclimab in period one, when they were re-randomized to continue taking 340 mg of Batoclimab in period two, they maintained their benefit. When these same patients were re-randomized to a dose reduction of 340 mg every other week, they lost benefit. 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. We will switch now to the initial results from our Batoclimab study in CIDP, where you will 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 two. I will not be reviewing any period two data today.
Recall that participants entered period one following a washout period in which they were required to worsen once their standard of care was stopped. In period one, participants were randomized to either 340 mg or 680 mg of Batoclimab delivered weekly for 12 weeks. For a combination of regulatory and competitive reasons, we chose not to underline 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 withdrawing. In terms of baseline characteristics, these are the baseline characteristics for all 73 patients who entered period one after worsening during washout. 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 one. 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 with caution. 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 one into two 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 analyses 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 mg of IMVT-IMVT-1402 will have an IgG reduction above 70%. This is also true for the large majority of patients on 680 mg of Batoclimab. On the other hand, other FcRn inhibitors generally reduce IgG by less than 70%. This is also true for Batoclimab at 340 mg.
The 70% cut point provides a nice division between what the high dose of IMVT-1402 can do, 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, iRODS, and grip strength. Our study used just INCAT response, which is stricter since that's just one part of the ECI composite. Let's look at some other efficacy scales in CIDP. iRODS is a patient-reported outcome, whereas MRCSS and grip strength are physician assessments.
In the blended Batoclimab period one data, we observed larger improvements across all three scales, likely driven primarily by the higher dose. Okay, let's settle the debate. I'm not going to read all the points at 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 subQ. Unfortunately, Batoclimab also lowers albumin, and it turns out that this lowering of albumin raises cholesterol. There is the good news that our second-generation asset preserves the ability to deliver the deepest IgG lowering in a simple subQ. However, the reduction in albumin and raising of LDL has been eliminated by engineering a different binding orientation to the FcRn receptor for IMVT-IMVT-1402.
The lower is better reads through to our second-generation asset that achieves lower without analyte abnormalities. Let me just show one or two additional data cuts to support this point that lower is better. Here we are looking at multiple different scales used for MG efficacy assessment, and you see a consistent dose response here across all three scales. 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 in those who achieved less than 70% reduction. Here we are showing MSE for patients who achieved greater than 70% IgG reduction, which was 53%. Again, deeper IgG reduction led to greater MSE rates.
Pulling it all together here, when we look at the totality of our data across Graves, MG, and 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 we expect for the vast majority of patients treated with 600 mg of IMVT-1402. We believe that a 10-point improvement in response rates between two active agents represents a meaningful differentiation in a commercial setting based on a wide variety of prior immunology precedents. These differences are all greater or much greater than that. Okay, what is our path forward in Myasthenia gravis? The IND is approved, as we've previously discussed, for IMVT-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 IMVT-1402 going forward in MG, given its superior tolerability profile without albumin and cholesterol changes. 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? It turns out that there is 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 FcRn approved, the bar 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.
The 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, IMVT-1402 is well positioned to deliver on this new and higher expectation. How will we show this with our IMVT-1402 trial? Here is a schematic of our pivotal trial in MG, and it is actually very straightforward. We are studying a similarly severe group of MG patients as we enrolled in our Batoclimab trial and as other phase III trials have enrolled. We are including AChR-positive patients as well as MuSK-positive and LRP4-positive patients in the primary analysis pool. This reminds me to mention that the results for MuSK-positive and LRP4-positive patients in the Batoclimab trial were consistent with those seen with the AChR-positive patients. We are confident to include all three groups in our primary for IMVT-1402.
Patients will be randomized to 600 mg or 300 mg of IMVT-1402, which are similarly or slightly more potent than our Batoclimab doses. A third of patients will then go to 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 doses that they were randomized to initially, and placebo patients switching to 600 mg 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 IMVT-1402, I want to make a point around translatability. A big, big theme for today is translatability. Translatability from Batoclimab to IMVT-1402 in terms of deeper IgG reduction driving greater clinical improvement.
As I said, we expect 600 mg of IMVT-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. IMVT-1402 will not have this problem. Here we show the results when we only include patients who didn't miss any of their last four 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 four doses prior to the primary endpoint at week 12.
