Good morning. I'm James Gordon, J.P. Morgan European Pharma and Biotech analyst, and today it's my pleasure to introduce the argenx presentation, and you're gonna hear from argenx CEO, Tim Van Hauwermeiren, and we're gonna have the breakout in here as well. So 20 minutes presentation and then time for your questions. So thanks a lot for joining us today, Tim. Good morning, everyone. A warm welcome to the argenx presentation. While we take a look at the forward-looking statements, James, I would like to thank you for hosting us today at this wonderful conference. We at argenx, we are on a bold journey, a journey to transform autoimmunity. Actually, we want to take autoimmunity away from surgery and blunt chemotherapy into precision medication, where we basically nail, with precision tools, specific molecular pathways which drive disease, offering a radically different benefit-risk profile to patients, a transformative benefit to patients. And the way we work is as follows: We think this space, this autoimmunity space, badly needs more novel targets. So instead of doing the technology push against the same old tried and trusted targets, we like to pioneer novel disease biology. We like to embark on novel targets, and we do that in close collaboration with world experts in translational biology. We work with antibody drugs going after these targets. We have a world-class suite of antibody engineering technologies, and we like to build molecules, which, when we promote them to the pipeline of the company, have the potential to play in multiple indications. So we create a ton of optionality within the molecules in the portfolio, but also between the molecules in the portfolio. In order to understand what transformation in autoimmunity means, I would like to invite you to take a look with me at Mike. Mike is an MG patient. He got diagnosed about 16 years ago with generalized MG when he was still at college, and the way he told to us the story is that he could not really participate to social activities, sports activities. He actually lost a full semester of classes at a given point in time, and basically, he was living his life with an MG ADL score, an activity of daily living score of about 8. That doesn't tell you a lot, but, guys, this is a miserable situation to live in. One day, his physician prescribed VYVGART. Mike went into what we call minimum symptom expression. That means an ADL of 0 or 1, like you and I have it, and he could basically reengage with his life. He went back to the gym, he became the coach of his son's baseball team, he started a new relationship. Basically, MG killed his first marriage. And then last summer, his physician switched him over from VYVGART to VYVGART Hytrulo, allowing him to enjoy the fast subQ injection, fitting it into his very busy life. Guys, this is transformation. Mike has his life back, and that's what we mean by bringing transformation to the autoimmune space. My agenda today is to walk you through three innovation horizons which run across the company. I'm gonna start with the VYVGART horizon, then I will take a look at the pipeline horizon with empasiprubart and ARGX-119, and then we will look at a third innovation horizon consisting of four new IND candidates. But let's start with horizon number one, the VYVGART horizon. We have two commercial products, VYVGART and VYVGART Hytrulo, and here from the podium, I would really like to take the time to congratulate my commercial colleagues, each and all of them, for printing a $1.2 billion revenue number across the globe in 2023. Day on day, we're two years into the launch of VYVGART, and I think this is an impressive achievement. Thank you. I would also like to applaud the CIDP team for submitting a high-quality sBLA on time before the end of last year. I want to applaud the ITP team for submitting the marketing authorization application in Japan, and I want to thank the clinical teams for pushing forward with 15 indications by 2025, and our Tech Ops team, working around the clock on the prefill syringe. We're developing leadership position in FcRn. I mean, you remember the business model I just explained? We are pioneering FcRn biology, as you can see from the numerous peer-reviewed publications. We're going after this novel exciting target with a unique antibody fragment, an Fc fragment, equipped with the proprietary ABDEG mutations, which preserve the pH-dependent nature of the binding, and that translates into a unique clinical profile. Remember the optionality, which we like, 15 indications by 2025. Yes, there will be attrition, but the way you protect against attrition is by creating this type of optionality. Now, stellar clinical data is one thing. Understanding how that translates to value in the real world is another thing. So that 45% minimum symptom expression we have seen in our clinical trials... Remember Mike, he was an MSE, right? ADL of 0 or 1. 