Immunovant Q2 2025 Earnings Call Transcript

Quartr
Provided by Quartr
November 7, 2024

Key Takeaways

  • Positive Sentiment: Immunovant said it has now cleared five INDs in 2024, ahead of its internal plan, and remains on track to launch 10 indications by March 2026 with several registrational trials starting before March 2025.
  • Positive Sentiment: In Graves' disease, the company highlighted strong batoclimab proof-of-concept data that it says can translate to IMVT-1402, including a notably higher ATD-free response in patients with 70%+ IgG suppression.
  • Positive Sentiment: Immunovant unveiled a new pivotal program in ACPA-positive, difficult-to-treat rheumatoid arthritis, supported by prior FcRn data suggesting deeper IgG reduction may drive better clinical responses in this biomarker-defined subgroup.
  • Neutral Sentiment: The company emphasized a novel RA trial design with an open-label lead-in followed by randomized withdrawal, which it says should improve enrollment, generate early catalyst data, and still provide registrational evidence.
  • Positive Sentiment: Management reiterated that MG and CIDP remain on track for data readouts early next year, while the thyroid eye disease readout has shifted to the second half of next year.
AI Generated. May Contain Errors.
Earnings Conference Call
Immunovant Q2 2025
00:00 / 00:00

There are 10 speakers on the call.

Speaker 3

Good morning. My name is Tara Sobreski, 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, 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, and the market opportunity for Immunovant's product candidates, including Graves' disease and difficult-to-treat rheumatoid arthritis. 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 for those indicated or anticipated.

Speaker 3

For more information, investors are encouraged to review Immunovant's most recent quarterly report on Form 10-Q filed with the SEC on November seventh, 2024. Joining me on this call this morning is Dr. Peter Salzmann, Chief Executive Officer at Immunovant. Following his prepared remarks, we will open the call for questions. With that, I would like to turn the call over to Dr. Salzmann.

Speaker 4

Thanks, Tara. Good morning, everyone, thank you for joining our call. At Immunovant, we're dedicated to enabling normal lives for people with autoimmune diseases. Today, I'm going to discuss two very exciting indications within the context of our overall development plans for our lead asset, IMVT-1402. First, though, I will highlight the very significant progress we've made in 2024 in advancing the development of IMVT-1402 since the phase I data were presented at the end of last year. Graves' disease is, of course, an exciting first-in-class indication, I will highlight some recently disclosed data that I believe you'll find very intriguing. After that, I'll have the great pleasure of introducing Dr. Peter Taylor from the University of Oxford. Dr. Taylor is a world leader in the field of rheumatology, I look forward to properly introducing him later in the call.

Speaker 4

He will help me unveil our pivotal trial in ACPA-positive, difficult-to-treat rheumatoid arthritis, where 1402 has potential for a best-in-class profile. I think you're all generally familiar with our lead assets, 1402. However, I want to emphasize a very unique combination of features. Other FcRn inhibitors might match one or even two of these features, I believe only 1402 combines the ability for maximum FcRn-mediated IgG suppression in the neighborhood of 80%, being achieved with a practical amount of medication that can be given subcutaneously and doesn't have an impact on analytes. This trifecta of features is what makes IMVT-1402 so unique. Given the strength of 1402's profile, also given the potential breadth of indications that could be pursued with an anti-FcRn, there is no shortage of great indications we might choose to pursue.

Speaker 4

Since we are waiting to disclose the individual indications until they are more or less ready to go from a study startup standpoint, I do want to provide our indication selection framework. At the top of the list are first-in-class indications. There aren't many of these left, but there are some, and they are uniquely valuable specifically for 1402. What I mean by that is when an asset is not only first in class but also best in class, then it's very hard for the competition to catch up. A first-in-class program which is not best in class can be matched with a later entrant. In fact, that's what we hope to do with our best-in-class offerings. Among the best-in-class assets, sorry, indications that we might pursue, there are those which are classic autoantibody-driven conditions.

Speaker 4

These have the advantage of a lot of data supporting the idea that deeper IgG reduction can yield better clinical efficacy. Another category of indications are more general autoimmune conditions where recent information suggests the importance of autoantibodies. In several of these indications, and we will review today ACPA-positive, difficult-to-treat rheumatoid arthritis, there is a strong suggestion from in-class data that deeper IgG reduction may yield better clinical efficacy. All three of these offer a lot of opportunity. Although we're talking today primarily about Graves' disease and difficult-to-treat rheumatoid arthritis, there is this wide portfolio of indications that we're working towards. So far in 2024, we have cleared five INDs across a range of therapeutic areas and with different FDA divisions. This includes announced and unannounced indications.

Speaker 4

For anyone who's ever been close to the development of a pivotal protocol and the submission of an IND for such a program, you'll appreciate that even a single or two INDs is a lot of work. To have achieved five INDs, all having been cleared by now, is really a tremendous accomplishment, and I'm very, very proud of our team for having achieved that. That's ahead of schedule that we set for ourselves, and therefore we're well on track to launch 10 indications by March of 2026, with four or five of those indications being started as potentially registrational trials prior to March of 2025. Along the way, our experience with the batoclimab offers many options to accelerate our 1402 development program. Okay, let's take a quick look at the Graves' disease opportunity and some recent data that we shared.

Speaker 4

As a reminder, for those of you who are following our story closely, you'll know this data well. For everyone, we recently disclosed data demonstrating a strong response rate in a population of Graves' patients who had insufficiently responded to antithyroid drugs. This is ultimately the target population that we hope to serve with 1402. This proof of concept study was, of course, done with batoclimab, but given the comparable IgG reduction between batoclimab and 1402, the findings that we have disclosed with batoclimab can be immediately translated to our 1402 development program in Graves'. On this slide, you see not only strong response rates in terms of normalizing T3 and T4, but a very strong response rate in terms of patients not only normalizing their T3 and T4, but being able to completely come off their antithyroid drug.

Speaker 4

This study employed a design where patients were treated with high-dose batoclimab for 12 weeks and then standard dose batoclimab for an additional 12 weeks. This design allowed us to explore the relationship of not only dose response, but also the relationship between depth of IgG reduction and clinical response, given that there is some variability in IgG reduction on the 340 milligram dose. This slide, I think, is maybe the most important slide from our Graves' disease program and shows, I think, remarkably, a large difference in patients who achieved the strict endpoint of ATD-free response, so normalizing their T3 and T4 while getting completely off their antithyroid drug. You see for those patients whose IgG was lowered by 70% or more, they had a 60% ATD-free response rate.

