Immunovant, Inc. (IMVT) Earnings Call Transcript & Summary

So good afternoon, everyone, and thank you for attending the UBS Global Healthcare Conference. I'm Colin Bristow, one of the biotech analysts here. It's my pleasure to have with me today, Peter Salzmann, CEO of Immunovant. If anyone has a question, you can scan the QR code, and it will pop through in the iPad I have with me, and I'll field it for you. Pete, thank you for joining us today. I know you have some opening remarks, so I'll turn it over to you, and then we can dig into some questions.

Yes. Great. Colin, thanks for having us. I will just do a quick sort of tasting menu across our program and then we can go deeper in the Q&A session. I will be making some forward-looking statements today, and so I direct investors to this slide, which is on our website to read that carefully. Okay. So Immunovant is developing batoclimab, which is a fully human monoclonal antibody, targeting the Fc receptor. FcRn inhibition is an exciting area within immunology for sure. How is batoclimab unique? There's really 2 things that sort of convert to a third feature. So the 2 core features for batoclimab are among the deepest IgG reduction that's been observed. And we've achieved that with a simple subcutaneous injection. So that's the first and the third feature there. When you put those together, then you get a -- that middle feature, which is really powerful, which is the ability to do tailored dosing. Simple tailored dosing, eventually, the kind of thing people could do at home, adjusting their IgG either based on symptoms or based on stage of disease, based on the data that we generate through our clinical trials. So this is how we plan to differentiate batoclimab in this really exciting market. We have announced programs in myasthenia gravis, thyroid eye disease and warm autoimmune hemolytic anemia. And then we are committed to announcing 2 new indications by August. August comes from a raise we did last August and we said we would announce 2 indications in 12 months. That's why. Some people wonder why August 2022. So that's just -- that's the reason there. Of the 5 programs that we'll be running, we plan to have 3 of them running as pivotal trials. The myasthenia program is just starting now as a pivotal trial. And then 2 out of those 4, 2 named, 2 unnamed, will be pivotals as well. So let me talk a little bit about our differentiation plan on myasthenia gravis because you can really see how those features, I think, can be translated to potential patient benefits in this program since it's obviously the most robustly disclosed; the other program is not yet being disclosed. So when we spoke with physicians and people with MG, we heard a couple of things. The first we heard is when a physician or person with MG is thinking about a new therapy, they're usually pretty symptomatic. It's a chronic condition, and there aren't that many approved therapy. So any change in therapy is taken very seriously. So at that point in time, when you're thinking about a new therapy, and you're quite symptomatic, the main goal is really to get the symptoms under control as quickly as possible. One of the most promising feature of the anti-FcRn class as a whole is that all of the data to date shows a pretty rapid symptom improvement, which is not true for the older nonsteroidal immunosuppressant therapies. So we designed a trial with high doses in the induction period, our anchor dose of 340 milligrams, which is kind of our standard dose similar to the other anti-FcRns in terms of its IgG reduction. But then we have higher dose, 680 milligrams, to test the hypothesis that those higher levels of IgG, which 680 has been shown to deliver, will translate into faster and deeper efficacy, again, which is what people want most right upfront. Once the symptoms are controlled, then -- people told us they don't want to go off their medicine entirely because of the risk of a flare. And many have experienced that or they have friends in their network that have experienced it, and a flare in the case of myasthenia can be pretty severe. But they do appreciate the opportunity to have their dose stepped down a little bit. So if they're well controlled on a medication, having an opportunity to take a little bit less over time, lower the dose in the maintenance phase is something that they -- many would appreciate. So we're testing that in the maintenance phase, can a lower dose maintain the benefit achieved in the induction period. And then finally, physicians mentioned to us that they often have people with MG who are doing really well for a period of time and then something happens and the symptoms get a little bit worse. And they would love in that case to have data to be able to go at a higher dose of their existing medication rather than having to add steroids on top or switch to an entirely new medication. None of the modern therapies have tested rescue with the medication that the patient is on. And therefore, you don't have any data to guide that kind of decision making, and it wouldn't be something that payers would approve. So this is built into our Phase III program to address that important need that physicians expressed to us. And turning quickly to thyroid eye disease. This is a simple