Good morning, everyone. I'm Colin Mytakis. I'm an associate here at J.P. Morgan's Healthcare Group. It's my pleasure to welcome Immunovant to the 42nd annual J.P. Morgan Healthcare Conference. Just a recap on the format, we'll hold Q&A questions at the end. However, throughout the webcast or throughout the presentation, feel free to submit questions through the Questions portal. Without further ado, please welcome CEO of Immunovant, Pete Salzmann.
Thank you, Colin, and thank you to J.P. Morgan for having us at this conference. Good morning, everyone in the room and on the webcast. I'm really excited about this conference. Colin and I were talking a little bit about the fireside chat format, which is great, with Q&A, which I really enjoy. But the timing and format of the JPM conference allows for a little bit of looking back and looking forward, which I think is really, really valuable. I'm gonna be making some forward-looking statements today, and I encourage investors to review the slides as well as our SEC documents for risks, both known and unknown, and uncertainties that may affect our results.
Okay, so in terms of taking a step back, I wanna start with a quick overview of our company, and then I'm gonna go into more detail with regard to our opportunity and our plans for 2024 and beyond. Our vision you see up on the slide is 7 words that I can remember without even looking at it, because it's short, it's meaningful. We want to enable normal lives for people with autoimmune diseases. Why do we come up with that vision? There's really a couple reasons.
First of all, having spoken to a lot of patients through market research who have autoimmune conditions, a common thread across all these conditions is a desire just to get back to normal, just to be a regular person, just to live their life, professionally and personally, without their disease constantly intruding or without their therapies constantly intruding. The other thing about normal for us is it sets a high bar, so we desire to make a big impact on the conditions for which we're studying either of our assets. And a lot of that has to do with the specific market we're in, which is the autoantibody market. So within autoimmune, there's been a lot of innovation, but within the subset of autoimmunity, which is autoantibody-driven conditions, there's been a lot less innovation.
The reason for that is, autoantibodies are polymorphic, which means they vary from person to person, and so that has made it traditionally very difficult to make targeted therapies. Until the anti-FcRn mechanism came to the fore, and it is a way to target, rather than the polymorphic portion of the antibody, the foot of the antibody, which is not polymorphic. So this is a really, really unique approach to targeting autoantibody conditions. A lot of the success that Immunovant has had in 2023 relates to the right side of this slide. The autoantibody market is really robust and strong. There's some great data that came out in 2023, both from Immunovant and other innovators in this space, as well as our second-generation asset, and I'm gonna get into that.
But I wanna start by talking about the left side of the slide, which is an important foundation for Immunovant. It's an opportunity in a conference like this to talk a little bit about the behind the scenes, and the most important foundational element for Immunovant is our people. I mentioned here on the slide, our C-suite and senior leaders, because you can look them all up on our website and see the diversity of their backgrounds, the strength of their experiences. But all of our employees are playing a huge role in delivering the results that we expect for the future and also those that we delivered in 2023.
We look for a very unique profile at Immunovant, and that is people who are exceptionally good at their area of expertise, but at the same time, tremendously open-minded to try new approaches. That's a hard combination to find, and we work very hard to find that, both in our leaders and employees. We also have a couple other key foundational elements beyond our employee base, and that is our intellectual property. We have a pending composition of matter patent on 1402, our second-generation asset, which, when issued, will go to 2043, and that's without any other extensions. So that's a lot of IP strength, and then financial strength you see on the slide as well. The...
What, what we're currently working on is reflected on this slide, and we have programs with batoclimab in four different indications. Three of those programs are pivotal, and I'm gonna go into those programs in a little bit more depth later in terms of how they're differentiating and how they could create value. But the point on this slide is that as we look to the future with 1402 and new programs, we're not starting from scratch from the standpoint of a newer biotech. We're a relatively young company. However, we're running pivotal programs across three different indications, global pivotal programs. So that requires us to have built a good amount of infrastructure that we can leverage to rapidly start a broad program with 1402. Okay, so that's a quick overview of our company and our opportunity.
Now, let's go a little deeper into a few of the most important aspects, starting with the market. This market is really, really unique within Immunology, I believe. It's actually one of the most important reasons why I chose to join Immunovant four years ago, having spent a lot of time thinking about Immunology and different opportunities within Immunology. The anti-FcRn mechanism combines two things that are very challenging to find in any other Immunology class. It combines a broad set of indications with a relatively straightforward biology. Usually, you only get to pick one. You either have a broad set of indications, but the mechanism is really foundational and has a lot of technical uncertainty, or you have a very targeted mechanism that's pretty easy to understand, but it's only likely gonna work for one or two indications.
