Good morning. Thanks for joining us for the first session at the 43rd JP Morgan Healthcare Conference. I'm Brian Cheng. I'm one of the senior biotech analysts here at the firm. I'm joined by my associate, Sean Kim , and also Mary Maggie , who are also in the audience. On stage, we have Immunovant, and we'll now pass the mic to their CEO, Pete Salzmann, for a short presentation, followed by a live audience Q&A. Pete, the stage is yours.
Thanks, Brian, and good morning, everyone. Excited to be here and give you some updates for what's coming in 2025 and some of the things we've accomplished in 2024. I'm going to start briefly with this slide because this is really our North Star. It's our vision to enable normal lives for patients with autoimmune disease. And it leads us to strive for the best efficacy, which we believe 1402 is positioned to across the anti-FcRn class, while also emphasizing a very simple and patient-friendly delivery device that I'm going to give you an update on today. Before getting to that, though, I want to go through a few of the accomplishments from 2024 that I think are really significant.
As many of you probably know, we disclosed some very impressive Graves' disease data from a batoclimab proof of concept that has allowed us to design a really robust program in Graves' disease with our 1402 lead asset. And importantly, that batoclimab study demonstrated a dose response, meaning that patients achieved greater clinical benefit during the period of time in that study when they were on the higher dose of batoclimab and had deeper IgG reduction. We spent a lot of time in 2024 advancing 1402 to be ready for a broad range of pivotal trials that can lead to registration. And in fact, we have five INDs cleared. For anyone who's worked on an IND, particularly for a potentially registrational trial, which is a much bigger set of information required than if you're just starting an early phase proof of concept, also be an IND.
You know that even a single IND is a big project to get right. And having cleared five of those last year was a tremendous accomplishment for our team. We have now initiated two of those five trials, both our Graves' trial as well as our trial in ACPA-positive, difficult- to- treat RA, are up and running and enrolling with sites open in the United States. We've achieved unprecedented speed to an auto-injector. All five of these trials are going to be run with an auto-injector, which is our eventual commercial formulation. So we're not going to be in a position to have to do bridging studies or wonder if we're going to be able to bridge. We're using the eventual commercial product in our trials for 1402, which is a tremendous accomplishment. And I'll show you some benchmarking data to put that accomplishment in perspective.
As I'm sure you all know, we completed enrollment for the MG trials. We're waiting for patients to work their way through the 24-week blinded period so that we can deliver that data this quarter. And then we announced a PIPE financing this week that meaningfully strengthened our balance sheet. So really a lot of that last one sort of came in right in the beginning of 2025, but I counted it as 2024 because there was a lot of work to set it up done in 2024. This slide, I'm not going to go into a lot of detail, but it's a nice one if you want to take a review of the various resources that we're bringing to bear on this opportunity. And it's not just that financial strength I just mentioned, but also a really tremendous intellectual property.
We have, as many of you probably know, an issued composition of matter patent to 2043. That composition of matter patent is somewhat unusually, we were able to get claims beyond just the composition of matter in terms of method of use and methods of manufacturing. So that's a very, very strong patent we're excited about. We have an experienced leadership team that's experienced individually and experienced working together, which is important because drug development's a team sport, as you guys all know. And this is an amazing market. I think that's maybe not fully appreciated. I know it's appreciated, but not fully appreciated. And I'm going to touch on a few reasons why I think the anti-FcRn market just keeps getting more exciting with each passing year and the data, not only that it's coming from Immunovant, but from other assets. This slide we usually have near the end.
I'm bringing it up front just so I can highlight one addition to our near-term catalyst roadmap, which is we now anticipate having additional data from our batoclimab proof of concept in Graves' disease. And that additional data will include initial six-month remission data. And I'll talk about that in a second. That'll come in the summer of this year. Okay, so very briefly, this is just beautiful data that probably many of you have seen. It shows a dose response between the dark purple when participants were on 680 of batoclimab and achieved a mean 77% IgG reduction. There was another part of the study where they were on the lower, more standard dose of batoclimab, 340 mgs, and had a 65% IgG reduction, which is pretty much the standard IgG reduction you see across the FcRn class, that 65%.