schematic, which just shows the role of autoantibodies triggering both underlying Graves' disease as well as Graves orbitopathy or thyroid eye disease. And what I want to point out about thyroid eye disease is, to share some data which we previously shared from our Phase IIb trial, looking at a very specific subtype of autoantibody. So most of the autoantibody data you see in anti-FcRn trials refers to just a general quantification of all the autoantibodies present. This data is from a cell-based assay that looks specifically at those autoantibodies which stimulate the TSH receptor, not just those that bind to it; because some bind to it, they don't stimulate it. And it's really only those antibodies that stimulate the receptor that are important in the pathophysiology. So this is a cell-based assay, which compares the activity of the antibody in the patient to a control. And there is a threshold of 140%. So that's 140% to control that is considered the threshold of abnormal. So if you're below 140%, it's normal or if you take someone below 140%, that's considered serologic remission. So what you see in the table on the right-hand side of the slide is the percentage of people within each dosing arm that achieved that serologic remission, that got their total antibody titer via the cell-based assay below 140% of reference. So half the people on the 680-milligram arm achieved that, whereas only 15% of people in the 340-milligram arm achieved it and no one on the 255 arm. What's shown in the curves is the total percentage of autoantibodies. So that's a little different than what's shown in the table. The importance of this is, we believe that in thyroid eye disease, it's likely that higher levels of IgG suppression are going to be needed to really drive disease control. The other thing that's really interesting about the thyroid eye disease market, it's very, very unique in all the immunology markets that I've worked in. There isn't one quite like this. And the -- what's unique about this market is that the labels are for a specified duration. So the ophthalmology division labels many of their products for acute or short-term use, and often includes in the posology section, in the dosage and administration section, the length of therapy. That's pretty uncommon for most labels -- across most FDA labels, but it's quite common within ophthalmology. It's important for a rare disease medicine, which is expensive because it's a very easy lever that payers then have to say, okay, we're only going to be able to treat the patient for the duration that's labeled. And again, most products don't get that type of restriction. The efgartigimod label doesn't have any specificity around total duration of therapy, and that's the normal label. So why is that important? Well, because although teprotumumab works very well in thyroid eye disease, once you've had your 6-month course, then you've completed the amount of time that you're eligible for in the FDA label. So based on that, there are 3 categories of opportunity that we see in thyroid eye disease, even recognizing that we've been transparent that we -- while we're confident that batoclimab will show an effect in thyroid eye disease, we don't believe it will necessarily be at the same level of teprotumumab, which has set a very, very high bar for efficacy. So why do we think we still have a really nice opportunity? Well, there's people who are more moderately affected. So still moderate to severe, but more on the moderate side of the spectrum. Often, physicians will choose a medicine that's a little bit better tolerated in that group. And to date, batoclimab doesn't have any irreversible side effects and no impact on hearing loss. And then there'll be the following 2 groups, which is people who've had success with teprotumumab but they still have some residual symptoms, either because they started out very severe, they got better but they're still not normal. Those people today are getting another course of medical therapy possibly with a steroid or some of them are even having surgery post teprotumumab, a much less surgery than they would have had without teprotumumab. So still a really good result for the patient but not yet fully well. So that's the opportunity, residual symptoms after teprotumumab. And then there'll be people who recur. So 6 months, 12 months after completing their course of teprotumumab, their symptoms come back. And again, because of that label restriction, they won't be able to get another course. And then, finally, just really quickly, warm autoimmune hemolytic anemia. There's a lot less data in this disease. There hasn't been as much innovation here. And when we look at what's currently being used, it's mostly steroids with occasional blood transfusion. So that's a standard of care we feel pretty confident that good data could supplant. I'll leave it at that. We'll see what questions we have in that -- in the Q&A. So anyway, that's hopefully quick enough that we left time for questions, Colin, overview of what we're up to and let's see where you want to take it.

That's perfect. Thank you. Yes. I mean maybe just to start high level, and there's several FcRn assets out there. And if you could just outline how you see yourself being differentiated?