This combination of indication breadth with relatively, straightforward biology is really unique within Immunology, and that has led to all this opportunity. The other thing that I already mentioned is that targeted therapy has been challenging for autoantibody conditions, so you've got many, many, many indications. That's what leads to that breadth. And then you have a very strong biomarker, which can guide development and accelerate development, and I'll get into that in a little bit more detail as well. What are the 22 indications that are being studied? There are two approvals in myasthenia gravis, and then there's another 21 indications listed on this slide. They span therapeutic areas. They have many different clinical manifestations, and some of them are more very, very classic autoantibody conditions like myasthenia gravis.
Others are conditions where autoantibodies are known to play a role, but the level of importance of the autoantibody until recently has been a little bit less certain. Refractory rheumatoid arthritis is an example there, where I think until we had the data from Janssen, many of us would have thought that, well, autoantibodies are present, but maybe not the driver of the condition. But with the Janssen data released at the end of last year, I think that it's clear that for a subset of rheumatoid arthritis, autoantibodies are playing a role, and reducing those autoantibodies can make a big difference. Okay, so this is a fabulous market, but differentiation is still very, very important.
In a fabulous market like this, you could probably have a reasonable base hit with an undifferentiated product, but we're not looking for a base hit. We're looking to be a leader, and so differentiation is very important. There's three elements of differentiation around our assets. The first at the top is the simple subcutaneous formulation. This is something that the original inventor of HanAll, which is HanAll, thought of right from the beginning. Both of our assets are, what I like to say, born sub Q. What does that mean? That means they went into first- in- human studies. Actually, they went into cynomolgus monkey studies with a subcutaneous formulation already available. That's pretty unusual. Usually, you start out with IV formulation, particularly if you have a monoclonal antibody that you're delivering at these doses.
The amount of Fc receptor in the body is high, so the amount of medication required in this class is high, and it would be more typical to start with a intravenous preparation, which is easier to formulate, de-risk the asset, the class a little bit before doing the hard work to concentrate the antibody. But if you take that approach, which our competitors have taken, then there are certain levers that are no longer available to you to pull. Whereas if you do the work upfront, then you're just much more likely to just, to, you know, succeed from the get-go. So we have two assets that were born sub Q. They're available in a simple subcutaneous format. That's a big differentiator.
The other two are probably even more important, honestly, and that is we can drive the deepest IgG reduction with a practical amount of medication. So others could get their IgG reduction possibly as low as we are able to achieve with batoclimab in 1402, but to accomplish that, they would need an impractical amount of medication. So we're able to get there with a practical amount of medication. I'll talk in a second for why that's so important. And then the other equally important component is tailored dosing. So not everybody needs maximum IgG suppression. So the ability to offer different dosing levels is going to be very important and honestly, has been important across a lot of Immunology conditions.
So let me go a little bit more into both of these points, deep IgG reduction and dosing flexibility. There have been now multiple studies with different anti-FcRn in different indications, where there was enough variability in the dosing to see variability in IgG reduction, and then look for a correlation with a clinical response. And every time that there's been enough information, where you had enough variability in the IgG... So there are some studies where you only had a one dose, and there wasn't a lot of IgG variation, so you're not gonna necessarily see this relationship. But in studies where there was variability in the dosing and the IgG reduction, you every single time you see a correlation with clinical response, whether that's in MG, TED, our most recent data in Graves' disease, ITP, or pemphigus.
Honestly, I think it makes sense based on first principles. I don't think this should be a surprise. The mechanism works by lowering IgG, so the idea that if you lower it greater, you're gonna get more efficacy or lower it less, you'll get less efficacy, I don't think should surprise any of us. Okay, what about tailored dosing? We have, I think, a unique development program in that we're looking at different dosing levels. We're using induction and maintenance. Our program in myasthenia gravis, I think, is the first one to look at induction and maintenance, which is a strategy which in other Immunology conditions has been very successful. We recently looked at the top 10 Immunology products globally, and they're all listed in the appendix, which is in the slide deck on our website.
If you look at those 10 Immunology products, which have a median global net sales in 2022 of $5 billion, the median account, you know, accounts—Humira would obviously drive the mean a little bit higher, but even using the median, you get to $5 billion. Those products have nearly 70% of them in terms of the indications. Those 10 products have 41 indications currently, and 28 of those 41 indications have either induction or a loading dose. So they're using not just straight dosing. They're not just using one dose and giving it for the entire duration of therapy. Rather, they're starting strong and then tapering down in many cases. So this is a proven approach in many Immunology indications, and the top 10 Immunology medications globally tend to use this approach.