45% of patients achieved that in the clinical studies. In the real world, when we follow a huge patient cohort out there, they have an ADL of 0-4. That means they no longer meet the threshold to enter a clinical trial, which is an ADL of 5. We also see, remarkably, a very fast ability to taper steroids. The world is quickly becoming more intolerant for the cumulative toxicity of steroids and achieving a meaningful steroid tapering within the first six months on therapy, guys, that's a big deal. We also made a commitment when we launched to make our innovation accessible to a broad range of patients. Well, we have shown now with My VYVGART Path, our patient support program, that patients get meaningfully faster on drug. And then last but not least, outside of the U.S., VYVGART has been reviewed now by so many HTA bodies, health technology assessment bodies, identifying the value of VYVGART. VYVGART is really shining through their models, and I was personally very pleased to see one of the leading HTA bodies declare that VYVGART has superior cost benefits over IVIG. The safety database of VYVGART is now becoming really big. We have more than 4,000 patient years of safety follow-up across the clinical trials and the real-world patients. Let's double-click on the commercial execution. We crossed the $1.2 billion revenue mark last year, and that represents a 21% CAGR in 2023. Already in Q3 last year, we passed the 6,000 patient mark, and what I want to call out is that 55% of our patients are coming straight from orals. That's exciting because that's where the real growth is in this market. We have been successfully broadening the prescriber base, crossing the 2,300 mark in Q3 last year, and that's a 25% year-on-year increase. Then last but not least, our promise, our commitment, most of the policies here in the States, 90% are favorable. That means patients can come on VYVGART after 1 or maximum 2 orals. And this is a growing market. When innovation enters an underserved rare disease space, it's growing the market. We're growing the VYVGART share. As of the first of January this year, we have a J-code in place for VYVGART Hytrulo, which will help in access. We're expanding the field force, not only benefiting MG, but also preparing for the CIDP launch. We are aggressively investing in the prefilled syringe, and at the end of last year, our partner, Zai Lab, got VYVGART on the Chinese NRDL. That's a hell of an achievement. We're also expanding the VYVGART total addressable market. We're investing in label-enabling trials, phase III studies, and externally sponsored research, and we continue the geographical expansion. And then last but not least, the magic happens when innovation enters this space. Jointly, as innovators, we are growing the overall market. Disease awareness goes up, diagnosis improves, and patients and physicians stand up to ask for better. They're no longer willing to accept the old status quo. Let's turn our attention to CIDP. We announced stellar data mid of last year. There is no other trial in the history of CIDP which showed this strong set of data. Very strong response rates, very strong reduction in risk of relapse, and for once and for all, we have shown CIDP is an IgG-mediated disease. We no longer have to guess how IVIG works. It's IgGs driving this disease. We have also set a whole new standard of how clinical trials will be done in the future from a quality and a global nature point of view in the CIDP rare disease. But then I would like to call out some of the magic of this study. 99% of the patients basically showed compliance in the study. That's not trivial. You ask these patients to give up their current medication to get on an unknown entity or placebo, that's risky for a progressive disease, and still we had such a high compliance. We also had a 99% rollover into the open label extension. Guys, what this means is that patients are waiting. They badly need new treatment options in the toolbox. From our own market research, we know that only 20% of patients achieve remission on their current standard of care. More than 50% of patients are dissatisfied with the burden of their symptoms, and we think there are more than 42,000 CIDP patients on treatment today in the United States and our ex-US argenx markets, excluding China. We're also working hard to transform the patient treatment experience. The key to understanding this slide is the exclusive license, which we hold to the Halozyme ENHANZE technology. This is a unique, commercially and clinically validated technology. It's a volume-enhancing technology, allowing us to get 5 ml of product quickly under the skin. And the second key to understanding this slide is the unique physicochemical properties of efgartigimod. This Fc fragment can be concentrated to 200 milligrams per milliliter without paying any penalty on viscosity. That means you can squeeze this formulation through a fine gauge needle without any back pressure. We have used these advantages to launch the first ever MG product in MG mid-last year, called VYVGART Hytrulo. We are working very hard on the prefilled syringe that's currently in advanced clinical trials, and we just promoted the auto-injector from prototyping stage into industrialization stage. This is just the beginning. So far, I have only been speaking about myasthenia. I have only been speaking about CIDP and ITP, but this year we get six phase II data points on deck. While in the background, we have the phase III trials ongoing for TED. Next year, we have another six data cards coming on deck, so we will be at least in 15 indications by 2025. Let's zoom in on the five