Speaker 4

Whereas for those patients whose IgG was not as suppressed, so their IgG was less than 70% suppressed at week 24, their ATD response rate was only 23%. We chose this 70% cut point because it highlights, I think, something that 1402 is uniquely able to achieve, which is to get the entire population treated over this threshold, whereas other anti-FcRn, including our own at their standard dose, would have a lesser IgG suppression on the left-hand side. This is what I mean by first in class and best in class in Graves' disease. Recently, at the American Thyroid Association meeting in Chicago, we had a chance to disclose some additional data from this trial, and specifically, during an oral presentation, finding extra-thyroidal findings.

Speaker 4

Here you're looking at a change from baseline in proptosis expressed in absolute terms, this is the median change for the population, which was two and a half millimeters already at 12 weeks and then three millimeters at 24 weeks. These are impressive changes in proptosis, and they were matched by changes in lid aperture as well. You do see a more pronounced impact during the first 12 weeks on a higher dose of batoclimab. The changes, both extra-thyroidal and thyroidal, yielded impressive improvements in quality of life, particularly for those patients who achieved that high bar response of being off ATD with normal T3 and T4. Among that group of patients, nearly 90%, 89% of them had a normal quality-of-life score. You see that in the left-hand graph by the end of 24 weeks.

Speaker 4

I remind you that the population we're targeting to serve with Graves' disease is a common and important population. Because there hasn't been a lot of innovation in Graves' disease, you may get a different perspective on the degree of unmet need from different physicians, and that would be particularly true if you're speaking with endocrinologists that don't specialize exclusively or nearly exclusively on the treatment of Graves' disease. This study here was done with 140 endocrinologists that do see predominantly Graves' patients, so they have a lot of clinical experience in the treatment of Graves' disease. We randomly pulled eight charts from each of those physicians to generate 1,000 patients' charts, which were objectively coded and analyzed. This is a very robust look at what's happening in actual clinical practice in the U.S.

Speaker 4

You see that 60% of patients did achieve a euthyroid state relatively easily with antithyroid drugs. Antithyroid drugs work well for a portion of patients with Graves' disease. However, at the other end of the spectrum, there were 23% of patients who actually never even became euthyroid. They did not achieve any degree of control in terms of normalizing T3 and T4, despite being treated by an expert physician for a good period of time. Then in the middle, there were 16% who did achieve control, but it was challenging. There was a lot of titration required, a lot of extra visits, a lot of blood draws to manage their T3 and T4. Some patients just have a much narrower therapeutic window. What I mean by that is small changes in their antithyroid drug can lead to wide swings in their thyroid control.

Speaker 4

This is something that we would not expect to be the case with FcRn inhibition, since you can't drive someone to become hypothyroid with FcRn inhibition, whereas you can drive someone to become hypothyroid with antithyroid drug therapy. Beyond just the ability to gain control, that's a primary benefit of anti-FcRn therapy. Having that control be achieved in an easier way is a second benefit. In order to validate that potential benefit, we've designed a pivotal trial. This is the first of two pivotal trials that will enroll a population very similar to the batoclimab proof of concept. Those patients will be people who are hyperthyroid despite antithyroid drug therapy, and they will be randomized to 14.02 or placebo. We're only using our high dose in this study because we believe that the lower dose may not be as successful based on the batoclimab data.

Speaker 4

We really think the high dose is uniquely positioned to serve patients with Graves' disease by achieving that mean IgG reduction of 80% with nearly every one above 70%. This is a trial that we're very excited about. There will be a second trial, which we are in the process of finalizing now. Taken together, that will be the primary data for our Graves' disease program. Okay. In addition to Graves' disease, today I'm excited to unveil our program in difficult-to-treat rheumatoid arthritis. This is, as I've said when I was reviewing our progress today on our portfolio, one of the five indications that we have an IND cleared in.

Speaker 4

It's one of our earlier indications because there are some unique elements of our trial design that we'll discuss in a moment, which allow it to provide not only an early data catalyst, but also for some parallel processing. Before I get to that, I want to welcome Dr. Peter Taylor to the call. Dr. Taylor is the Norman Collisson Chair of Musculo-Skeletal Sciences at the University of Oxford, and he is a fellow of St. Peter's College at Oxford. He's the head of clinical sciences at the Botnar Research Centre, where he directs the Inflammation across Tissues Theme and leads the Rheumatology Clinical Trials group and related translational research program at the Kennedy Institute of Rheumatology. Dr. Taylor has special clinical interest in rheumatoid arthritis and early inflammatory arthritis.

Speaker 4

He has over 20 years' experience in clinical trial design and international study leadership for multiple biologic and small molecule therapies in rheumatology. I'll also note, is really an outstanding clinician with a very nuanced and fine appreciation of what patients experience every day with these conditions. That insight is invaluable for companies like us working to design a trial in one of these conditions. With that, I'm going to turn it over to Peter to talk about some of the background here.

Speaker 5

Well, thank you very much indeed, Pete, for the generous introduction. Good morning to everybody. I have to confess that time marches on, in fact, it's probably well over 20 years of experience now, we might need to add another decade to that. That's another story. Actually, it's an appropriate remark in some ways because I'd like to introduce our audience to how the landscape has changed over the course of a generation in order to contextualize contemporary unmet need and the relevance of the dialogue that we're having today. You'll all be aware that rheumatoid arthritis is a very unpleasant condition. There's no cure currently. It's a chronic progressive disease that's going to last a lifetime once it starts. It causes not only joint inflammation and pain, but potentially it causes a great deal of joint destruction with accompanying loss of function.

Speaker 5

Now, a generation ago, when I started out in rheumatology, our clinics were full of poor souls in wheelchairs. Basically, if a patient had developed rheumatoid arthritis, they were going to lose their employment within a very short time. People came out of work. They had a really awful quality of life, they died prematurely. Matters changed some years later when the first targeted therapies came about, this came about really for two concurrent reasons. One was a much better understanding of the pathobiology of disease, the second was the development of protein engineering, which allowed us to pick off key therapeutic targets. Of course, over more recent years, we've had advances in chemical engineering, which has enabled the development of small molecules.

Speaker 5

All of this has been a tremendous success story to a degree, in as much that now we don't see this awful structural damage to the same degree as shown in the radiographs here. It can happen. It's less common, thank goodness. Patients do have functional deficits. It does impact on employment. The reality is that many of the symptoms that patients have today are not so readily visible to the observer, but certainly impact hugely on quality of life. This is a common condition. About 0.5% to 1% of the population have rheumatoid arthritis. It's the most common systemic autoimmune condition. Although we have this really quite expanded array of effective therapeutics now, the difficulty is that they're all similarly effective.