Those same 10 medications have multiple doses available in maintenance phase. Sometimes that's because different indications require a different intensity of dosing, and sometimes it's within an indication because different patients require a different intensive dosing, intensity of dosing, even within an indication. So the fact that we're able to offer meaningfully different levels of IgG reduction with a simple preparation, our pre-filled syringe, gives us a lot of flexibility and matches us more closely to the other proven leading immunology compounds to date. So we've got a lot of opportunity to differentiate. How are we applying that differentiated asset to this exciting market? Well, to date, as I mentioned up front, we have programs in four different indications. These are batoclimab programs, and each one is a little bit different.
So we've selected to so far focus on neurology and endocrinology, that we think are both really nice therapeutic areas for an anti-FcRn. I imagine eventually we'll be in other therapeutic areas as well. There is a benefit to concentrating a little bit in a therapeutic area. You get to know the physician thought leaders. You get to understand the approach to development, and there are some differences, therapeutic area to therapeutic area, so there's a capability there. Within neurology, we have programs in MG. I mentioned already that we have an induction and maintenance design. You can see a little bit more detail on that in our website. This is an approach which is common in other medications used in MG, and it's even the older standard of care medications.
It's an approach that's very, very common in other Immunology programs. But our myasthenia program was the first one to use induction and maintenance, and as we've been rolling this program out globally and have had discussions with investigators who've been in part of many, many other myasthenia trials and treat many patients with myasthenia gravis, they're really excited about this because myasthenia is a very variable condition. Some patients get a lot worse all of a sudden and then require intensive therapy for a while. Others have a more modest degree of impact that's a little bit easier to treat. And in spite of that variability in disease course, most of the modern therapies just have a single dose that's labeled for a one regimen.
So whether it's weekly or biweekly or monthly, whatever the course is, it's the same dose with the same frequency. So the physician doesn't have the ability to modulate the medication based on the patient's course. We wanna bring that to physicians. In CIDP, this is an area where there was some new data in 2023. CIDP is a condition that definitely has autoantibodies involved, but prior to the efgartigimod data, I think it wasn't as clear that this was an autoantibody-mediated condition. There was more risk in this program before the efgartigimod data than there was in MG, which is a more clearly classical autoantibody condition. And we see a big opportunity to apply the same approach with MG, essentially, in CIDP.
Moving a little bit to endocrinology, we have a program in thyroid eye disease that was a first-in-class program, and others have talked about following us into thyroid eye disease. In 2019, when I first joined Immunovant and was speaking to investors, there was a uncertainty about how much patient need there really was in thyroid eye disease. It was a condition that didn't have a lot of innovation prior to 2019, and consequently, physicians had become accustomed to a relatively modest or even poor treatment outcome. That's typical when you haven't had an innovation for a long time. So if you talk to physicians, they're... the quality of the unmet need wasn't so apparent.
But we spoke with patients who were affected, and it was very, very clear that there was a lot of unmet need in thyroid eye disease, and obviously, the Tepezza launch has really validated that. This is no longer a question. Now, the question is, what's the best mechanism for treating thyroid eye disease? And we believe that based on the fact this is a autoantibody, classic autoantibody-driven condition, that an autoantibody-lowering mechanism, like an anti-FcRn, can and should play a big role in thyroid eye disease. We got interested in Graves because the more physicians we talked to about TED, the more they told us: "Hey, how come you're not thinking about Graves? That's an even bigger opportunity. TED is a nice opportunity, but Graves might be even better." And the biologic rationale is equally strong there.
And we had some data at the end of last year that we released, showing a positive impact in a trial with batoclimab. Okay, another big part of our story in 2023 was our second-generation asset. So we have 5 programs running in 2023, the 4 I just mentioned with batoclimab, and then a first-in-human study with 1402, our second-generation asset, which was designed to achieve the same degree of IgG lowering that batoclimab achieves with a same simple subQ formulation. But avoid the reduction in albumin that batoclimab drives because of steric hindrance. 1402 binds to the Fc receptor in a different orientation. That lowering of albumin, which you see with batoclimab and some of the other FcRn inhibitors, secondarily causes an increase in LDL.