phase two proof of concept studies for VYVGART on deck this year. It's Sjögren's syndrome, it's post-COVID POTS, and then three subtypes of myositis, which we're proceeding with in a basket trial. What these five indications share is a very strong biology rationale. It's very plausible that these diseases are driven by pathogenic IgGs, as you can see from the literature, convincing evidence from different models, suggesting that pathogenic IgGs drive the disease. Each of these indications is going through the discipline of a randomized controlled phase 2 trial of 24 weeks. The myositis basket study is actually a seamless phase 2, phase 3 trial, and there are accepted clinical endpoints for each of these indications. And then invariably, all these indications have the same in common. There's a significant number of patients out there waiting for new transformative tools in the toolbox. The current treatment options are either non-existing, like in PC-POTS, or very dissatisfactory, as in Sjögren's syndrome or myositis. Let's move our attention now to innovation horizon number two. We start with empasiprubart. Let's call it EMPA today, but here's the argenx playbook. We are pioneering a novel target, complement factor C2. We're first in class. We're approaching this target with black belt antibody engineering. This is a sweeping antibody. That means that one antibody can take out multiple times C2 before it is cleared itself. It has a half-life of about 80 days, supporting very favorable dosing. And again, we create optionality within this molecule. We're already in three indications in clinical development, and today we will be talking about MMN, multifocal motor neuropathy, where we're redefining the textbooks of immunology and say that MMN is a pathogenic IgM-driven disease. These are data from the first of two dosing cohorts in the phase 2 proof of concept trial of MMN. You need to know that MMN patients have only one treatment option, it's IVIG. So every MMN patient you find on the globe is on IVIG. So in the run-in phase, what we do is we establish the IVIG dosing cadence for each patient. It's a very high dose of IVIG, typically every two to three weeks. And once we established their cadence of IVIG, at the peak of their last IVIG administration, we randomize these patients over placebo or EMPA, and we monitor the risk for needing an IVIG rescue. What you can see is that EMPA is reducing the risk for an IVIG rescue by 91%, which is pretty spectacular. But what we're most excited about is that 94% of patients declared their health condition to be better as compared to their baseline when they were on IVIG. Guys, that's transformational. 55% of these patients say they were much or very much improved compared to non-placebo. The safety profile of EMPA continues to be favorable and in line with the very extensive phase 1 safety and tolerability study, which we performed. MMN patients are waiting. The diagnosis of an MMN patient is lengthy, it's frustrating, and it's an emotional rollercoaster. Many of these patients first get diagnosed as an ALS patient, then they're being re-diagnosed as an MMN patient to find out there is a treatment option out there called IVIG, but it's imperfect because the chance of progressing on IVIG is real. So we think the MMN space, MMN patients are ready for a transformation, and we think there are more than 10,000 patients waiting in our argenx markets. Taking a look at ARGX-119, enhancing the neuromuscular junction. Here, the novel target we're pioneering is MuSK. Again, we're working with the world experts on the neuromuscular junction. We made a pretty cool agonistic antibody. It's a very special antibody. And again, we create optionality by pursuing multiple indications where enhancement of the neuromuscular junction can create a transformative event for a patient. We're just concluding a very extensive phase 1 safety and tolerability study, warranting advancement of this molecule into proof of concept studies. On the left-hand side, you see a preclinical animal model for congenital myasthenic syndrome. This is the first indication we're going in with ARGX-119. This is an ultra-orphan indication. It's a genetic mutation which is leading to genetic myasthenia. And this animal model shows that normally when these pups are born, that is the short gray line at the bottom, they die. Their muscle function is very weak, their diaphragm doesn't really work, so they don't live long. And what you see is that the single administration of 119 upon birth is rescuing that phenotype from lethality. They have a normal body weight development, a normal restoration of the phenotype. Of course, at a given point in time, the antibody has left the system, and the single re-administration is rescuing the relapse in these animals. So this is a very robust preclinical animal model based on which we are marching forward into CMS patients this year. We do not have such models in ALS. There are no robust predictive animal models, so we're reverting to kind of second-generation advanced testing. Here you see a neuromuscular junction on a chip. It's interesting to see how these motor neurons innervate the muscle cells. They can stimulate the cells to contract. And now you can see in black how neuromuscular