If we look at a deep responder metric, which is those patients who not only normalized their T3 and T4, but were able to come off their anti-thyroid drug, you see a 56% ATD responder rate while on the high dose and 36% ATD-free responder rate on the lower dose or the standard dose. Not only is Graves' disease a first-in-class opportunity for us, but we feel that this data, along with some other data that is in our corporate deck, provides a compelling reason to believe that in order to truly succeed in Graves' disease, you will need to be able to provide deep IgG reduction. At the moment, we're the only ones that can do that with a practical amount of medication. You could achieve it with a large amount of medication given intravenously.
When Momenta owned nipocalimab, they were able to show similar reductions, but it was with a large amount of medication given intravenously. If we're talking about a practical amount of medication that can be given by a simple subQ, then batoclimab and now 1402 at the high dose are the only ones reporting these levels of IgG reduction. And within Graves' specifically, there's a lot of information that we have reviewed and shared to articulate the size and qualitative nature of this really compelling opportunity in Graves' disease. This is a large market among rare disease opportunities. It's not so large that it sort of breaks the rare disease paradigm. We're talking about people who are unable to achieve a euthyroid state on anti-thyroid drugs. So that subset that we're targeting is a very meaningful group of patients.
You can see an annual incidence conservatively estimated at 20,000, but not so large that you would go outside of rare disease pricing bands, which is important. And if you look at the bullets three, four, and five, you can see that we took a look from several different angles at, well, what percentage of patients who have Graves' disease fall into this category that they're unable to either ever achieve a response with an anti-thyroid drug or maintain a reasonably consistent response with an anti-thyroid drug. And we looked at that by doing surveys. We looked at that by doing blinded chart reviews. And then we did, and so the surveys were done with both physicians and patients. And all of these methods came to about the same estimate, which was 1/3 .
Interestingly, that estimate was arrived at in a setting where no one had seen any new data in Graves' disease in 50 years or so. And so in a context where people, physicians in particular, couldn't imagine any new therapy, we think that their estimate of unmet need was probably conservative. If you don't think you have a solution for something, you're a little less likely to appreciate that there might be a problem. So this is really, really interesting information. And it just shows kind of two data points. In July of 2024, this was a different survey that was similar to one on the last slide. Physicians basically said a 1/3 of their patients needed a new medical therapy, people with Graves' disease treated with an anti-thyroid drug. Now, in December, we updated that market research.
This is all done, by the way, with thyroid specialist endocrinologists, not general endocrinologists, but thyroid specialists who see a lot of patients with Graves' disease. So these would be the target physicians you would eventually be promoting the product to if it's approved. Well, now many of them are aware of our Graves' data just because it's been in the public domain, but we also reviewed with them in the context of this market research, kind of product X, it was blinded to batoclimab, but showed them the information that was on that previous slide, as well as some other information to highlight that there's a solution potentially on the way, and then after that, asked them how many patients that they treat with ATDs need a new therapy.
And you can see it increased 60% versus a different group of patients who didn't have that awareness of a potential solution. So this matches qualitatively what we are feeling as we work with investigators setting up clinical trial sites for our Graves' trial, where we can just feel tangibly the enthusiasm for a new therapy in Graves' disease based on a greater appreciation of the unmet need growing. These physicians are also very excited about. I'm going to skip forward a slide and back a second. Our auto-injector and the fact that the clinical trial will be run with an auto-injector.