Right. Right. Right. So these 2 differentiating features that I mentioned upfront really are with the other anti-FcRns in mind. So the ability to deliver among the deepest IgG suppression. Nipocalimab has also reported IgG suppression in the 80-plus percent. But the doses that are being studied, at least those that have been disclosed, aren't anywhere near those highest doses. So Momenta tested doses as high as 60 milligrams per kilogram, it's like almost 5 grams of drug given intravenously. Whereas the studies in myasthenia are using a dose that's much, much lower than that. So it's not going to get near the 80%, certainly not in the steady state, maybe not even at the peak. So there's that piece. And then the second element is the simple subcutaneous injection. So while we believe Halozyme is a good technology and it's certainly better than intravenous infusion in a health care setting, it's not a technology that has been used chronically, and it's not as easy as a simple subcu from our perspective, which is really well validated across a lot of different biologics. So again, you put that deep IgG, simple subcu together, now you can do tailored dosing, which our programs are going to be built around that opportunity.

And then one thing you've obviously seen is some LDL elevation. And so can you talk about whether you think that's unique to batoclimab or whether you think there's any evidence of it with other assets so that it would likely appear at some point?

Right. So batoclimab causes reductions in IgG as its primary impact, and then also decreases albumin. And albumin is recycled via the Fc receptor. The albumin binding site is distinct from the IgG binding site but near it. And so there's, we believe, some steric hindrance based on the way the batoclimab sits on that Fc receptor. Albumin lowering was the one thing which correlated most strongly, and it was a very strong correlation to LDL changes when we looked at all of our data during our program-wide review last year. So we're pretty confident that it's the albumin lowering that's causing the increase in LDL. Nipocalimab has also reported changes in albumin and has acknowledged that they have LDL changes, although they haven't reported the degree of those. I think the key thing is that the LDL we see, first of all, we're seeing it primarily at the highest doses. So when you lower the dose, then the LDL comes down as the albumin becomes more normal. And then we recently did a study looking at 680 milligrams of batoclimab, which is our highest dose, combined with 40 milligrams of atorvastatin, which is the most commonly prescribed dose of atorvastatin, which is the most common statin. And those data are on our website, but just to describe them briefly, the 40 of atorvastatin was given during a 2-week run-in period. You saw the 50% reduction in LDL that's typical with atorvastatin at that dose. And then after batoclimab was added at 680 milligrams, the LDL was essentially the same over that period of time. So that was a very small study. There's more to be learned, but it confirms what we heard from experts, which is that they expect statins, probably even at a lower dose, to control the LDL changes caused by batoclimab in some patients.

So as we think about -- I mean, the MG, for example, in the Phase III trial design, you're excluding patients with high LDL. And so -- I mean, a couple of questions around this. What size of the population do you expect to exclude? And then is that something we should expect to see in other trials in terms of high LDL exclusion? Or would dosing or duration of dosing be short enough that you think that wouldn't be necessary?

Right. Right. So we're excluding patients. I mean, I don't know if I'd say high or very high, but patients who have an LDL over 190, which is pretty high. How did we choose 190? Well, there's no CTCAE guidance for LDL specifically. But there is a CTCAE category for total cholesterol. And for most people, LDL is about 65% of total cholesterol. So when you look at the CTCAE for cholesterol grade 2 -- and grade 2 abnormalities are pretty significant. Normally, you don't want to enroll people in the clinical trials if they'd have some abnormality outside of the disease of interest with a grade 2 or higher. So 190 is roughly a grade 2 abnormality for LDL. How many people is that? 5%, 10% max of the population. And it's only people who aren't treated with a statin because if you had somebody who had -- let's say, they had 190 at baseline and then they were treated with a statin and their LDL comes down, they're now stable. Those people can be enrolled. It's just really somebody who is probably untreated, who shows up for screening and has a high LDL or somebody who's treated with a statin and then their LDL is 190, there's probably something else going on. They probably have a quite significant cholesterol abnormality. So it's a group that I think probably is best left out of the clinical trials anyway, and it's a relatively small group. There's a second group, which is people who have existing cardiovascular disease, but that's a pretty small group. They have a slightly lower threshold. By excluding those people, again, which is a small percentage of the population, what that allows us to do is something very important, which is to study batoclimab for 24 weeks without having unblinding labs going to the investigator. So of course, LDL will be measured in the background but because the highest elevations will be in the 12 -- first 12 weeks when there is induction and then the second 12 weeks when most people are coming down on dose, you expect the LDL to go down, there won't be any unblinding required in the trial. And that means also no statin use during that 24-week blinded period, which would complicate the analysis. So there's many things which would make the trial more challenging to run if unblinded statin use were required in that first 24 weeks, which is not based on the models that we've developed and reviewed with the FDA.