Speaker 5

After failure of the first particular agent, if you don't have an adequate response to treatment, the switching to any of the others gives an almost exactly similar chance of response. The chance of responding meaningfully is around about 50%. On the one hand, you could argue that we have a perfect biomarker because it's just a flip of the coin. In seriousness, the reality is that if you've got a 50% chance of responding at a not all that impressive level, we're left with a problem. What happens is that patients cycle through different advanced therapies, and at each point in the cycle, they often get more and more refractory to responding to the next drug. This is a real issue in contemporary practice, and the size of that population is increasing.

Speaker 5

That begs the question as to why might there be an interest in anti-FcRn in this situation. The advances in understanding the pathobiology that I mentioned really have been to note the role of cytokines, and the key pro-inflammatory cytokines, IL-6 and TNF, have become really very well-validated targets over the last quarter-century and form the backbone of our therapeutic armamentarium, biologics targeting these particular cytokines. Of course, we also have other agents, B-cell depleting agents, co-stimulation blockers, and more recently, JAK inhibitors. Each one of these agents has a different benefit/risk ratio, with the nature of the risks associated with drug being somewhat different. We don't currently have biomarkers that will reliably inform which drug a patient will refer to or respond to.

Speaker 5

FcRn is the neonatal Fc receptor, and the biologists among you will know that, of course, the name comes because this is the molecule that enables transfer of potentially protective Immunoglobulin G from the maternal circulation to the fetal circulation. In the first few months of birth, a fetus has some degree of protection to environmental pathogens. In actual fact, the FcRn receptor is also responsible for the homeostasis of Immunoglobulin G. IgG is in fact the most abundant protein, or one of the most abundant proteins in peripheral blood of human beings because of this receptor, because it rescues the IgG from being degraded within the cytoplasm of a whole variety of cells. If you were to block the FcRn receptor, you would prevent that rescue process.

Speaker 5

In the situation in the face of any condition that has autoantibodies that are driving the pathogenesis, this would be advantageous. Furthermore, there'd be a theoretical advantage here because although you would diminish the concentration of pathogenic autoantibodies, you would not disable the ability of the whole cellular adaptive immune system to respond to another pathogenic insult. There could be many advantages of inhibiting FcRn. Of course, it presumes that there would be an IgG that's pathogenic. In rheumatoid arthritis, we've known for a long time about rheumatoid factors, which can be of any isotype, but the majority that we measure are IgM, and that's not affected by the FcRn mechanism. IgG rheumatoid factor is also, we know, of interest and pathogenic relevance in rheumatoid, but there's also this interest in ACPAs and the role that ACPAs may play in the pathobiology of the disease.

Speaker 5

Let's look at that a little bit more closely. Sorry, it skipped two slides. We'll just go back to ACPAs. There's been a lot of interest in ACPAs over the last 20 years or so. These are very good diagnostic autoantibodies. They're not so good at actually reflecting disease activity as rheumatoid factor is, but they're also poor prognostic antibodies. Patients with higher levels of ACPA and rheumatoid factor tend to have more destructive erosive disease. We know that the whole process of developing autoantibodies against citrullinated proteins, it may be one of the initiating factors in rheumatoid. The hypothesis is that there may be certain bacteria that citrullinate proteins, particularly those in the lung. In smokers, this is a problem. Smokers and the association with ACPA is very high.

Speaker 5

If you have the five amino acid susceptibility sequence in the HLA class II system, that's the DRB susceptibility allele that's referred to at the top right-hand of the slide. One of the earliest features of rheumatoid arthritis can be ACPAs, anti-citrullinated peptide antibodies. The presence of these antibodies, in fact, may predate the onset of clinical symptoms and signs by more than a decade. What we find is that there's this regulation right across all arms of the immune system in rheumatoid, but a proportion of patients will have these autoantibodies, about two-thirds to three-quarters of patients through the lifetime of disease. We've learnt that these autoantibodies play a proactive part in disease in many ways. There's data to show that they increase osteoclastogenesis and contribute to joint destruction in rheumatoid.

Speaker 5

There's also data to suggest that they're related to some of the pain signaling that occurs in rheumatoid through modulation of chemokines. Among the contemporary patients that I described that have been better treated than was the case a generation ago, so they've had earlier exposure to therapeutic doses of methotrexate and may have been experienced on one biologic, let's say. Actually, the pain that remains for many of these patients may be related to chemokine production and ACPAs. ACPAs are a very interesting set of autoantibodies in rheumatoid. There's undoubtedly a need to look at this so-called difficult-to-treat group of rheumatoid arthritis. What do we mean by that? Well, what we mean is that the ideal treatment target from a clinician's point of view is to achieve low disease activity or remission.

Speaker 5

In early phase rheumatoid, we aim to achieve remission and can do that very successfully. Unfortunately, half of those patients will lose their remission status over time. Of those patients who need to go on to an advanced therapy, meaning a biologic or a small molecule such as a JAK inhibitor, a proportion of those will either not respond or will lose responsiveness over time. This is a huge problem with biologics in particular because they're all immunogenic, being proteins. The immunogenicity of administered proteins leads to loss of effect. About 50% of patients will lose effect to their first biologic anti-TNF over two years, sometimes even less time than that.

Speaker 5

The consequence of all this is, in an era where the belief is that when a patient's not responding adequately to current therapy, that you should then switch and move on to another mechanism of action therapy, is that over the course of time, there's an enrichment of patients who still have really very debilitating symptoms, but nonetheless have active disease. When we talk about active disease, in some cases it might be highly active disease, but in other cases, it may simply be patients who are not achieving low disease activity. By having moderate disease activity, that might be enough to increase the likelihood of needing orthopedic intervention. It increases the likelihood of joint destruction. It majorly impacts on employment prospects, both in terms of what we call presenteeism, meaning being able to go to work but being relatively non-productive because of the impact of disease.

Speaker 5

Even in terms of absenteeism, those patients who simply can't get to work, and of course, in terms of unemployment. Difficult to treat rheumatoid has an impact on the individual, it has an impact on their families and carers, and it has actually a very significant impact on broader society because these patients who have inadequately controlled disease get all sorts of comorbidities, and of course, the healthcare costs in dealing with those become exponential. We really need to do something about it, and we need further therapies. The problem with the existing array of treatment therapeutics is that we simply don't have the biomarkers to tell us which patient might respond best if you switch from one mechanism of action treatment to another.