junctions of healthy volunteers are performing on such a chip... how the neuromuscular junctions of an ALS patient perform. You see a marked reduction, which you can rescue with an ARGX-119 dose with a nice dose response. Turning our attention to the third innovation horizon running across the company, we're going to talk about four new pipeline assets. Last year, here on this podium, I promised you one, at least one. Well, we announced four molecules, ARGX-213, which is a new molecule targeting FcRn. We're bundling all our know-how on FcRn in this molecule. We believe the universe of opportunity is so big that we cannot just tap it with VYVGART. We need a second molecule to do that. We have ARGX-109, which is known to some of you. It's an ultra-potent, long half-life IL-6 blocker, and then ARGX-121 and ARGX-220 come straight from the argenx innovation playbook. These are first-in-class novel target antibodies, and they're all racing towards IND. They should all have achieved that IND before the end of 2025. So this company is firing from all cylinders. In 2024, there's gonna be a ton of news. We will have approval news from Switzerland, Australia, Saudi Arabia, and South Korea for VYVGART and gMG. We're initiating a seronegative trial, and for ITP, we're expecting a Japan decision on approval. For VYVGART sub-Q, in gMG, we're expecting a Japan decision on approval, a China decision on approval. CIDP, we're expecting a launch around the middle of the year, and then steaming forward into regulatory submissions in Japan, Europe, China, and Canada. We are also investing heavily in the prefilled syringe development, and we will be giving you data-based updates in the course of the first half of this year. As I told you, we're expecting five phase 2 data cards in Sjögren's, PC-POTS, and three myositis subtypes. We're expecting the full phase 2 data for MMN, and you will see ARGX-119 getting to the first two proof of concept studies in CMS and ALS. A few words from the financials of this company. We're in a very healthy state with such a continued strong execution on the commercialization front, with such a strong cash position of $3.2 billion at the end of last year, and a disciplined investment in R&D and SG&A at or below $2 billion, we can guide for a cash burn of around $500 million, and that basically means that this company is on a firm trajectory to become financially self-dependent. To conclude, this year, we're rallying the troops behind important strategic priorities. On the commercial front, we want to broaden the MG leadership, we want to launch CIDP, and we want to advance the prefilled syringe as fast as we can. We're preparing for six phase 2 data readouts, leading to multiple phase 3 indications, and we're working around the clock to get our four INDs filed by 2025. With this, I would like to really thank you for your attention, and I would like to open the floor for questions. Great, so we'll now kick off the Q&A part of the session. Does anyone have any questions they'd like to start with? In that case, maybe I'll start with a high-level question, which was... So lots going on in the presentation. VYVGART already a blockbuster, but where are you now seeing VYVGART's peak potential, and how long can VYVGART go for? I think VYVGART has a really long time horizon in front of itself. I think we have a very long patent life. What we said is that the patent life is now known to be further extended by another 2-3 years due to PT and PTA, so there is an enormous volume of opportunity in front of us. It's just the sheer volume of indications, you know, which we need to tackle with the molecule, which makes us believe that there is space for a second molecule in the pipeline. Clearly, you had very strong data for MG and CIDP. You have had some setbacks towards the end of last year for ITP and PV, but does that change your view on all these other indications much, as should we read through from MG and CIDP, or does PV change how you think about all these other indications? I'm glad with the question because I don't think these indications failed from a biology point of view. That is the whole point, so I think VYVGART worked. These are clearly IgG-driven diseases. Actually, as a reference, the whole class of FcRn antagonists has already shown in eight out of eight indications, convincing proof of concept. The lesson we learned for one of the two ITP studies and the pemphigus study is: how do you run a clinical experiment in autoimmunity without being tricked by background medication? That's a very important question we run into. We're drawing the lessons we need to draw from this experiment, and we're reapplying them across the pipeline now in all the other indications. A question from the gentleman there. Hi. Just quickly, Sjögren's, what gives you the real confidence there? Obviously, difficult disease, untreated, is kind of the point of it. So kind of how should we be thinking about the increase, going forward? Yeah, I think that's an excellent question. Maybe in case some people didn't hear the question. So I think... Well, in summary, the question was Sjögren's and confidence, isn't it? Yeah, I think that's an excellent question. So when you do the homework on biology, and you start to look at the pattern