So we wanted to remove those two issues with 1402, which binds in a different orientation. And our cynomolgus monkey data, which we disclosed at the end of 2022, looked very promising in that regard, and that's a pretty good historical model for predicting impact on albumin and LDL in humans. But I think the proof is really in the pudding when you see the phase 1 data, and that's what investors and we were waiting for last year, and we delivered that in the second half of last year. And we're super excited about what 1402 can now bring to the table as a potentially best-in-class asset in a market with so many different opportunities. So how are we gonna attack all these different opportunities?
What you all want to know, I'm sure, is which indications are we gonna start when? That information we're not gonna share for a little bit for strategic, competitive reasons, but I think it's important and fair to describe our approach. How are we going to march through the different opportunities? I think this first row on the top is perhaps the most exciting. There's still a phenomenal amount of white space in the FcRn class, and so that gives us some first-in-class opportunities. I've only listed one here because it's one that we've talked about, and we have a program in Graves' disease with batoclimab. So that's the other ones that we've thought about, we're not yet disclosing. But where we're gonna go first in class, what are we looking for?
We're looking for two things. First, strong biologic plausibility. You won't have any FcRn data, obviously, because it's, if it's first in class, you don't have that data. So you wanna be confident that there's a role that the autoantibody is playing, and there are many things about Graves' that give us that confidence. And then the second thing, which is equally or maybe even more important for a first-in-class opportunity, is that we're really confident that there's a high level of unmet need. Because if you're doing a first-in-class, if you're executing a first-in-class program, there's going to be a lot of trailblazing required.
The more unmet need there is from a patient perspective, then the more value to be created, and therefore, the more willingness and ability to have to, you have to trailblaze and work out those details, which are always hurdles when you're first in class. There's also a lot of best-in-class opportunities when you have a potentially best-in-class asset, and I've grouped those into two categories. The first one is those indications where there are... I think there's broad acceptance that it's an autoantibody condition. And in these, we'll be looking to differentiate primarily based on being able to deliver deeper IgG reduction, which we think will deliver better efficacy for a meaningful subset of patients. And then, of course, our simple subcutaneous delivery device.
Then the third category is also really exciting, and these are conditions like refractory rheumatoid arthritis that I referenced a little bit earlier in the talk, where emerging data suggests there is a therapeutic potential in lowering autoantibodies. These, I think, are probably the conditions that are most likely to require deeper IgG reduction to achieve maximum efficacy because there are more things in the immune system activated than just the autoantibody. Even if the autoantibody was kind of what got things going, there are generally in these kind of conditions, there's a multifactorial immune system activation. So if you're going after just one component of that, which is the autoantibody, as a solution, then you need to, I think, lower that autoantibody in, you know, maximally. So this could be...
This third category could be the group that is most where we're most differentiated by having deepest IgG reduction with a practical amount of medication. Okay, so what does that look like? What's the so what in terms of our catalyst roadmap? This is our catalyst roadmap as of today. We'll be adding many things to this as we build out our 1402 plan, and I included the two most recent catalysts because they're very, very fresh, even though they're in the rearview mirror, and that is the 1402 healthy volunteer data and the Graves' initial data that we disclosed at the end of last year. We have data coming up in the first half of this year, 2024, with CIDP.
That's the interesting trial, which includes sort of almost a proof of concept built into a pivotal trial. We're using two different doses in our open-label lead-in. Otherwise, this trial is very similar to the very nicely designed trial that argenx ran. And those two different doses in the lead-in period will give us an opportunity to look at, test the hypothesis of whether deeper IgG reduction matters in CIDP, which we believe strongly that it will. MG, those are the full top-line results in the second half of this year, and then TED are the same thing in the first half of 2025. So, just my last slide before I jump over to join Colin for Q&A is, you know, bottom line, what are we excited about?
This is a really, really exciting mechanism. Really, really exciting class. It's having spent, I don't know, the last 10 years or so, thinking a lot about Immunology, I think this is a very, very, very unique, special class within Immunology. And that's not only because of the breadth of indications, but because of the biomarker. That kind of links between the first and the second box here. The fact that IgG is such a specific biomarker is what enables an asset like 1402 that's just coming out of phase 1 to contemplate going straight to pivotal trials. What do you need to do to start a pivotal trial? You need dose design and effect size.
Normally, you don't get dose and effect size until you do a phase 2, because even if there are other in-class assets, you don't really know, how do I translate my dose to their dose? Because most mechanisms don't have a biomarker as strong as IgG. But in a phase 1 anti-FcRn trial, you know, we know that our 300 milligram dose of 1402 matches our 340 milligram of batoclimab in terms of IgG lowering, and our 600 matches our 680, so we know dose already. We know effect size because IgG correlates with clinical response from our own programs and other programs.