And just as you think about this in the future for more chronic dosing, what and how do you plan to collect data, potentially dosing concomitantly with the statin?

Right. Right. So I think there's 2 types of data that's important, and we'll -- I'm sure we'll end up collecting both by the time of launch, and they're -- it's both relatively easy to collect. So there's, of course, the healthy subject data, but I think what's -- there's 2 types of data from patients. So one is sort of what I'll call real world and -- or usual practice, and that's what we're doing in MG trial. So in the long-term extension, once the controlled period has passed and people are in the long-term extension, then the investigator will get the LDL panel along with other labs. And if they choose to treat the person's LDL based on the absolute level and what else is going on, with an anti-lipid, which would probably be a statin, then of course, we'll collect that information. So the good thing about that type of information is, it's very real world, it's very based on what practicing physicians kind of feel is appropriate. But it's, of course, not a standardized because everybody is going to do a little bit -- take a little bit different approach. Even though there are pretty standard guidelines for statin management, there's still a lot of diversity at the level of the clinical practice. So the second type of data would be, what I'll call, standardized data or per-protocol data where you have a expectation that a certain anti-lipid therapy will began at a certain level. And that -- the advantage of that type of an approach is you then get sort of population-level data of how much anti-lipid therapy yields how much LDL-lowering. So I think we'll have a little bit of both by the time of launch. Physicians told us in market research that they assume that statins would control the excursions of the magnitude we are reporting but that they'd like to see a little data to validate it. And so we'll have that data at the time of launch, that they're not having to just guess in terms of what dose to start with or that kind of thing.

And you're still on track for a first half '22 initiation?

Right. Right. It's getting close, but yes.

Yes, just checking. And what's the threshold for success in this trial? Like, what do you want to see at the 12-week endpoint?

Right. So I think it's not just the 12-week endpoint, it's the -- but that's an important one. I think success in this trial is really validating the -- a couple of hypothesis. The first hypothesis is that greater IgG reduction yields greater clinical benefit. So that's -- I mean, that's been published, and I think it's relatively accepted as directionally right but there's not a large body of data to say, well, is there a ceiling? Do you get a ceiling effect at 60%? I'm not sure why you would, but you don't know for sure. What's the exact magnitude of improvement? Most of the data that shows a relationship between IgG lowering and clinical response has been done with cyclic dosing or in a Phase II setting where you gave a dose and then just watched the IgG return and the symptoms return. So that's a little bit artificial. The setting I think you want is, okay, when you have a steady reduction at a certain level, then what's the steady improvement over time. So that already is a tremendous step forward, I think, in terms of what physicians will have in terms of information. And our bet is that, that will pan out that the higher IgG reduction will be important for some patients. This won't be like 100% 1:1, but I believe that there'll be an important minority of patients for whom deeper IgG reduction yields 1 of 2 things, either get some kind of over the regulatory line, meaning they have a 2- or 3-point improvement of MG-ADL that they might not have had otherwise. But maybe even more importantly, gets them deeper down the MG-ADL curve or up the Christmas tree if you're used to the Christmas tree plots. So not just having a 3- or 4-point improvement in MG-ADL, but a 5- or 6- or 7-point improvement. And that's important because those are the patients that make a really big impact on the prescribing physician. It's great if you have somebody who's impacted by myasthenia and are able to improve their symptoms. Everybody feels good about that and they should, but if you get somebody almost back to where they were before, that's the kind of experience that nobody forgets. So success is having more patients like that. I think if you had 1 in 10 patients more that get to almost symptom-free, that's going to have a big, big impact.

Just with regards to one of the points of differentiation being the subcu dosing, I think we recently saw some subcu data from argenx. And I'd just be curious on your thoughts there.