Here you see an even bigger reduction in MG-ADL 680R, nicely clearing a 6-point reduction in MG-ADL bar that previously seemed unattainable in the controlled portions of the trial. I'll conclude here with a high-level summary of why IMVT-1402 is so exciting. It's exciting based on the compelling results we shared today showing that lower is better. Based on IMVT-1402's profile, which can deliver deeper IgG reduction without analyte abnormalities. Based on the composition of matter patents until 2043 for IMVT-1402. Based on having six INDs cleared with many other exciting indications to come. Based on all of these reasons and more, I believe that IMVT-1402 has an exceptionally bright future. With that, I'll turn it over to questions from me and Matt.
Great. Thank you, Pete. At this time, we will be conducting a question-and-answer session with our speakers.
To our analysts on the line, we kindly ask that you limit yourselves to one question and one follow-up. Please hold for a brief moment while we pull for questions. Our first question comes from Brian Cheng at JPMorgan. Please go ahead, Brian.
Thanks for taking our question this morning. Maybe just first, Pete, to walk through the super responder at week two 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 four to week eight. Can you talk about just how the MG-ADL response looks here at week four, specifically tied towards your high dose and the placebo arm? From week four and on, how does that look over the course of the 12 weeks? Thank you. I have a quick follow-up. Thank you.
Right, Brian. I think there's a couple of important points there. There's a lot of different ways that you could cut the data. We were trying to focus on what's going to be most important for patients when we introduce the concept of durability. 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. 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. The 340 mg 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 during the 680 mg- 340 mg is a good way to do that. Whenever we looked at that, when we looked at a single point in time, when we looked at durability, the 680 was 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.
Hey, 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 four-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 four-week data.
I think the reframing that's important to me is to take a step back and say, okay, but why is the field looking at four-week data? The field's looking at four-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.
The reason we've shown two 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. I think it's important to us that we focus on the unique attributes that IMVT-1402 is going to have in MG. We'll talk more about other indications, obviously, over the course of this call. Specifically in MG, what we're clearly going to be able to do better based on this dataset is get deeper faster and hold those responses for longer.
That is the impact of the deeper IgG suppression that we deliver. That is what we are focused on.
Okay. 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 IMVT-1402, do you think you will ultimately need to run a head-to-head trial against VYVGART? Thank you.
No, I do not think that is going to be required. We have a big advantage in having two doses. I focused today primarily on the additional benefit that can be achieved with a higher dose. Having two doses is also a big advantage just in and of itself in MG. Neurologists appreciate the ability to have dosing flexibility. That is why we are including both doses in our IMVT-1402 pivotal trial.
Again, that standard dose, the lower dose of IMVT-1402 will serve as essentially an internal reference arm and internal head-to-head. 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 being on this call is Pete's an actually more conservative person than I am. 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. 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 in such a study. I think the market would be forced to pay attention if we were running one. By the way, just one last point on the four-week thing. Just to be clear, 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.
Thanks for the questions, Brian. Our next question comes from Derek Archila at Wells Fargo. Please go ahead, Derek.
Hey, good morning and congrats on the data. Thanks for taking the questions. Just one in the follow-up from us. Obviously, there's a lot of focus here on the absolute rates versus placebo-adjusted rates.
Obviously, got to ask the question, why do you think these are more relevant for comparison? And then just a quick one on, it looks like in the IMVT-1402 trial, I guess you're going to look at 600 mg weekly in period two, I guess, was the driving factor of that from the BATO switch to 340 mg from 680 mg. Did you see kind of those patients worsen, kind of confirming the dose response? Is that the driving factor? Thanks.
Yeah, thanks, Derek, for those two questions. I think the emphasis on the absolute treatment response is based on a couple of things. First of all, placebo-correct, it's important. It's important for getting approval. You need to be placebo to get approved.
When comparing different agents, our discussions with clinical neurologists who treat a lot of MG patients consistently say that they prefer treatment effect because it gives them a better sense for how the patient's 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 did not even have a placebo, so everybody knew they were getting efgartigimod, essentially reported a very similar treatment effect in terms of MG-ADL as compared to the placebo-controlled phase III trial. The treatment effects are really consistent across different agents and therefore gives us the ability, I think, to compare in the way we did.