Speaker 5

In the case of an FcRn inhibitor, we've got some pointers that there may be a companion diagnostic that might not give a precise likelihood of response, but will give a pointer to response, because those patients with higher levels of anti-citrullinated peptide antibody are the patients who are most likely to respond to this mechanism of action. As Keith alluded to earlier, there's already been a proof of principle study. I was the chief investigator for this study, which used another antibody called nipocalimab. That's an FcRn inhibitor. What this study was designed to do was to look at short-term exposure in anti-TNF inadequate responders in a relatively small number of patients, 53 patients. It was a placebo-controlled study with an intravenously administered drug.

Speaker 5

The idea really was to see whether in either rheumatoid factor or ACPA positive patients, whether or not there was any benefit of the drug. In fact, when we looked at the primary endpoint, the study missed its primary endpoint looking at the cohort as a whole. Nonetheless, when we look at some of the other outcomes that were actually in the statistical analysis plan, we can see that looking at those participants with a higher than median ACPA, that there's really a very striking response at ACR50. You can see that in the histogram on the left-hand side of this slide. In the subgroup with above median ACPA, you see this very nice response that differentiates from placebo.

Speaker 5

If you look at all comers on the left-hand side of that histogram, you can see again there is a difference between placebo and looking at the patients on nipocalimab. That's looking for ACR50 responses, which as rheumatologists we would consider to be really a very clinically meaningful response. The primary endpoint in this study was looking at absolute change in DAS28, that was the outcome measure that didn't meet statistical significance for the study as a whole. If you now look over on the right-hand side of this slide, what we're seeing here is that there's a relationship between the magnitude of improvement, either in terms of DAS28-CRP remission, which is the type of outcome we'd like to see, or ACR responsiveness, which again is the type of outcome measure that we would like to see in our difficult-to-treat patients.

Speaker 5

There's a very striking relationship between the reduction in ACPA IgG level. The ACPAs are IgG, whereas most of the rheumatoid factors are IgM, as I mentioned earlier. You can see this striking relationship. In fact, the implication of that from a pathobiology point of view is that this is probably one of the first pieces of data outside of in vitro data that directly implicates ACPA as one of the key drivers of disease in this subgroup of patients. We've learned that rheumatoid arthritis is, in fact, a very heterogeneous condition, and there are probably many different sub-diseases that have a similar clinical phenotype. The attraction of FcRn inhibition is that we've got a biomarker that's readily available in the clinic that might identify those patients who are most likely to respond.

Speaker 5

We have the potential to inhibit driving autoantibodies, but without actually disabling other aspects of the adaptive immune system. That also is an attractive possibility. Really, this is the reason for our interest and the interest of Immunovant. If we look at the size of the patient population that might be affected, the data that are shown here are for a U.S. population. In fact, I can tell you that the proportions are very similar if we look at Europe. The proportion of patients of the total involved that are autoantibody positive is around about three-quarters. Particularly, that's the case when they get to what we call the established phase of disease. The proportion of patients who have an inadequate response to prior exposure to a biologic or targeted synthetic DMARD is around about 20%.

Speaker 5

That figure tends to go up, if anything, over time. The longer the disease duration, the higher the figure tends to become. What we can see is that this emergence of more and more and more patients with difficult-to-treat disease. Despite the enormous therapeutic advance over my lifetime in rheumatology, we've also seen this rapidly accruing number of patients who failed to respond adequately to multiple therapies. Really, we have this enormous problem of what do we do next? At the present time, they just tend to cycle through a number of drugs unsuccessfully, incur the various adverse effects that might be associated with these drugs, but without the benefits of improvements in quality of life. There really is a very major unmet need right around the globe, let alone in the U.S.

Speaker 5

You can see here that the likely target addressable population is thought to be about 70,000 and climbing, I would say, in the U.S. I would have thought it's very similar in Europe. Probably a higher figure across Europe as a whole. Really, those are the points that I wanted to make today. I'm going to hand back over to Pete, who's going to talk you through the path forward from the perspective of Immunovant. Thanks for your attention.

Speaker 4

Thanks, Peter. That was a tremendous overview. I really appreciate that. Taking those learnings that Peter just shared with all of you, and some additional thoughts, for example, that there are many studies in rheumatoid arthritis, where medications have been studied versus an active control. The reason that's important is it gives you a sense for the response that patients might be expected to have in a non-placebo-controlled trial, which helps from a trial design standpoint. Taking all that into consideration, we designed this trial that you see before you. Starting over on the left-hand side, I want to highlight a couple important things. This study will investigate a group with active disease.

Speaker 4

I'm going to ask Peter to comment on that for a moment, but you'll see some criteria here that are designed to ensure that patients have at least moderately active disease at the time of entry. They're, of course, going to be ACPA positive based on the information that Peter just reviewed, then they will have had an inadequate response to a couple of different classes of medications. That's a group that I think is right in the bullseye of what Peter was just describing. We then have what I would say is a little bit of a unique approach within rheumatoid arthritis, but it is an approach that's been used in other rare disease studies. It's a common approach, actually, in pediatrics. Which is to begin with an open label lead-in. That has several different advantages for us.

Speaker 4

One is that from a patient and clinician standpoint, these are people who are really struggling, who might be considering either a therapy that's a little bit of a shot in the dark without a biomarker in clinical practice or enrolling in a trial. By offering an open label lead-in at the beginning, they know that they're going to at least have active therapy right up front. Not only active therapy, but active therapy with our most potent dosage form of 1402. That's nice from an enrollment perspective. Also, by having that open-label lead-in, this allows us to generate data both for internal decision-making in terms of when we would start a second trial in rheumatoid arthritis, and also from a catalyst perspective prior to the eventual top-line readout of the placebo-controlled regulatory component that I'll talk about next.

Speaker 4

That open-label period really has a lot of advantages. For patients who have an ACR 20 response in period one, they meet a minimum threshold of response, they advance to period two, where they will be randomized. That's essentially the beginning of the actual controlled experiment, the regulatory portion of the trial, or primary regulatory portion of the trial. They're randomized to then maintain their dosing with 600 or step down to 300 or go to placebo so that you have a control group to compare. The primary, actually, for the study is how many of them maintain that response 12 weeks out. Of course, we will also look at more stringent measures of improvement, and that will allow comparison across different trials and also be ultimately really interesting and important for clinicians.