Before I go into a little bit more detail about the auto-injector, I just want to highlight what's really, I think, unprecedented, profoundly amazing accomplishment from our CMC and quality team to put us in a position to run these pivotal trials with 1402 with an auto-injector just about a year and a half after our first in-human dose with a vial and syringe. So why do I say that's so impressive? Many of you may not have a context for what does that usually take. So we looked at 16 products. You can look at them in the footnote if you're interested, but it's products you would recognize of a variety of immunology products, some approved, some still in development.
The median time from the first time they dosed a patient in a phase I trial, usually with a vial and syringe or intravenous formulation, usually the very, very first one is actually intravenous, till they had auto-injectors introduced, approved by regulators in their supply chain, dosing patients in a clinical trial was seven and a half years. Now, part of that is if you miss a window, you kind of miss a long time. So if you start your pivotal trials with a prefilled syringe or with an on-body infusion site, then you sort of got to wait until the entire trial is done. And then there's a rule that you can't, you got to wait for your first package to be approved with that first formulation and then submit something else.
Some of this is a consequence of the challenging project management from a regulatory standpoint that companies face in bringing an auto-injector to bear. But we managed all that complexity and got ahead of it. Batoclimab helped us in this regard because we did some initial engineering work with batoclimab on the same platform, which allowed us to make some good decisions far in advance of what we would have been able to do without batoclimab. And it's a nice example of how batoclimab as a first-generation asset has set us up for speed with our second-generation asset. So this platform, this pen right here, it's the YpsoMate 2.25 mL auto-injector that delivers a 2 mL amount of medication. It's the same. This is the same pen, same platform used by Cosentyx. It's probably the most famous product, a blockbuster product.
It's treated many, many, many thousands of patients, and they use this as their 300 milligram dose is in this auto-injector, which is super easy to use. It doesn't even have a button. You just press it on your skin. You just put it up to your skin and press it, so it's very, very easy to use. It's established. There are many other products that are approved in development. This is like this is a standard platform, so this is. We're not developing our own auto-injector. We went to a standard platform, and it's a very important part of our strategy, as I said, back to our vision of normal lives for patients with autoimmune diseases that they can deliver their medication in their home by themselves easily. Okay, so we've accomplished a lot. We have an auto-injector ready to go.
I showed you some exciting Graves' data. I do want to take just one step back and share one slide on our market, the FcRn inhibitor market, which I think is still certainly appreciated, but maybe not as even as appreciated as it should be. I think it's an extremely unique mechanism within immunology in terms of the amount of de-risking, not only on the efficacy side. There's many, many studies that have shown positive data and the few that actually have failed have often been because of a trial design issue from my perspective, but also now on the safety side, there's just thousands and thousands of patients in trials and also treated commercially with FcRns, and so there's a predictability to what to expect that is really powerful when you're looking across a lot of indications.
Last year, we had new data in Sjögren's from a very large trial that Janssen ran and a smaller trial that Argenx ran. Janssen released a lot of information from that trial that allowed us and would allow you to, I think, form a pretty strong opinion that there was not only a very good biological effect, but almost certainly a dose response probably going beyond the dose that they studied. Janssen generally is studying 15 mg/ kg q2 weeks of nipocalimab, which delivers 60%-65% IgG reduction. In the same neighborhood as our batoclimab 340, which I showed you from the Graves study, and the same as we expect from our 300 of 1402, but lower than what we expect from our high dose of 1402.
So even with that standard dose, they showed signs of a dose response going beyond that standard dose, which is great for us and also for the class. There was obviously the approval in CIDP that Argenx achieved. And around this time last year, actually probably wasn't this week, but a couple of weeks after JPM last year, there was a lot of noise from our perspective, swirl around other mechanisms. Were all these patients going to go to CAR-T? What about IL-6? And I think there were mixed results from certainly the IL-6 trial and MG. And I think CAR-T is an amazing technology for very, very severe patients. The data that we're seeing from the various companies there is bringing into focus the importance of B- cells and autoantibodies in a way that is really interesting.