In terms of why we designed the trial to include, essentially, have 600 mg for six months versus 300 mg for six months, we're just doing the primary endpoint at week 12. 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 mg arm, and I expect it to show deeper and more durable responses. That provides sort of an internal head-to-head up to six months that is going to be very compelling data eventually for prescribing neurologists.
Got it. Thanks, Pete. Just one clarification on the consistency that you're seeing. Does consistency on MG-ADL also allude to consistency on QMG for the data that you saw across the doses? Thanks.
Yeah, right. 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. Whether you looked at MG-ADL, QMG, or MGC, you saw the same thing, same trends.
Excellent. Thank you.
Thanks, Derek. Our next question comes from Tom Smith at Leerink. Please go ahead, Tom.
Hey, guys. Good morning. Thanks for taking the questions and congrats on the data. Just one question, one follow-up, please. Just on the phase III 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 datasets.
I'm just wondering whether there are any changes you can incorporate into the IMVT-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.
Yeah, 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. That leaves you with just expectation bias that when you're enrolling and a principal investigator discusses an FcRn trial with you today versus five, six years ago, they're doing so very, very enthusiastically. That expectation bias is hard to engineer out. 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 in MG-ADL, or some are using a two-point or three-point responder. It's a little bit like ACR-20 in rheumatoid arthritis. The most important endpoints are going to shift to these deeper and more durable responses, which will be secondary endpoints. 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. The expectation bias is mostly getting a little bit of intermittent response and a more modest response. That's maybe the best thing that helps us from a not worrying about placebo standpoint is the performance we're seeing on these deep and durable endpoints.
Hey, just one or two comments on that. One is, just as a reminder, 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. I think that just gets to the point that, look, placebo kind of is what it is here. 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 at the prior call about whether we would run a head-to-head, that is certainly one change we could 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. 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. Whatever this headwind looks to be in this specific study, it's something that is really specific to MG to this point in time, etc. I think most of the answer is on the breadth of indications.
I at least am not that worried about it.
Got it. That makes sense. Just a quick follow-up. Maybe just talk a little bit about the learnings from these two studies and how you plan to accelerate development of IMVT-1402 in these registrational studies and drive enrollment in these increasingly competitive indications. Thanks so much.
Yeah, thanks, Tom. Obviously, we've designed both of these trials, the MG and the CIDP trial and IMVT-1402, a little bit at risk because we wanted to be in a position to start them very rapidly once the Batoclimab data was available. In the case of MG, we designed this trial that I shared today for the best-case data, for the case where the deeper IgG suppression was consistently associated with deeper and durable responses. In that sense, there really aren't any adjustments that need to be made.
If the data had not been as strong, we might have had to make some adjustments. Given how strong Batoclimab data is, we do not need to make any adjustments in our best-case scenario for IMVT-1402. The CIDP trial, that one is still being finalized, but largely the same idea applies, which is we have got really strong dose response. I think because there was less data in CIDP available than MG, the uncertainty around showing a dose response in CIDP was a little bit higher. The dose response we saw on the INCAT responder was really, really strong. That gives us a lot of confidence in emphasizing the higher dose for the CIDP trial.
Thanks for the questions, Tom. Our next question comes from Yaron Werber at Cowen. Please go ahead, Yaron.
Great. Thanks so much. Kind of two 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? Secondly, as I think you very nicely highlighted, the challenge here is we're trying to compare sort of four-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. You showed us the two-week data. What does the four-week data look like? Is there a correlation between the MSE was like 40% at week two, and I think 65% or 70% at week 12? What was it like at week four?
I'm just trying to even trying to get to an apples-to-apples comparison. Thank you.
Yeah. 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. I think when you look at the group that got a deeper than 70% IgG reduction, which was a little bit more than half 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, iRODS, MRCSS change from baseline. Those aren't maybe talked about quite as much as the response rate is, but they're publicly available. You can go look them up, and we have them on our slides.
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, blended Batoclimab data. I don't have the four-week, but your MG question, I don't have the four-week data at my fingertips, but it looked very good. I mean, you see an improvement from week two to week four to week six. By then, at that point, you're sort of peaked. For those patients who are on the higher dose therapy, as we showed with the maintenance of MSE, they mostly maintain it through week 12. Not just from week six and then again at week 12, but in every single week, that's a very, very high bar, that maintenance of MSE.