Speaker 4

ACR 20 is the primary to maximize the ability of patients to move through the trial. We do expect that we'll need two trials for approval in rheumatoid arthritis, the second trial would, of course, need to be a more standard trial where patients who meet inclusion criteria are immediately randomized to therapy or placebo. There are some different advantages of that style, more classic trial design from a regulator's perspective, they're going to want to see that information. This allows us to get started and generate data more quickly, and again, is sort of nice for patients who are struggling with disease control even after having been treated with multiple therapies. This is kind of a unique trial design, I'd love, Peter, if you don't mind jumping back in and give your perspective just on the trial design itself.

Speaker 5

Yes. Thanks, Pete. I actually think this is a terrific trial design for this particular population for a number of reasons. The first comment to your question regarding disease activity, to set these entry criteria as given here, historically, we've always seen that if you use these type of entry criteria, the average patient will in fact have higher disease activity. Nonetheless, even if some were included within the moderate disease activity range, that's still really relevant because these are patients who have had an inadequate response to a couple or more drugs and actually have a pretty miserable quality of life because there are so many different ways in which the disease activity impacts on quality of life. That's important to note that these are patients with genuinely active disease at baseline.

Speaker 5

The second point to note is that from a recruitment and feasibility point of view, I'm very sensitive to this, having spent many years trying to recruit patients to clinical trials, it's always challenging. People worry about a lot of things, one of the things they worry about most of all is will they be exposed to placebo for any length of time, and could their disease flare and get even worse than it has been? This particular study design is very attractive from that point of view because everybody's exposed to test drug and therefore, it is likely if there are benefits of this, to receive them. Of course, they're aware that this is a test drug. Going into period two, we'll also derive very good data about the durability of response to drug as well as the optimal dose for maintaining response.

Speaker 5

It's a very attractive clinical trial design because it addresses exactly the type of things that contemporary physicians need to know, whilst at the same time talking to the needs that are necessary for regulators from the point of view of trials that are relevant to registration. If it turns out, as we all anticipate, that this will potentially form a valuable part of the future therapeutic armamentarium, this way of actually going about a trial in the more difficult-to-treat and refractory patients can potentially catalyze how rapidly the drug might get through to clinic. That's also really important, I think, because some of the more traditional routes may be very protracted indeed, and the sooner we can get effective and safe new therapies for this particular tranche of patients, the better. I hope those comments are of some use, Pete.

Speaker 4

Yeah, that's excellent. Thanks, Peter, for that insight. Great. In summary, I'm not going to read through these because Peter's made them so eloquently. We've got a biomarker-driven strategy for a high unmet need population where there is evidence from another FcRn inhibitor's trial of the relevance and potential impact of FcRn inhibition in this group. The study design is enhanced in a couple different ways that we just highlighted. Based on the data that Peter shared, which showed a correlation between the degree of ACPA reduction, those who started out at a higher level were more likely to be the ones who got a deep response, and those who got a deep response were more likely to have a larger change in their ACPA.

Speaker 4

Kind of looking at the correlation between ACPA changes and clinical improvement from two different angles, there was good evidence that a deeper reduction yields better efficacy. We're really excited to have the IND cleared and to get this study started in the early part of next calendar year. There's some similarities between the two programs that we've so far highlighted, the Graves' disease program and the rheumatoid arthritis program, in the sense that we really, first and foremost, are looking for a group of patients that really need a new therapy. That's kind of always our starting point from a clinical and market opportunity standpoint. We're looking for scientific evidence that FcRn inhibition is going to matter, and that actually deeper IgG reductions from a more potent FcRn inhibitor could matter even more.

Speaker 4

We have evidence, I didn't review it today, but you'll be aware of the data that batoclimab lowered not only IgG but TRAB levels. Today, Peter reviewed the information showing the reduction in ACPAs in the nipocalimab trial, which we expect to not only replicate for those patients in the 300 dose during the randomized withdrawal, but potentially exceed for those patients on 600. Finally, from a trial design standpoint, we're really looking hard at how to have the most informative trial design possible, because in rare diseases, the number of patients is lower, and you don't have study programs that have thousands of patients where when you do have thousands of patients, there are many different questions that could be asked.

Speaker 4

Even if the trial is a relatively straightforward design, when you're looking at trials that are more in the 100 to 200 range, the trial design needs to be done very thoughtfully, so that not only do you generate information required by regulators for approval, you're able to generate data that can differentiate the product for clinicians. With that, I want to loop back to where we started, which is maybe one of the main points of today, even though we didn't spend as much time on it, because a lot of the information is as yet undisclosed. Behind the scenes, there's just been an amazing amount of work to ensure that we stay on track for our development program for 14.02.

Speaker 4

I think, again, to highlight that having 5 INDs already cleared, which exceeded our goal, we were hoping to have three by the end of the year to be well on track to launch four or five indications by the end of the fiscal year, which is March 2025. To already have 5 of those cleared is just an amazing accomplishment by the Immunovant team, and it gives us a lot of confidence in our broad development program. We also have data coming up from our MG and CIDP programs. Both of those are fully enrolled in terms of the people who will contribute to the initial data readouts. In the case of MG, that's the entire trial. In the case of CIDP, it's all of the participants who will contribute to the period one data release.

Speaker 4

Both of those are closed from an enrollment standpoint, and the patients are just moving through the studies for that data disclosure. In the case of our Thyroid Eye Disease Program, that data will now be expected in the second half of next year. Thyroid eye disease is very interesting. The primary focus in the last several years has been around those patients with high disease activity and who are acute, meaning they're very early in their journey with thyroid eye disease, and they haven't been diagnosed with thyroid eye disease for very long. That's actually a relatively narrow slice of the entire thyroid eye disease population, but it's where all the clinical trials are currently happening, there's a lot of competition for those patients specifically.

Speaker 4

Having attended multiple thyroid conferences this year, including most recently ATA, where there's always a good discussion around thyroid eye disease, even at the thyroid conferences, it's clear that the clinical opportunity, I think, is kind of moving sort of out in both directions. What I mean by that is there's a large prevalence of more chronic long-term thyroid eye disease. That's a population of patients who have had proptosis for a while, may or may not have residual inflammation, but the key thing is they've had the condition for quite a while. Those patients are probably going to remain best served either by surgery or, in the case of medical therapy, insulin growth factor inhibition. The real excitement is to treat patients earlier in their disease course.

Speaker 4

Remember that people who qualify for a thyroid eye disease trial have not only active disease, but have to achieve certain thresholds of severity in terms of their exophthalmos. Earlier in the course of Graves' disease, there's many more people who have mild thyroid eye disease. Some of them will progress to moderate to severe thyroid eye disease, along with their thyroid-specific autoantibodies remaining high and/or their Graves' disease remaining uncontrolled. The big opportunity we see in thyroid eye disease is actually to catch it earlier and treat it along with Graves. Peter mentioned in some ways there's an analogy to rheumatoid arthritis. Peter mentioned that earlier in his career, patients who he saw in the clinic or was enrolling in trials would come in wheelchair-bound, or he would be worried that if they hadn't already become that disabled, that that might be right around the corner.