Yes. I mean I think it looked good, which they're from a pharmacodynamic standpoint. They reported a high percentage of injection site reactions, but it wasn't really clear whether that was just the way the study was done or something else. I think the main uncertainty with Halozyme from our perspective is how does chronic Halozyme, particularly chronic Halozyme given weekly because I think in many cases people will be dosed weekly across a variety of chronic conditions, how is that tolerated? My understanding is that of all the various co-formulated medications approved for use with Halozyme, I think only one of them is weekly, and that one has a limitation of use for a year. Most of the other ones are, I think, every 3 weeks. So unlike a simple subcu biologic where there's many products that have been approved, some of them for decades, and you have people who've used -- and by simple subcu, I mean like a normal concentrated formulation in a prefilled syringe or autoinjector, people have used those for years and years and years. Some people have used the TNFs, I think, we're probably approaching 2 decades now. So you have a huge body of experience that it works for a long time for many people. With Halozyme, we don't know if that system of kind of dissolving a little bit of tissue below the skin and creating a potential space and then injecting the medicine and then it has to grow back, does that work week on and week off for years and years? We'll see, maybe, but there's some uncertainty there, just technical uncertainty. But I think that -- but I think the -- you see everybody moving towards subcu as the way to go because that's what the people with the disease tell us. If you ask physicians, you get a little bit mixed perspective, some prefer this, some prefer that. But if you go to the source, you ask people with these conditions, which would you prefer, I mean, it's a very skewed answer towards subcu. So eventually, medicine follows what the people affected by the condition want.

Okay. The -- obviously, your Phase III design and path forward here in MG has been blessed by FDA. Any early discussions with ex U.S. regulators on the path forward just given the LDL changes and with regards to what they would see -- they would need to see to feel comfortable and how you're factoring that into your development plan?

Yes. Yes, we've had discussions with regulators across the globe and across different programs, and I think the feedback has been quite consistent.

Okay. That's great. Maybe switching gears to WAIHA and TED. In WAIHA, you -- I don't think we've seen the study data accumulated prior to the study termination. So any plans to share that at a conference or just publicly?

We did share it, but it's so sparse that you probably don't remember, but I don't fault you for that because it's a sparse data set. We had -- we only had 3 patients who completed the 12-week of treatment. And actually, one of them only completed 11 weeks. So we had 3 people that really kind of completed a course of therapy. And -- in those 3 people, all of whom were quite refractory, so they had had multiple prior medications, including some pretty significant off-label use of cytotoxics and things like that. And they had just been -- really had no improvement for a long time. They were all in this group of on a moderate dose of steroid and occasionally off and on getting a transfusion. So in that really, really refractory group, very small, one of them had a very good response. So I mean this was -- we showed this slide back in June of last year. So we can -- it's out there in the public domain, and they had almost a 3-gram improvement after 4, 5 or 6 weeks, and then they held that throughout the treatment period. That's a big, big response. The regulatory threshold is a 2-gram per deciliter improvement and -- because this was a small study, we had several discussions -- it was open label, we had several discussions with the investigator. He was really impressed, like this person had not -- nothing was touching them. Then we had the 3 patients, one of them had sort of a so-so response. They got a little bit better and then a little bit worse. They had a steroid taper during the trial, so maybe that changed things a little bit. And then 1 didn't respond. So again, it's only 3 people, but 1 out of 3, if that's even directionally close to the percentage of people who get a big response, I think that's a good opportunity.

And then the buckets you outlined in TED, the buckets of opportunity, obviously, post teprotumumab, which one of those you're seeing as your sort of most optimal chance of success? Or is it just you're simply going to go after all 3 and you think they're all completely viable?