If you miss even a single week where you went to an MG-ADL of two, then you're not counted in, or you're not part of the 70%. We are seeing early responses. We are seeing durable responses. To the point Matt made, placebo-corrected and absolute differences in the deep durable responses, we think is best in class.
We will eventually get all of this data, probably including time point curves and everything, into 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 two-week data and their durable response data as well so that we can compare across all the fields.
Great. Thank you for the questions, Yaron. Our next question comes from Sam Slutsky at LifeSci Capital. Please go ahead, Sam.
Hey, good morning, everyone.
Thanks for taking my question and great work on today's update. Just assuming a dose response is also shown in phase III with IMVT-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 mg and 600-mg doses, as well as just switching patients from other FcRNs who might have suboptimal responses?
Yeah, absolutely. 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 like to joke. There's no question that we could beat, I think, any other FcRN. At some point, we may do that.
It is very, very cost and time efficient to just use our own standard dose, which is 300 mg, IMVT-1402, as a comparison. The beauty of that, then, is you have comparative data you can show physicians. I imagine a DTLA that will have a wide variety of efficacy endpoints on depth and durability of response, and it will show it at 300 mg or show it at 600 mg. You might say, "Why bother with 300 mg? Why not just use your higher dose versus placebo?" There are some patients who do well on the standard dose, and physicians really like the ability to titrate between the two doses. There are many drivers to studying both doses in our, at least in MG. This will not be necessarily true in every indication in our IMVT-1402 pivotal trial.
That is just going to give us a wealth of head-to-head data, head-to-head high dose versus low dose. I think we will then get to your next question, which is, "Okay, who is going to get the high dose?" It will be those people who are not getting a deep durable response. On an existing FcRn inhibitor, I think at the time that we launched IMVT-1402, most patients who are on a modern therapy for MG will be on an FcRn inhibitor because that class is preferred or strongly preferred to other classes by neurologists. Some of those patients are going to be doing great, but many of them are going to be doing okay. They are great one week and less great the next week. They have residual symptoms. They have breakthrough symptoms. Without IMVT-1402, there is nothing really they can do. They can add prednisone.
They can add some other concomitant medications, but they do not have a product to upgrade to. With the launch of IMVT-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 a physician to gain experience with the high dose of IMVT-1402 by upgrading them to this more potent medication. It is going to be available in a super form factor, which will be a nice icing on the cake.
Hey, just one point on switching. Look, I do not expect us to live in a competitor refractory, VYVGART refractory patient population at all. If you just look at the overall MG-ADL 2-point responders, for example, I think there are a million different ways to count this, but the VYVGART number was called at 78%, and our number was 93%.
Just as a reminder, what that means is you were basically 3x as likely to fail to generate a response on VYVGART as you are on Batoclimab. I think one point about switching is there actually are a bunch of patients who will be underwhelmed by performance of some of the competitor agents. I love the phrase Pete just used, first-generation FcRn, and will 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.
Great. Thanks for the question, Sam. Our next question comes from Dave Reisinger at Leerink. Please go ahead, Dave.
Thanks very much, and congrats, Matt and Pete, on the data. I just wanted to step back to a couple of high-level questions.
First, looking ahead to future commercialization of IMVT-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? Second, with respect to the timing for key indications beyond MG and CIDP, could you please group them and highlight which indications IMVT-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 so much.
Thanks, Dave.
Look, on the first question, and Pete's done a lot of the doc calls, so he 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 totality 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. 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 and 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. The docs are going to tell you this drug is easier to take because of the autoinjector and has a higher response rate, better MG-ADL improvements, etc. I believe the absolute efficacy is how most docs will think about this on a practical basis. On the timing point, Pete can give a more specific answer or not, but look, obviously, in indications like Graves, where we've announced a phase III program that no one else has begun, we're definitely ahead. I would say there's one or two 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.
If you're looking at an indication and it's not Graves and it's not MG and CIDP, you can assume that we will be aligned from a timing perspective with our competitors.
Thank you.
Thanks, Dave.
Yes. Thank you for the questions, Dave. Our next question comes from Alex Thompson at Stifel. Please go ahead, Alex.