So now you've answered dose and effect size, and then design, there are many indications where others have run a successful program, and we know the design, or in some cases, an unsuccessful program, which has told us which designs to avoid. So this is the strength of this biomarker is really a big part of why our development program can be so accelerated with 1402. And then none of that would matter if we weren't ready to take on the opportunity. So if we didn't have all the good work that we've done with batoclimab, which, by the way, of course, will generate some meaningful benefits for patients all by itself. But secondarily, what it's doing is allowing us to build a capable company, ready to take on multiple indications simultaneously with 1402.
So with that, I will jump over to join Colin for Q&A.
Great. Thank you. Maybe I do need to stand here.
Maybe I need to stand up here just so the mic works. Okay.
We've got one question: Has the IND for 1402 been cleared in the U.S.? Are you actively enrolling U.S. patients?
Yeah, so the 1402 had like many, many other... I think actually all the other anti-FcRn programs had their phase 1 trial outside the U.S. There are different reasons why companies select to choose to do phase 1 trials in the U.S. versus outside the U.S. We're conducting, because it's just finishing up, the phase 1 trial for 1402 in New Zealand, where they have an exceptionally good phase 1 center in Auckland that's been running for two decades and has produced many, many phase 1 data that's accepted by the FDA. So we will be opening various INDs for trials in patients, and as those are established, then we will announce what they are.
I'll get the mic here for you.
I guess two very unrelated questions, but one is, you know, with the argenx trials not playing out the way they expected, what do you make of that for the class? And then the other is kind of more broadly, great mechanism, but four companies, three that are big, that are... So how do you see this playing out three to five years from now in, in terms of differentiation of, you know, who wins and what indications?
Yeah, yeah. So I think in terms of the, let me start with the argenx trials. So first of all, I would start with CIDP, which I don't think was a slam dunk at all, and that turned out not maybe how some people expected, but for the positive. That and quite positive. So prior to that trial, I think there was a good amount of uncertainty about whether autoantibodies were pathogenic within CIDP versus bystanders, and whether an FcRn inhibitor would work, and the fact that it worked and worked really well, I think changed our perspective, increased our conviction that there were many, many indications beyond the classic ones, that would work. Then you go to ITP.
Okay, ITP is very unique in that it's one of the few indications on that list of 22 where there is a targeted therapy. So the vast majority of those 22 indications have no targeted therapy. But ITP does have a targeted therapy. It has thrombopoietin receptor agonists, TPO-RAs. So what's that? It's a platelet growth factor. And those work very well, and there are a lot of them. So in the case of ITP, again, this is different than almost every other indication on that list of 22. You have first, second, third line platelet growth factors. So by the time you're studying a refractory population, they've really, they've really failed a lot. That's a tough, tough population that they were looking at.
When you look at tough populations, sometimes a disease is just burned out and no longer amenable, you know, whereas it might have been amenable. It's, I mean, ITP is almost certainly driven by autoantibodies, and I think if you used efgartigimod or any FcRn very early on, it would work well. But that's not practical because you have TPO-RAs at the front of the line. So if you have a refractory condition, sometimes it's just not going to be amenable. Maybe ITP is not the best indication for FcRn inhibition. I don't think that says a lot about other indications. Or possibly, you just need deeper IgG reduction. You know, if you're treating refractory patients in any condition, sometimes you just need to be much more potent. Pemphigus, I think, is another different story.
So in the case of pemphigus, that's, you know, when you do a trial design that includes induction and maintenance with steroids, and you don't force anybody to go off their steroid, that's a really high-risk design. And it's a good reminder that you need to be very, very thoughtful about how you handle background medications in immunology. And certainly, if you're starting a different medication at the same time you're starting your investigational product or placebo, that's got to be done extremely thoughtfully. So I think, you know, on balance, the argenx data over last year was really positive. They're doing a lot of trailblazing. When you're first in class, there's gonna be some things that go really well and some things that don't go as well.
But I think you know, the mechanism is more promising today than 12 months ago, based on all the data from last year. In terms of you know, the number of competitors, look, I think if we all do the thought experiment, what's gonna be the FcRns? What's the profile of a leading FcRn 5, 6, 7 years down the road? It's got to be an FcRn that offers dosing flexibility and a simple subQ. I mean, these across Immunology, you don't have a first-in-class asset that's good but not great maintain a 70% share for decades. They get replaced by better-in-class assets. That doesn't mean they don't retain some share.