At the same time, I don't think that that's a modality that's likely to compete for the main type of patients, which are those patients who are severe, but not hyper-hyper-refractory. So I think it's in a lot of ways a complementary modality to FcRn. And then the other thing that supports that is that physicians who are using FcRns or those who are anticipating using them based on trials that are happening in other indications have an increasing enthusiasm for earlier line use. If you talk to a neurologist who's used a good amount of Vyvgart, what they're excited about is using it even earlier. They want to start with an FcRn because they see this mechanism is so favorable.
If you talk to physicians who are excited about CAR-T, they're not saying, "I'm excited to use this first line." They're excited to use it in the patients that don't succeed with an anti-FcRn or an anti-cytokine therapy, depending on the modality. So I really think there's just different populations that we'll be going for. And this enthusiasm for earlier line use in FcRn, I think, is going to play out across a lot of different indications and grow the class. So this is a super exciting class. In spite of that, we want to be differentiated. Our goal is not just to be a player in an exciting class. Our goal is to be a leader in an exciting class. And in order to be a leader, you need to have differentiation. You got to have something that's unique.
So in that lower right-hand corner, this is the most important differentiating factor for two reasons: the rapid and deep IgG reduction. It's most important because it's very important to patients. If you're a person who needs deepest IgG reduction to get full symptom control, then that's really, really critical. And probably before everything else. And secondly, I think it's the one that's going to be the most challenging for anybody to match. I don't see other assets currently on any type of trajectory to get to 80% steady, consistent 80% IgG reduction. That's even true outside of the class. And then on top of that, you have the simple subcutaneous delivery mechanism that I showed. And by having a subcutaneous delivery and having the high dose and the standard dose, then you get the lower left-hand advantage, which is dosing flexibility.
Not everybody is going to need the 600 dose of 1402. Not everybody's going to need the high dose. But for a physician to know that I can go to the high dose if that patient needs it, or I could step down if they're doing really well, that flexibility is very attractive to many physicians and pretty unique. Last year, we showed that most of the most successful immunology drugs generally have at least two doses, and we have two doses. But within the FcRn class, most of the others have a single dose, either that they're studying or that they've gotten approved. So our tailored dosing is unique within the class. This just summarizes some of the points I've already made as a nice kind of one-pager. So what do we have coming up for 2025? So we have data from our first-generation asset, which I've already highlighted.
There are many ways that batoclimab is sort of accelerating the development of 1402, and we expect data that we're really excited about in the first quarter for MG and CIDP and then later in the year for TED. Those trials are designed to take advantage of batoclimab's higher dose to demonstrate and reinforce this correlation that we've already observed in a lot of other studies between greater IgG reduction and greater clinical efficacy. I mentioned early on that we plan now in the summer of this year to disclose some updated information from our batoclimab proof of concept in Graves' disease, and that will include remission data. For 1402 to be successful in Graves', what we need to do is get people who can't become euthyroid who aren't euthyroid, euthyroid.
The main success factor of the Graves program is to get people to a euthyroid state and ideally off their ATD. If, however, once they've gotten euthyroid for some period of time, taken 1402, they can go off their medication and stay in remission, stay euthyroid, that's a huge upside. The Graves treatment guidelines are all written to support 12 months-18 months of therapy, ideally, not 10 years of therapy. Physicians, endocrinologists have a very, very strong desire to get Graves patients in remission. That could be because long-term anti-thyroid drug use has a variety of problems associated with it. Whatever the reasons are, it's a real part of the market dynamic in Graves' disease.
So if we're able to show that not only are we able to get people to euthyroid, but get them to maintain that euthyroid state, put them in remission, which we believe we can do because the people who historically achieve remission in Graves are those whose antibodies come down. And that's exactly what we're doing, is driving the antibodies down. So I think there's a good reason to think we could get remission, and that will be a big upside. It wouldn't be part of our initial submission or label, but it would be additional data that would come after the launch and I think be very favorably received. We're going to have potentially registrational trials enrolling. Two of them are already enrolling in Graves' and rheumatoid arthritis, the ACPA-positive, difficult to treat.