Speaker 4

Whereas today, with more advanced therapies, we're not seeing people generally with that degree of disability, even though he highlighted that they have other disability. I think we have the same hope for thyroid eye disease over time, that if the Graves' disease program works as we expect, then the numbers of people who are progressing to that moderate to severe TED requiring surgery in many cases will be much reduced, because you catch it earlier. With that, I think that concludes our prepared remarks on a lot of different topics, and I will turn it back to Tara to open the line for questions.

Speaker 3

Great. Thanks, Pete. Please hold for a brief moment while we poll for questions. Our first question comes from Samantha Semenkow at Citi. Please go ahead, Samantha. You might be on mute.

Speaker 7

Sorry. It toggled back and forth on mute for some reason. Hi, good morning. Thank you so much for taking the question. I have actually a couple for Dr. Taylor on RA. First off, do we know much about the heterogeneity of RA patients that have high ACPA? Is this a more homogeneous population based on their ACPA status, or is this group still quite diverse in terms of pathogenesis? Then just building on that, what are your thoughts on how effective an FcRn could be as a monotherapy in this population, dependent on how heterogeneous it is? Do you think we'll need a combination therapy to better control it as one of the competitors in this space is running? Thank you.

Speaker 4

Yeah. Thanks, Sam, for those questions. Peter, I think those are two good questions we've talked about before. The heterogeneity, I guess, applies broadly to patients with rheumatoid arthritis. Sam asked specifically about any heterogeneity within the ACPA positive. Your ideas on drug development with monotherapy versus combination therapy would be appreciated.

Speaker 5

Yes. Thanks, Samantha. It's an important question. There's been a very considerable advance in our understanding of rheumatoid in recent years. It's complex. It's clear that the ACPA positive patients and the ACPA negative patients are very different in many respects. We have also learnt that one can subdivide the syndrome we call rheumatoid, in other words, people meeting classification criteria according to synovial histomorphology and a number of other markers. It would appear that the ACPA positive patients, and particularly those who are strongly ACPA positive, are more homogeneous than the enormous heterogeneity that we observe in the seronegative patients. The attraction really of looking at FcRn as a therapeutic target is related to the sub-analysis that I referred to earlier, where we were seeing a very nice proportion of patients hitting ACR50 criteria and even DAS28 remission criteria.

Speaker 5

That, of course, was a monotherapy antibody. What was also publicly disclosed as part of the nipocalimab data was that the magnitude of total IgG reduction was a lot less than the magnitude that Pete's been talking about in the various studies where the Immunovant antibody has been explored. In terms of how well patients might respond to monotherapy, well, of course, that's the reason we do clinical trials, to address hypotheses and find out. The expectation based on information we already have and based on theoretical knowledge about this new antibody would be that a good proportion of patients would respond at exactly the type of level that people like myself, as practicing clinicians on a day-to-day basis, would like to see. In other words, significantly relieving the aspects of life that are impacted by rheumatoid arthritis.

Speaker 5

Really further comment than that can't be made because, of course, that's precisely why these sorts of novel trial designs are necessary and then carefully scrutinizing the data that arises.

Speaker 4

Thanks, Peter. Tara, back to you.

Speaker 3

Yep. Thanks for the question, Sam. Our next question comes from Sam Slutsky at LifeSci Capital. Please go ahead, Sam.

Speaker 6

Hey, good morning, everyone. Thanks for the questions. Got one for Dr. Taylor and then for the Immunovant team to follow up for that. I guess for Dr. Taylor, for the population that IMVT-1402 is being studied in, I guess what level of efficacy would be clinically relevant to make this an interesting therapy to you? Then also just given the novel trial design they're using, would that have any impact at all on interpreting these results versus drugs that have used other trial designs for RA?

Speaker 4

Yeah. Great questions, Sam. I think I'll reference a point then allow Peter to comment on whether he agrees or not. I mentioned that one of the benefits of studying patients with rheumatoid arthritis is there's so many other trials that it gives you some benchmarks. There have been some meta-analyses which, when you look at patients who fail the biologic, generally, they average across a lot of different trials in terms of ACR50 is about 25%. Of course, looking at the higher ACPA-positive patients that Peter showed, those had ACR50 of 27% or so. Something that I think would be a very competitive response in this difficult-to-treat patient.

Speaker 4

I guess just generally, Peter, would you agree, without getting into all the details today, that it's going to be possible for clinicians and investors to form an opinion about what sort of response rate would be a really good response rate in this trial?

Speaker 5

Yes. Absolutely. I think the key point here is that in order to really understand the relevance of the findings of the study, one has to look at the totality of data. If, for example, you were just to take the ACR categorical levels at any one time point as being the sole indicator, that would have a very limited value. It's important to stress that even a 20% improvement for these people who have not had an adequate response to other therapies may be very impactful in terms of improvements in their quality of life. When you look at the totality of the data, which will include other measures, some of which will be continuous measures of response, where you can look at maintenance of response, for example, area under the curve and so on, will be extremely informative.

Speaker 5

I think, in fact, this is a very clever study design because it will give us that total set of data that will point in the right direction to allow nuancing of design for any study that follows. At the same time, it will also allow the type of ballpark in direct comparison because of the choice of regulatory endpoints that's going to be used. It's an ACR20 outcome, for example, which will allow indirect comparison and benchmarking with other mechanism-of-action drugs.

Speaker 4

Awesome. Thanks, Peter. Sam, maybe just quickly to the Immunovant question, in the interest of time.

Speaker 6

Yeah. Just actually going to the Graves' disease data that you recently presented. For the patients who had Graves' orbitopathy, what was the range of severity at baseline? Was it all moderate to severe patients, or were milds mixed in? Just any additional clarity on that.

Speaker 4

Yeah. I'm glad you asked that. I didn't mention that, but I should have. These were not patients, for the most part, who had moderate to severe disease. More of them were mild. They might have been moderate to severe on one dimension. For example, by moderate to severe, I'm using the criteria that are typically used for enrollment inclusion criteria in a TED trial, whether ours or others. You generally require short duration of disease, high CAS, and proptosis finding that meets a minimum threshold, among some other things. Many of these patients had one or maybe two of those, but most didn't have all three. It's generally a group that had more mild disease. Nevertheless, you see a meaningful change in their proptosis values, which really is a whole interesting separate discussion that the population averages for what is a normal amount of exophthalmos.