Remicade retained a decent amount of share, even after you had, Enbrel and Humira. But the leader in Immunology classes, Stelara, is still a leading product in spite of the fact that IL-17s and the new, IL-23s have taken a lot of share. So, the first-in-class product is gonna continue to do well, but the leader, I think five years from now, is gonna be a profile like ours, so we're excited to have that profile today.
Can you talk about some of the feedback you've gotten on the LDL issues in batoclimab and, kind of maybe some of the rationale behind continuing to progress that when you have a next-gen molecule that doesn't have that issue?
Right. So I think the question is hard to answer in the abstract, so it's easier to kind of march through the various programs because we have four batoclimab programs. So Graves’, we started that program, we announced it a month or two before we announced 1402, so we knew 1402 was coming. And as I've said right from the beginning, the Graves’ program is designed to answer some of these questions around dose design and effect size faster with batoclimab than could be answered with 1402, because 1402 wasn't ready, and batoclimab was. Our plan has always been that if the Graves’ ... the proof of concept with batoclimab was positive, that we would switch that program to 1402. So that's the plan there.
Thyroid eye disease is interesting because it's fixed-duration therapy, and the changes you have in analytes are much less of an issue over a short period of time than a long period of time. And, you know, we have a first-in-class program there and what I think is a very, very exciting therapeutic area that needs new mechanisms, not just a fifth or sixth or seventh insulin-like growth factor. So that's sort of unique because of the fixed-duration therapy. Myasthenia is really interesting because we believe that induction maintenance is gonna work very well there. And many patients probably will do quite well with a lower dose of IgG suppression and therefore a lower change in analyte after an initial induction with more intense IgG reduction that will have a bigger change in analytes.
So I think batoclimab offers a unique new profile for at the time of its anticipated launch versus anybody else. Obviously, efgartigimod will have a really... They've done a very nice job with their MG launch and but not everybody gets the perfect results with any product. So I think there'll be opportunities for batoclimab there. And then CIDP is kind of in the middle. You know, I think I believe pretty strongly that we're gonna see a dose response in CIDP that's probably gonna suggest that that program, in terms of what we take to registration, should be switched over to 1402 as well.
Maybe we can take one more from the iPad. How important is self-administration via simple subQ?
Right. So with the exception of thyroid eye disease, which is a short-term therapy, pretty much all the other indications are chronic therapy. There are some specific elements of this mechanism, and particularly the fact that there are so many receptors, and that you have target-mediated disposition, which means that you block the target, and then that actually accelerates the disposition of your own product. You know, an FcRn makes the half-life of a monoclonal antibody shorter. So putting those things together, the net result is you're gonna have relatively frequent dosing. I think it's gonna be very challenging to get Q8 or Q12 dosing with an FcRn without doing something that's really bleeding edge, you know, putting it on to another molecule or something like that.
So, you have a chronic condition and relatively frequent dosing. That's not gonna work for an IV. I mean, come on, nobody's gonna do an every two-week IV infusion, unless they're really, really, really sick, and this is the only product that's working for them. So, even if you have a cumbersome subcutaneous administration, something where you have to have a nurse monitor you or you have a lot of, you know, setup, that's not gonna be ideal if you're taking the product every week or two for years. So I think the simple subQ is really, really important, and that's why we're so glad that we have two—that we're actually far ahead, I think, on the simple subQ dimension. Thank you.
We will go one more from the iPad. Given your Graves' trial didn't include a placebo, how can you be confident in the results?
Yeah, it's a good question, Colin. So, our design, and you can look on our website for a little more information, but it's pretty straightforward. We're enrolling people who are insufficient responders to an oral antithyroid drug, and that meant they've been taking it for a while at a pretty reasonable dose, and in spite of that, they're still hyperthyroid. That group of patients doesn't spontaneously just get better, particularly over 12 weeks, or even 24 weeks. There are people who are doing well on their antithyroid drug, meaning they're taking a low dose and their euthyroid, their thyroid function's normal, who stop needing their antithyroid drug. So you do see spontaneous remission in people who are doing well, but in insufficient responders, you don't see, you don't see spontaneous remission. So that's why we feel confident.
Great, Colin. Well, thanks. This has been fun and we're really looking forward to 2024 and proud of what we've accomplished in 2023. Thanks, everyone.