We've also said we're going to start the trials in MG and CIDP after the batoclimab trials read out, and then we have a soon-to-unveil fifth indication. These studies are all running with the auto-injector, which I think is going to be very exciting. We're on track also to initiate the 10 studies that we talked about last year by next March, which is the end of our fiscal year. This just kind of summarizes that same information in a different way, and with that, I'll say thank you and see what questions Brian or the audience has for me.
Great. Let's begin the Q&A session. For those of you who are in the audience, if you have any questions, you can raise your hand, and we do have a runner on the floor. For those who are joining us virtually, you can submit questions on the conference portal. Pete, thanks for joining us. I think one of the key questions going into the MG readout had always been, what do we need to focus on? I think it's interesting that the deeper the reduction, the better have been signaled across multiple indications. But this is really the first time that we see it, particularly in an indication that a lot of investors have looked at in the past and they're highly familiar with.
There is a lot of focus around what do you need to see in MG-ADL and the low dose going to expect it to perform like efgartigimod. What do you think that a win case is for the upcoming pivotal phase III for MG?
Right. So I think that, I'd say, first of all, that the MG trial in particular is very, very well set up to show a difference between the doses and to show general comparability of the 340 to other FcRn data, which achieves a similar IgG reduction, so I think what we need to see and what we expect to see is, first of all, that the 340 dose is broadly similar to other FcRn data in MG, and that is a big enough population that's similar enough treated in a standard way, so people enter the trial and are randomized to either placebo, 340, or 680 for 12 weeks.
So we'll have 24 weeks of data, but that first 12 weeks of data where the patients are treated for those participants that get 340, I think what you're going to see is broadly similar data to efgartigimod and the other FcRNs, both in terms of IgG lowering, in terms of MG-ADL, in terms of QMG. So that's the first point is do we show that? Then the other thing that, that trial is well designed to do is demonstrate a difference between the participants who get randomized to 680 versus those who are randomized to 340 and placebo. Because, again, it's a good-sized group and it's the same trial, so all the same clinical trial sites, so a little bit less bias, those kind of things. And on top of that, we have all the patient-level information, so it's easiest to do an apples-to-apples comparison.
We expect the 680 dose to be faster in IgG reduction and clinical response and yield deeper responses. So not only deeper IgG, but deeper MG- ADL. What do I mean by deeper? So a two-point improvement is clinically significant for patients and is the minimal clinically important difference, MCID. But there are people who get a four-point, five-point, six-point improvement in their MG- ADL. Remember, people start these trials generally with a baseline MG- ADL of eight or nine. So if you're at eight or nine and you improve two points, that's noticeable. But what's really impressive is you improve four or five points. Those people are just, they're in a very different place in their life. And it's obvious to them and obvious to the physician. So we expect to get more people to those deep responses with the 680 dose.
That will translate to an average improvement at the population level. But I think what will be most tangible to neurologists will be the number of people who are getting a deeper response, which we expect to be higher with 680.
Just to confirm, the top line, are we going to get data from both induction and the maintenance portion?
Right. Yeah.
I think primary endpoint is focused on the end of the induction period.
Right.
What will you look for in the maintenance period? As patients start to transition into the maintenance portion, what is your focus to better understand the dynamics of these, I guess, the outcome of the deeper reduction in IgG?
Right. So first and foremost, in order to register a project product in MG, and this was particularly true at the time that we were designing this study, what regulators both in the U.S. and Europe wanted was a 24-week controlled study. So one option is to treat everybody the same for 24 weeks, randomized to drug or placebo. We didn't really want to do that to have people randomized to 24 weeks of placebo. So in order to have a 12-week endpoint with two control periods, we did this study design where we have an induction period and a maintenance period. So that was kind of one of the main drivers for why we had that versus why just you could have had 680, 340, and placebo for 24 weeks. I think it would have been a little harder to enroll and a little bit less interesting.