Speaker 4

It's a little bit like anything else in the population, height, or something where there's variability. Some people clearly had exophthalmos that was abnormal for them because they improved a lot on therapy, even if they weren't above the average value for the population based on their gender and race. It's also what gives us a lot of encouragement that we can see some benefit in a more Graves' enriched program that we're going to be running that those are mostly going to have mild or TED, but yet we expect to see some findings based on this data.

Speaker 6

Awesome. Thanks.

Speaker 4

Thanks, Sam.

Speaker 3

Our next question comes from Brian Cheng at JP Morgan. Please go ahead, Brian. Brian, you might be on mute.

Speaker 9

Good morning. Thanks for taking our questions. I'm Mary. I'm on for Brian. First for Pete, can you talk about how the extrathyroidal benefits that you presented last week at ATA read through to your ongoing TED trial with batoclimab, any color on the timing of the updated timeline for the TED readout? We have a follow-up.

Speaker 4

Sorry, I couldn't quite hear you there, Mary. You said the extrathyroidal findings. Then I missed something.

Speaker 9

Yeah. How the extrathyroidal benefits that you presented last week at ATA read through to your ongoing TED trial with IMVT-1402, any color on the timing of the updated timeline for the TED readout. We also have a follow-up.

Speaker 4

Right. The thyroid eye disease program's obviously blinded. As I just highlighted to Sam, the populations are different because the TED trial is enriched for moderate to severe, whereas the Graves' trial was selected for Graves' disease activity in spite of antithyroid drug therapy. Those patients happen to have, for the most part, a mild disease, but mostly not moderate to severe. I think at the end of the day, though, the fact that we're seeing not subtle changes in proptosis, even in that Graves' population, is encouraging for our overarching goal within our program for IMVT-1402 in Graves', which is to address thyroid eye disease before it gets to be that severe.

Speaker 4

That relates to the comments I made around the thyroid eye disease program, which has been chugging along, but there's been increasing competition for patients who are in that narrow slice of acute and very active. We wanted to keep our trial consistent with others and just maintain that narrow slice of patients for the TED trial so that cross-trial comparisons would also maybe most easily done. I think the bigger picture is that IMVT-1402 has an opportunity through its Graves program to get to TED early in the disease course, which is maybe the main value driver there. I'm probably going to have to ask you to have your second question short. We do need to finish by 9:15 A.M., and we have some other questions in the queue. You want to ask your second one, Mary?

Speaker 9

Yeah. For Dr. Taylor, down the line, how do you think about sequencing FcRn in the real world? Do you see any potential for it to move into earlier line?

Speaker 5

Theoretically, absolutely there could be, and certainly given that we may have the biomarker to indicate responsiveness. Of course, it's important to point out that in a world where we're seeing many biosimilars now and many of the small molecules will become generic, a lot of the potential prescribing choice is restricted in many healthcare economies. Actually, the area of biggest unmet need is potentially around this difficult-to-treat population. In principle, yes, that's a possibility.

Speaker 4

Thanks, Peter, for that. Tara, turn it back to you.

Speaker 3

Yes. Our next question comes from Alex Thompson at Stifel. Please go ahead, Alex.

Operator

Great. Thanks for taking our questions. I guess sort of at a high level heading into the CIDP and MG readouts early next year, maybe, Pete, you could sort of talk about what you want to see to really validate the best-in-class profile you're thinking for 1402. Then sort of with that, are there any scenarios at this point where batoclimab moves forward towards FDA registration? Is it really still all 1402 at this point? Thanks.

Speaker 4

Thanks, Alex. I think you see in the data that was presented today, particularly the Graves data, a strong correlation between degree of IgG lowering. We didn't go into all of the various dose cuts that I presented a couple of months ago, but when you look at the totality of that data, there's a lot of evidence for deeper IgG reduction correlating with better clinical response, which is a fundamental thesis of Immunovant's value creation story. In the Nipocalimab data that Peter presented, you see that correlation as well. The reason you're able to see that correlation, although the average reduction, as Peter pointed out, was closer to 60% at the population level, there was variability. You see some small number of patients who got a deeper response. We see that in our low dose as well.

Speaker 4

I think what we want to show with MG and CIDP data is the same thing. That in the case of myasthenia gravis and CIDP, deeper IgG reduction correlates with clinical improvement across multiple parameters. Peter made a very good point about assessing particularly the impact of a biomarker and the correlation between that biomarker and disease, that any single time point, any single measurement is not going to be convincing one way or the other. The totality of data, when you look at endpoints over time and you see a correlation, particularly over time between a biomarker and disease activity, that's the kind of information that gives you a lot of confidence that there's a correlation there. That's what we're looking forward to seeing and plan to see.

Speaker 4

That's why we designed the trials to be able to test this correlation across a lot of different dimensions. Thanks for that question, Alex.

Speaker 3

Our next question comes from Andy Chen at Wolfe Research. Please go ahead, Andy.

Speaker 1

Thank you for taking the question. One question for Dr. Taylor. In these ACPA positive patients, do IgG antibodies, do they account for the majority of disease pathogenesis and disease activity? Is it much more so than other pathways and cytokines from TH1, TH17, and maybe CD8 T cells? Just trying to understand how much more important IgG may be in disease activity. Maybe just one follow-up for the Immunovant team. The 70,000 U.S. prevalence, is that the diagnosed population or is that the estimated prevalence? Thank you.

Speaker 4

Yeah, thanks, Andy. Maybe I'll start with that one. Patients who are difficult to treat, almost by definition, they're in the healthcare system because they need to be seeing physicians, getting treatment in order to tick off those boxes of having disease activity, having failed different therapies. This is essentially the current population estimates of people who are in the clinic with and meeting those criteria. As Peter pointed out, that prevalence may be growing over time as people cycle through the anti-cytokine therapies and as more people, possibly due to availability of biosimilars and things like that, get more advanced therapy earlier, some fraction of them will unfortunately progress to being difficult to treat. That group could be growing in size. I think Peter, I'll toss it over to you for the disease heterogeneity question. That's a Big topic.

Speaker 4

Maybe you could just give your thoughts on, which I think you kind of already did, but again, on the relative homogeneity of an ACPA positive, difficult to treat population.