Great. Thanks for taking my questions and congrats on the data. I guess to follow up a little bit on timelines here, I guess now that IMVT-1402 is officially greenlit on the path forward, could you give us a sense of really what the catalyst path could look like here over the next 12-18 months in terms of some of the initial IMVT-1402 readouts? And then with that, curious what happens to patel-camab 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? Thanks.
Yeah, thanks, Alex. In terms of the catalyst path, that's going to be rich as it unfolds. We have six INDs approved. We've only unveiled four of those: the Graves program, the difficult-to-treat pathophobic RA, MG, and CIDP. The other two will be unveiled very shortly here. The difficult-to-treat RA study includes an open-label run-in with just the high dose and then a randomized withdrawal. That gives us an opportunity to generate data earlier. Some of the new indications that we're launching, sorry, that we'll be unveiling also incorporate designs that will enable us to get some data a little bit earlier. The Graves and the MG programs are optimized for fast-to-approval.
Those are they won't have data in 2026, for example, but they will get faster-to-approval. Finally, with our indications 7 through 10, some of those will also be POCs that can generate data sooner. Essentially, over the next nice 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 2026 and 2027. 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 composition of matter patent until 2035. We have plenty of time to make that decision. In the short term, we're really going to be focused on launching a wide variety of trials for IMVT-1402 cross-indications.
That's our main effort.
Great. Thanks for the questions, Alex. Our next question comes from Yatin Suneja at Guggenheim. Please go ahead,
Yatin. Hi. Thank you for taking my question and congrats on the data. Just a clarification question on the MSE data. There are two sets of data you presented. One was on slide 14, the other one on slide 27. Can you just talk about how you are calculating these MSE at week 6, the 75% number that you report? On slide 27, there seem to be a bunch of patients that do not qualify for week 12 analysis. How do you get to this number, and what is going on in those patients? That is a question on MSE. I think in the past, you have 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? Thank you.
Yeah, thanks, Alex, for those questions. 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? The idea is that with deeper IgG suppression, you're going to be more consistently at the MSE if you achieve it, meaning 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. 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. In order to generate those percentages, we used our PERI-1 data. That is 12 weeks of placebo-controlled data. That way, we were able to show 680 performance, 340 performance, and placebo performance. We wanted to have six 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 are not six weeks left in the 12-week period. For everybody who achieved MSE, regardless of which arm they were randomized to in weeks 0 through 6, they are 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 the disease. That is kind of how that one goes.
I think you're referring to the you're talking about the MSE where we looked at the performance in two groups. Those who achieved a greater than 70% IgG reduction, those that achieved less than 70% IgG reduction, and that was defined as at the end of week 12. We didn't have there were a few patients we didn't have an IgG for, so that sample set is slightly different. That's the reason that those ends are a little bit different, but not a big difference. In terms of indication prioritization, I think we've consistently said that we're really, really excited about Graves. 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 one of the benefits, which gives us an opportunity to be best in class.
If you can be first in class and best in class, that's very, very hard to catch up to for competitors. On top of all that, it's among rare diseases. This is the population of patients who have Graves' disease and are not responding to an anti-thyroid drug, which is the group we're going after. That's a large group. It's on the high end of rare disease in terms of size. There is 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 have kind of stacked up waiting for something new. At the time of launch, in addition to having just a regular pool of incident patients, you have this big group of prevalent patients.
Everything is really lined up well to make Graves' disease an inordinately large opportunity for Immunovant. Across the rest of the indications, they're all sort of similarly sized. This data, I think that we've connected your question around MG, this data that shows 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 IMVT-1402 in MG, but it's still not as large an opportunity as Graves'. Sorry, just two quick things. One is, Pete may have said this, but just because I happen to have a slide in front of me.
If your question is about the 20 patients who just are not included in the ± 70% number on slide 27, that is just literally they did not have an IgG measure at week 12, and so they could not be included in the cut. And why they did not have one ranges from, well, anyway, it is because they did not get to the doctor on the right day, basically. It is not a significant thing. Cool. Everything else I totally agree with. Thanks, yeah.
Great. Thank you for the questions, Yatin. Our next question comes from Sam Semenkow at Citi. Please go ahead, Sam.
Hi, good morning, and thanks very much for taking our question. 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 a competitor trial.