Right. I think -- so one of the things, I have been involved in many, many product launches. At one point, I had them all summarized, I think, 17 or something around the globe. And there's one thing that's really common across all the product launches I've been involved with, particularly the more recent ones, which is you need a very specific patient type at the time of launch. Who's going to -- where is the physician going to get their first experience? And that's even I think maybe even more important today than in the past because there's a short window to get some kind of experience before the various payer restrictions, which are usually not quite as tight on day 1 of launch, can be quite tight 6 months in. And so if you get 6 months in or 9 months in, and the physician just hasn't gotten an experience, then you sort of fall back into the noise and then the next product launch is coming. So if -- you need know who you're going to get your first couple of patients from so that the physician can get their own experience. But then equally importantly, there should be a patient for whom you really feel you're the best. And that may not be the same person because maybe the person who is going to be -- really benefit the most or the type of patient that's going to benefit the most, they may not be available like immediately in large quantities at the time of launch in a physician's practice. So what's really nice about the thyroid eye disease groups that I showed you, there's sort of 2 groups that are both represented. So the people who will be available, I think, for really great candidates for batoclimab if it works in Phase III and gets approved, at launch will be those people who've failed or gotten an incomplete response on Tepezza. There'll be a lot of them. Tepezza is being used in a lot of patients. It's demonstrated for everybody that there's a lot of them that need in this category. So somebody who's just finishing their course of therapy or maybe finished it 6 months ago and their symptoms are just coming back, they're a perfect candidate at the time of launch. Probably, those types of patients aren't going to have quite as robust of a response as somebody who's brand new -- brand newly treated. And you want to have some patient group for whom you're first to have a long-term brand that's going to be among the winners and that's what we think we can have. So that other group, the people who have more moderate symptoms, they're still in the moderate to severe, they're still within the same group of patients that are studied in the Tepezza trial and were studied in our IIb trial, but they're just a little bit on the milder side. That's the group that we think is going to be sort of the best pool for batoclimab first. So why do we think that? Well, I've also been involved in a lot of products -- promoting a lot of products that were very efficacious, often the best efficacy in their class, but had a little bit of something that needed to be managed. It sounds a little bit like batoclimab in the other indications. And what's true about those types of products is physicians often use them for kind of their middle group of patients and the more severe ones because it's a bigger gun, if you will. The people who are a little bit less severe, if you have choices, often those are the patients who will get the product that's a little bit -- has a little bit lower efficacy because there's just a general sense that with a little less efficacy there's also a little bit more tolerability. And as I mentioned, we don't -- haven't yet observed any irreversible side effects with batoclimab and haven't observed any hearing issues. So that group, I think, will be the one that longer term gets used -- or batoclimab works first. The other thing that's nice about having 2 products is you can sequence them, particularly in a category like this. So I think you if you have a person who has a not-as-severe thyroid eye disease, treat them with batoclimab; if they get better, great, you're done. You don't have to worry about a irreversible side effect. If they don't get fully well, then now you know that you're using that bigger gun, sort of having tried the other asset first.

Okay. Great. So you showed us a slide, we've got 2 -- MG, TED, WAIHA and then 2 other indications. And 2 out of those 4 are going to be pivotal trials or the next step is a pivotal trial, correct? What is the -- what are we waiting, or what are you waiting on there? Is it discussions with FDA? Is it that they -- or is it you already know and you're just waiting to disclose them? Is it resources that you're going to pick 2 of the 4? What's the processes going on behind the scenes?

Right. Right. Great question. So the first, we made a strategic decision, which I think was a really good one. And it was based on feedback we got from a lot of regulatory consultants, people who had a lot of experience, many of them have worked at the FDA previously. And they said that in the unique situation that the anti-FcRn classes where you have multiple divisions working on your asset at the same time, when you have a particular safety finding that you want to work through like we had, best to run it to ground with a single division versus kind of having it -- having open discussions with multiple divisions at once. And then it's even hard for them. They're not quite sure who's on first and who to best coordinate. So because we were most ready to go into a pivotal trial with MG, we decided that we would have that interaction with the neuro division. So we did that. In the short term, that was a little bit slower because we wanted to make sure that we, again, had everything sort of wrapped up with the neurology division before we went to other divisions. But long term, I think it will be faster because if we had gone the other route and there had been some miscommunication between the divisions or 1 of them had a different idea versus the other 2, then I think it would have been a much longer path to try to recover from that. So we got that just at the end of last year. End of 2021 is when we announced that we had achieved in line with the neuro division. After that, then we started all the other regulatory interactions for thyroid eye disease. I mentioned previously that we're meeting with the ophtho division this quarter, and with the heme division for warm autoimmune hemolytic anemia and then interactions for the other indications. And the other thing -- so that was the one thing which -- so that's been happening this year, 2020 year -- '22. And the second thing is we have these again, these 2 features and particularly the IgG-lowering being at the top end. We spent a fair amount of time working with external thought leaders looking down the list of potential anti-FcRn indications and saying, okay, which ones is the best indication that higher IgG-lowering will matter more, with a desire to kind of play to win versus trying to find like a niche indication where nobody was at.

Has the thought process around subsequent indications changed since the discovery of the LDL issues? Or were the next 2 indications you're following, have they -- were they just happened to be the same?