Having designed it this way, we also appreciated that there are some, there's a lot of kind of, I don't know, clinical experience that people with MG, which is different than CIDP, can achieve a period of disease quiescence. I hesitate to call it remission because I'm not sure they're totally in remission. But after treatment with IVIG or PLEX historically at a very intense level, you can also often get people's disease in MG to quiet down, and then they don't need treatment for a while. They need a lot less intense treatment. And with IVIG, you might be able to spread out the doses. We thought, well, let's see if that's true also for FcRn inhibition.
After intensive induction with the 680, can we keep people controlled with lesser dose, maybe even as little as every other week, which could have a benefit in terms of ease of use? So I think the every other week in period two will do better than placebo, but probably not as well as every week. And if that's the case, this plays into this tailored dosing. So physicians, if they see that some patients can handle every other week and some need weekly, that provides them flexibility, which is attractive. And to have that in the label ultimately is a positive for the product. The primary outcome, though, not just the primary endpoint, but the most important part of the trial is to demonstrate that 680 is better than 340, better than other FcRNs. Period two will generate a lot of extra data.
That's the kind of data that's nice to have when you're talking to physicians about how they're going to use the product and help drive commercialization.
I'm going to ask one more question on MG before I open up the floor for any questions. I think you brought up an interesting point about phase II generating data for the potential tailoring experience for 1402 in the future. So how do we think about your design for the pivotal studies for not just MG, right, MG and CIDP? So how do you kind of frame that to make sure that doctors also have the ability to also adjust the dosing as they to optimize the dosing for the specific patients that they're treating?
In terms of 1402 eventually?
In terms of 1402 eventually.
Yeah. Yeah. Well, I think for 1402, we plan to study generally the 300 and the 600 dose in most indications. Back to Graves for a second, our first trial only has the 600 dose because we believe that, as I showed you, that there's a strong dose response. But our second trial in Graves may well have both doses because I think having two doses is a nice advantage for physicians. And then back to MG, I would expect that we'll study both the 300 and the 600 dose. Having the ability to go to 600 for those people who need it is a real advantage, but having the flexibility is a second advantage that you can add without getting rid of the first advantage. So how do physicians use the data from the batoclimab trial in the context of 1402? I think that'll be relatively straightforward.
IgG is such a strong biomarker that you can basically make the link between two assets. We'll have batoclimab data. Even if we end up not commercializing batoclimab, which is our base case, we'll still have that data to share, and showing a correlation between IgG lowering and clinical response will be relevant for 1402.
Okay. Maybe just on the top of your comment there, do you think that there is potential to commercialize batoclimab for TED?
For thyroid eye disease, so from a corporate strategy standpoint, we're just 110% behind 1402. And there's so much to do. There's so many opportunities that anything we would do with batoclimab is a potential threat to our focus and a trade-off versus moving 1402 faster and broader. With regard to the opportunity in endocrinology, Graves' and thyroid eye disease, I think the opportunity that's growing is mild to moderate thyroid eye disease. And the reason is that those people are increasingly in the healthcare system. They're seeing Tepezza commercials. They know their eyes are uncomfortable. They're going in to see their doctor, but they're not severe enough to get an insulin-like growth factor inhibitor, and they're not severe enough for surgery. The group that is severe enough is pretty well treated with insulin-like growth factors and surgery.
Tepezza and surgery are finding a balance that physicians are pretty happy with. There is an opportunity there, but that opportunity is becoming, I think, a little bit smaller, particularly as new insulin-like growth factors come to market. On the other hand, the mild to moderate thyroid eye disease patients who also have Graves', there isn't anything for them. There's no medical therapy. There's no surgical therapy. And that group is large, and they're not necessarily getting larger, but the group that's in the healthcare system seeking a solution with mild TED is getting larger. So all that's a big introduction to say that I think our main focus for Graves' and thyroid eye disease is going to be milder thyroid eye disease in the context of Graves'.