I'm curious on your thoughts of if you were to include both iRODS and grip strength in a 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. Just secondly, just following up on the last question, recognizing that there is competition in both MG and CIDP with approved FcRn inhibitors. 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 Graves, RA, and some of your other indications you're advancing with IMVT-1402. Thanks very much.
Yeah, thanks, Sam.
In terms of the CIDP response rates, for those patients who achieved a deep IgG reduction, they have such a high response rate just with INCAT alone. If you include iRODS response or grip strength response, it is going to be a little bit higher. It probably would impact the other group more because the lower dose group did not have quite as high of an INCAT response. If you added iRODS or grip strength, it would be a little bit higher. There are some differences also in terms of how patients got into the PERI-1. We decided that that just was not the best comparison to try to replicate. Given how strong the INCAT response was, given how strong the mean change in baseline was across all the scales, I think that is the best comparator.
In terms of the peak revenue for different indications, as I said earlier, Graves is an inordinately large opportunity. Difficult-to-treat RA is a little bit technically riskier. It's not sort of a slam dunk like Graves and MG and now CIDP, although we think the Nipocalimab data provides a really, really strong proof of concept. There is 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 failed a couple of different anti-cytokines and have a high ACPA, most people who failed a couple of different cytokines do have a high ACPA. That is a good-sized group. For those patients, there are really not any good options today.
There is not actually much in development for that group. That difficult-to-treat RA group is really, really good size. Of course, we have a couple of other indications that we are about to unveil that I think will also come into the really exciting. There is a portfolio of opportunities that I think are really, really good. Just to keep saying it, I think Graves is the one that is inordinately large.
Just two quick things. One on the CIDP question, just as a reminder, I know we said this and it was not specifically your question, but just to reiterate it. The reason we showed the ± 70% cut is because we decided not to unwind the data to dose.
I think that is a pretty good proxy, in our opinion, for what dose response would look like in IMVT-1402 or in the study when it is ultimately done. That is why that data is not available here. In terms of market opportunity, this is one of the things, by the way, that on various relevant calls I have been focused on pointing out is I do think there is a little bit of a myopic perspective around slicing up what I used to call a little slice of pie that is MG. I will now say it is a big slice of pie that is MG, but still it is only one slice of the pie.
Obviously, after today's data, 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 two weeks ago, just based on the quality of this data. That is still just one slice for MG. When I think about things like Graves' disease, for example, there are 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.
I think the other thing to keep in mind is 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 is about expanding the treatment options within each indication. It is about unlocking a whole number of new market opportunities, including new patients within MG, but also lots of patients in other indications who do not currently have any options.
Thanks for the question, Sam. Our next question comes from Yasmeen Rahimi at Piper Sandler. Please go ahead, Yas.
Good morning, team. First of all, congratulations. I think listening to the Q&A, I think in my view, the most important thing that you have proven that is incredible is the debate on whether deeper matters.
I think this data today, this morning, really put that to rest. I 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. Two 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 in relation to MG? Question one. Question two is, given that IMVT-1402 has a, given the better tolerability, it could drive a 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 two doses? I appreciate that.
Yeah, those are really astute questions, Yas. Back to the question around the trial design.
The IMVT-1402 trial design, as I said, was kind of done at risk for best-case data, which we have. 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 the Tolkamab is the SAP, meaning what do we include as a key secondary and what's the hierarchy there? Luckily, that's not on the critical path to getting the study started because that's the kind of thing you can alter as long as it's done in the database it's logged. It's not a problem. 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.
This trial will be way, way, way overpowered on that dimension. I think even between doses, normally it's a little challenging to power between dose comparisons, but for things like durable MSE 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 secondary so that they're promotable, easily promotable. That's a change that we'll make.
If I may ask one last question, given that a deeper IgG response drives greater efficacy, could you talk about what work 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? What type of initiatives will be ongoing before the phase III's readout?
That is a very, very good question.
The short answer is a ton of them. If you go, some or maybe many investors and analysts have asked neurologists the last three months or so, kind of in the lead-up to this data, whether IgG reduction matters in MG. Mostly they've said, "I'm not sure or no," because nobody's talking about it. The approved therapies have only a single dose and do not have any real reason to talk about the correlation between IgG lowering and clinical scales. It's not been a topic. What has been a topic is even at a recent neurology conference, there were posters on, there were more posters on MSE. As you get to MSE and maintenance of MSE, the natural next question is, who are the patients that are achieving durable MSE?