Right. So I would say initially, when we were -- when we had some uncertainty, we sort of put a pause on thinking about other indications, while we just sort of decided what we actually had. And what we found was we had a reversible lab abnormality that was likely manageable and we validated that the IgG-lowering probably mattered. And we went into a lot more detail on our R&D Day about the dose-dependent response that we believe we've observed in thyroid eye disease. And of course, there's the myasthenia data. So with that in mind, we pretty much returned to where we were before. We had the LDL signal, which is we've got -- what's our key differentiators, deep IgG reduction, simple subcu. What does that translate into in terms of your best indications? And if you believe you can compete on the main stages we do, then the best indications are going to be the best place to compete.

And you previously mentioned that the -- you were going to kind of run it through the LDL issues with 1 division and then you hope that there will be sort of cross-talk between the others. In your subsequent interactions with these other divisions, have you found evidence of that cross-talk? Or have you kind of -- how efficient has that been?

Yes, it's hard to parse that out, to be honest. But we've gotten -- we've been -- even across regulators, they share information or sometimes request documents from other -- official documents from other regulators from FDA, sometimes OUS regulators. So there's a fair amount of cross-talk. It's a little bit vague sometimes to the sponsor what have they actually talked about or -- you only see at the end of the day, do you get different requests. And for the most part, the feedback we're getting when it comes to kind of nuts and bolts, do they agree with the safety and monitoring plan, that's a very specific item, the answers have been quite consistent.

Okay. From a timeline perspective and a sort of event path for the company, I guess all we know right now is MG trial initiation first half '22, data 2024. And then we're kind of waiting on the -- you too kind of open the [indiscernible] and tell us what the other 2 indications are and what's starting? What can you tell us about potential data updates between now and 2024?

Right. About all I can say is we're working on it. It's a priority for sure, we understand. And that's important to investors. It's important to us. We don't want to be too skewed in one direction where we only have very long-term programs where you only get an answer after a couple of years. The beauty of a pivotal program is it's the -- if you're ready to do it, it's the fastest obviously to approval. And we have a very long-term value-creation focus. So that's positive. But it's also the longest to learning anything. And so having a mix of some prepivotals, some proof-of-concept studies that will generate data in the 2023 timeframe is important not only for catalyst, that's important, but it's also important to continue to build our knowledge base of how does IgG-lowering relate to clinical response across a range of indications.

Maybe switching gears just quickly on funding, obviously, an important consideration for the space, especially where things are right now. Just remind us where you are and what that -- what the runway that gives you is?

Right. So as of our last disclosure, which was our fiscal year ending in March, so our last disclosure was our Q -- for the quarter ending in December 31, at that time we had $527 million in cash. And when we -- in the first quarter -- first calendar year quarter of this year, we disclosed that that cash would get us through 2025 or into 2025 based on the assumptions we have, programs we're running, that kind of thing. So a pretty decent cash runway, I would say.

Okay. So do you think that will get us -- would that get you through to approval in MG, do you think? Or do you think we would -- there may be additional funding required between Phase III data to an approval?

Yes. I mean, I think kind of slicing it that thin around MG specifically, it's hard to say because, again, we still haven't made a final decision, and we haven't communicated a final decision in terms of what our other pivotals will be, and proof-of-concept. And so we had enough information -- we made enough decisions to have confidence that we'll have cash into 2025, but that specific, we haven't made a decision. But what I will say, as you look at the opportunity across the anti-FcRn class, again, there's many, many, many indications, we will -- at some point in the future, we're going to be raising money again before we're cash flow positive. So when that will be exactly, we'll have to see.

Sure. And maybe just on the healthy volunteer program with the statins. I think we're in a follow-up period right now. Should we expect to see any data from that follow-up period publicly?

Yes. Yes, eventually, we'll see all of it. I'm not sure that that data will be so interesting just because it's really just a safety follow-up that you have after a study like that, kind of for good measure. The data that I think will be interesting is we do have additional cohorts with lower doses of batoclimab and lower doses of statins. We haven't disclosed what exactly they are yet, but I think that will be the data that will come in the second half of this year that will be interesting.

Okay, fantastic. And I presume you'll let us know when MG trial initiates, right?

Yes.

Fantastic. Well, I think we're actually at the end of time. But, Pete, thank you. This has been really interesting. I look forward to the updates.