So with all of that, I think it's a little bit unlikely that we find an opportunity in thyroid eye disease that's large enough for batoclimab that it warrants the trade-off with 1402. But we'll see. We'll see what the data shows.
Any questions from the audience? Maybe let's switch gears into more I mean, I'm sure we can spend an hour talking about the different data catalysts upcoming this year. But I think one important question that we've been getting is more about just the evolving landscape. I think especially last year, I think there are just so many questions on how you compete against protein degrader, the IL-6 class, which is now put aside. And there's also that question of the advantage of your auto-injector. I think you framed it really well today, but maybe just can you kind of frame there are two key questions here, right? So one is, how do you think about your auto-injector compared to the auto-injector formulations that are coming out from competitors?
And then, secondly, it's just protein degrader, how do you think about yourself in position and compared to where they stand today?
Right. So our primary competitive advantage that I think is really, really strong and hard for anyone to replicate, and I don't see anybody on a path to replicate it, is the deeper IgG reduction. That said, as we sit here today, I think we have a route of administration advantage. And the reason I say that is we have our investigational product in a standard platform in the clinic. And that's different than having it on a slide or having signed a contract with YpsoMate. YpsoMate is a very proven platform, but any individual product has various engineering challenges that need to be solved. And there are so many ways to face a challenge that can be very time-consuming to solve.
You can see that by just the data that shows that many, many products don't take two or three years, but five or six or seven or eight years. These are big products where the economic value of getting them into a simple subQ is very strong. The products are performing well, maybe in an IV. There's a lot of money to solve the problem. It's not a financial problem. It's a time problem. The fact that we have overcome all the various engineering challenges and have our product in a standard platform in the clinic, that's a big advantage. Others probably will eventually catch up, but there's still some they face more twists and turns. Even having a prefilled syringe is not. Depending on your prefilled syringe platform isn't exactly the same as being ready with an auto-injector.
So I think that we'll see what happens with the other platforms. But we have a system that's working now, and that's what I'm excited about. In terms of other modalities, degraders in particular, theoretically, degraders will some degrader, whether it's some of the ones that are out there today or some new ones in the future, should be able to reduce IgG deeply. That's not the main challenge. The big challenge that degraders will have is yielding a consistent IgG lowering. You can overshoot with a degrader. With an FcRn, when you completely maximize the mechanism, so what I mean by that is when you have every Fc receptor in the entire body bound with a monoclonal antibody, you get about an 80% IgG reduction. You're not going to go deeper than that. And that's because you're not actively degrading the IgG. You're preventing its recycling.
And so the balance that's achieved with an FcRn is about 80%. And it turns out that if you go deeper than 80%, you start to get into some problems with too low of IgG. So this is a little bit technical, but the PK/PD of degraders is tricky. And I think getting to a nice steady state, 80%, without overshooting some patients and simultaneously undershooting others, that's another big engineering problem that degraders face. So they're many years behind, and they face a lot of challenges that the FcRn class and 1402 specifically have already overcome.
I guess last question for us is maybe just looking at the pipe that you announced yesterday.
Yeah.
Yeah, it felt like a week ago, but it's only day two. How much does that add to your plan here? Because you have the plan to start off 10 trials, 10 potentially pivotal trials over the course of the next 12 months-15 months or so. So how do we think about the role of the pipe? And does that effectively remove some of the financing overhang that I think that's some of the focus of some of the investors today?
Yeah. So look, I think that $450 million pipe with the cash we already had puts us in a tremendous position to execute for a long time. And we don't have any near-term need to raise capital. That doesn't mean we wouldn't opportunistically, but there's no immediate need to raise additional capital.
Great. That concludes the end of our Q&A sessions. Thanks for listening.
Thanks, Brian.
Thank you.