It is going to be the patients who have deeper IgG reductions who we have shown. We have a lot of data from PERI-1, from PERI-2, multiple cuts that you guys asked about that we did not show today just in the interest of time. That gives us a very, very nice opportunity to share that data at various medical meetings. I do expect that will generate a lot of conversation about the importance of both deeper IgG reduction and the importance of achieving durable MSE and the link between those two. This is a topic that we intend to release a good amount of data on to drive that discussion in the neurology community. By the time we are launching, I think it is not going to be a question anymore that it is important to achieve the deepest IgG reductions in order to achieve the best clinical response.
Thank you. Congrats again.
Thanks, Yas.
Yas, thanks for the questions, Yas. Our final question comes from Jason Gerberry at Bank of America. Please go ahead, Jason.
Hey, guys. Thanks for squeezing me in. Just on CIDP, I was wondering if you can give us a sense of the sample size of the +70% threshold or below 70% threshold on IgG, either specifically or directionally. 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. Thanks.
Yeah. 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 mg and 340 mg in equal numbers because the vast majority of the 680 mg patients get there and a few 340 mg patients get there. Generally, whenever you're looking at those cut points, they're kind of the sort of the group size is about equal. In terms of focusing on the higher dose, I think for certain indications, we'll have some studies where we only use the high dose or we primarily use the high dose. You already see that with Graves. With Graves, 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 had less than 70% reduction. That's just a spectacular difference in size, the response rate.
As a consequence, for our Graves trial, the first one, we only used the high dose. Many divisions, particularly in the U.S., prefer to see two doses if you have two doses that both have efficacy, even if the higher dose is more efficacious. I imagine that for many indications, we will study both doses. There is definitely going to be an emphasis on our higher dose.
Just one comment, just literally to repeat something Pete said, because I think it's important. We expect the vast majority of patients on high-dose Batoclimab or high-dose IMVT-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'll be a difficult, it'll be an easier bar to miss than to meet.
The vast, vast, vast majority of patients on high dose will be over 70. 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 mg patients are getting there, it's a relatively small percentage of patients on low dose who are getting there. 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. Second of all, what we believe is that 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.
Below 70, it's going to be more densely competitive. 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.
All right. Thanks, guys.
Great. Thank you for the questions, Jason. This concludes today's Q&A session. I'll now turn it back over to Pete for closing remarks.
Yeah, thanks, Tara. 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. It's a lot of preparation because there's so much data. There's not just one or two cuts that show this relationship between deep IgG reduction and clinical response, but really every cut.
What we tried to do is put together a series of cuts that kind of flow logically and link to what we believe all patients are really going to want, not only in MG, but in other indications, which is a deep durable response. The same is going to be true in Graves' disease. Patients want to get euthyroid and off their ATD, and they want to stay euthyroid and stay off their ATD. This concept of being able to deliver a deep durable response is really the future direction, I think, for many autoantibody conditions. I think IMVT-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 large.
Can I just make just a couple quickly closing remarks?
First of all, something that I can say that Pete can't. I just want to thank Pete and the Immunovant team. These things are a lot of work, both to run a study and then to see through. Thanks to them. Thanks to the patients and the investigators, obviously, who participate in these studies. Thanks to the Roivant team who also works alongside the Immunovant team on this. The other two comments I want to make, one is I've said this in a couple of other forums, and I've struggled 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 table. I get that there's going to be debate today about placebo-adjusted deltas, and there's people who have opinions on these things. We'll watch it.
I think we've proven today that deeper IgG suppression yields better clinical benefit. I think we've proven it in what is more or less the most difficult setting, and my esteemed graph is to demonstrate that. 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. 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.
We are not going to be blind to data. We are going to think really carefully about how we spend money, what we spend it on, what indications we run at, how we compete. I just want to be clear that you can think about this however you want to think about it for the next couple of months. In the next couple of years, we are going to generate a consistent set of data showing that deeper IgG suppression matters. We are going to get out there in the market, and we are going to compete aggressively. I think that story is going to win the day for patients. I feel pretty excited about that from here.
Very good. Thank you, everybody.