Speaker 5

Well, Andy, thanks for the question. In brief, I don't know the answer to the exact question you posed, and I don't think anybody does. What we do know is that when you look at all the different mechanism of action agents that are currently approved, that they all have similar benefits in a similar proportion of patients. The groups of patients who respond to each are not necessarily the same. Furthermore, for patients who become refractory to one, the responsiveness to another different mechanism of action may vary. The current hypothesis is that there's an immune dysregulation in both the adaptive and innate immune arms, that there's a sort of bottleneck hypothesis whereby TNF and IL-6 may be the key cytokines that are driving.

Speaker 5

The reason for the aberrant control of those cytokines may be multiple, and that perturbing those dysregulations within the entire immune network at any point may give rise to similar outcomes. What we do know already is that FcRn is a validated target in a subgroup of individuals. We'll learn more in terms of answering your question through studies with drugs that optimally decrease pathogenic autoantibodies and particularly obviously IgG. It's also important to mention that rheumatoid factor, whilst it's predominantly IgM rheumatoid factor that we measure, it's long been known that IgG rheumatoid factor plays a role in the pathogenesis. We'll learn more in answer to your question.

Speaker 4

Thank you. The other thing to maybe, because it's a good question that's been asked by a couple different people, maybe a follow-up point, Peter, could also be that, again, this strong hypothesis has been generated with the Nipocalimab data. We're going to test it. If it pans out as we expect, then it's readily implementable in the clinic. This isn't just an austere biomarker that's going to be hard for rheumatologists to get their head around, right? If this works, the translatability to clinical practice, I think should be high.

Speaker 5

Exactly.

Speaker 3

Thanks for the questions, Andy. Our next question comes from Yasmin Rahimi at Piper. Please go ahead, Yas.

Speaker 8

Thank you, team. Congrats on the really brilliant design. Thank you, Dr. Taylor, for your thoughtful comments. This is directed to Pete. Pete, could you talk about, given that it has an open label portion, would you be in a position to provide updates from the open label before you go into part 2, or is the strategy to finish part 1, go into part 2, and then the top-line data will be post part 2? That's sort of question number 1, just for housekeeping. In regards to it's a very difficult to treat population. You would think in terms of a treatment effect, any statistical separation in the primary and trends in case secondary would be a very, very attractive opportunity.

Speaker 8

Am I thinking about this the right way, or is there a specifically magnitude of change that could be clinically meaningful for this very tough population? What are we powered for in part two of the study? I guess that's what I'm trying to get at. Sorry for the long-winded questions. I'll jump back in the queue.

Speaker 4

Yeah, no problem. I think to the first point, yes is the answer, this is part of the reason we chose this design. It wasn't the main reason. The main reason was based on the scientific rationale and the ability to advance our program quickly to registration if we're seeing good data as we expect. There's a nice side benefit of having this open label period, which is we'll be able to define a certain number of patients less than the, potentially less than the entire 120, where there's enough information to warrant a disclosure. That'll be a nice side benefit from a catalyst standpoint. This is a potentially registrational pivotal trial, it's fully powered for the primary.

Speaker 4

Many of the secondaries are reasonably equally powered because the placebo arm is likely to have a very low rate of response, and the placebo-corrected delta is often kind of in a similar order of magnitude, no matter which cut point you're using. One of the things maybe I'll say, in terms of, ask Peter to comment on the clinical magnitude in the DAS28 remission was shown in one of the slides. Could you put that in context, Peter, for a group that starts out, I don't know what the mean or median was, but I'm guessing it was maybe five or more in the Nipocalimab trial. For a population like that, how meaningful is DAS28 remission as an outcome?

Speaker 5

Well, it's enormously meaningful. Just for the benefit of the listeners, there are many different definitions of remission, but basically, we want to approximate as closely as possible to the absence of symptoms and signs that impact on quality of life. Perhaps it is only fair to point out that one of the findings from the Nipocalimab studies was that it didn't impact significantly on CRP, which is one of the components of the DAS28. There's another measure called the CDAI, the Clinical Disease Activity Index, which doesn't include an acute phase marker that's probably even more meaningful. What really matters is that the patient's quality of life is significantly better. The sort of proportions we were seeing with the DAS28 remission, I would say were pretty impressive in the difficult-to-treat population.

Speaker 5

In fact, when you look at metrics that don't include a CRP, that becomes even more impressive.

Speaker 4

Yeah, that's a really important technical point. A lot of the anti-cytokine therapies tend to move CRP a lot. The patient doesn't necessarily feel CRP, but it is a part of a lot of the scoring criteria because of that point. When you look at the, as you did, I know in a study, in data we didn't show today, when you sort of disaggregate the DAS into its component parts and also ACR into the pain and swollen joint changes, there were many changes across all those subparts, which gives you a lot of confidence. That's a very important point you just made. I think we have time maybe for just one last question, we'll wrap up.

Speaker 3

Great. Thanks, Pete. Our next question comes from Louise Chen at Cantor Fitzgerald. Please go ahead, Louise.

Speaker 2

Hi. Thanks for taking my question. Just wanted to ask you if you thought your FcRn for RA would always be in a refractory patient population based sort of on the premise of how you're designing your study, or does it have opportunities in earlier lines of treatment? Thank you.

Speaker 4

Yeah. Thanks, Louise. I think there's a overwhelmingly practical component to the answer I'm gonna give you, which is the anti-cytokine therapies are already some of them available as biosimilars, and many others will become available as biosimilars. They have a proven track record in a certain percentage of patients, and before them, even methotrexate works in some patients. I think healthcare systems are going to require patients to go through those therapies, which will be much less expensive because they're generic or biosimilar prior to using an advanced therapy like an FcRn. I think for most patients, that's probably reasonable.

Speaker 4

Therefore, our program is targeting the subpopulation of patients who are difficult to treat, which makes sense from a clinical standpoint, but is also something that healthcare systems can absorb from the standpoint of the difference in price between a modern therapy and a generic or biosimilar. Excellent. Well, I appreciate everybody joining today and the robust dialogue we had. A huge thank you to you, Peter, for providing such a really nuanced and detailed and engaging overview of the history of rheumatoid arthritis, also the specific subpopulation of ACPA-positive difficult-to-treat RA and your thoughts on our clinical trial, which I'm really, really excited about. I guess I'll close again with where we started, which is that maybe what I'm most excited about is just the progress we've made across multiple indications, including many that aren't yet disclosed.

Speaker 4

We wanted to let everybody know that that progress is real in the sense that we have five indications have now been approved by the FDA, which is a big, big step forward. For those whose questions we didn't get to today, I do apologize. Just in the interest of time prior to market opening, we need to wrap it up. Thanks again to everyone, and I'm sure we'll be talking to you soon.

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