of evidence, there's actually quite a lot of evidence that it's immune complexes driving this disease. I think there has been a hyper-focus on B-cell biology, but I think the trigger are immune complexes, which are formed by autoantigens in complex with the autoantibody. You basically see pretty convincing passive transfer data. For example, moms with Sjögren's delivering babies which have lupus-like effects. The autoantibodies correlates, the titer correlates with disease severity. And basically, what we do in the Sjögren's study is try to prove the concept, that this is indeed IgG mediated. We're not only looking at specific clinical endpoints, which are typical in Sjögren's, but we also take a real deep dive in our patient cohort from a biomarker point of view. We can zoom in on subsets of patients where you have the highest chance of success. Thank you for the question. There's a gentleman at the back there with his hand up. Yeah, any guidance on 213 in maternal fetal medicine indications? I think... Was the question on 2, 1, 3? Yeah, ARGX-213, any, any direction in terms of going into maternal fetal indications? No, we're not public on any indication for the molecule. I think we're in a bit of a more competitive space than a couple of years ago when we were alone. So give us the time to further develop the molecule and announce indications when the time is there, okay? Thank you. There's a person second row here with his hand up. I think if you just wait for the microphone. Thank you so much. Just two questions. One, to remind us of the sort of advantage and disadvantage of the FcRn therapy versus the immunoglobulin, and also how much of the CIDP patients' market, the patients' share you are going to... you're likely to, sort of, capture in the CIDP market. Thank you. Could you repeat part one of the question, please? Sorry, there is a lot of going on. Immunoglobulin, you know, compare to immunoglobulin, the... What's the sort of advantage of the VYVGART. Thank you. Yeah. So today, I think the mainstay of therapy in CIDP is steroids and IVIG. You're correct. IVIG can also be part of the diagnosis, so it's a difficult diagnosis. And when there is a suspicion of CIDP and patients respond to IVIG, it's further evidence that this is a CIDP patient. I think there's plenty of room for improvement. I think you will see a typical adoption ladder when we launch the product. There are patients, of course, which do not respond to IVIG or who cannot tolerate IVIG, or who do not want to carry that burden of therapy. Then, of course, you have patients, you know, which weaken in between IVIG cycles, who could also be open, you know, for an alternative tool in the toolbox. So I think in general, this is a space which is, I think, ready for multiple tools in the toolbox, not just one. And then I think the 42,000 patients we reference in our markets, these are patients which are on therapy. I'm not excluding a similar dynamic as the dynamic which we've seen in myasthenia, where for the first time when precision tools entered the space, you uncover that the space is bigger than you thought. So awareness going up, diagnosis improving, and basically more patients and physicians coming out of the woodworks asking for better. Thank you. A question just there. Thank you. In terms of indications for FcRn inhibitors, how do you think about IgG proteases and their competition? I think, was the question on... Sorry, the acoustics aren't great. Was the question on competition for FcRNs for other mechanisms? Yes. How you view IgG proteases as a potential competitive approach? IgG proteases, IgG degraders, I think, is the question. Well, there are little data for us to navigate by, so we like to be science-based and data-based. I would like to see a bit more data, not just concepts, you know, or early-stage animal model data. But let's see how these new molecules pan out before we make any conclusion on this generation of technology, okay? We're just lacking the data. Question here. Could you elaborate a little bit on the? If you could just wait for the microphone, please. Could you elaborate a little bit on the trial design learnings from the studies that didn't go well? Because it's incredibly important what you said, not only for your drug, but for the whole class. Yeah, I mean, so in summary, the two lessons we learned is the following: When you go in autoimmunity on top of background medication, it is important that you single variably test what is the impact of that background medication on the disease state. If you compare a pemphigus trial with, for example, an MG trial, what we did well in MG is patients were on a stable dose of background medication and still symptomatic, right? And then you, you randomize them into your trial. What we did in the pemphigus trial is these patients were not on, on active therapy. You randomized them over active and control, but your control actually also contains active medication. So you put the patients in both arms on active therapy, and the steroid dose, which was assured to us to be suboptimal and not able to push patients into complete remission, was very effective putting patients into complete remission. So two lessons learned: randomize patients which are symptomatic despite being on a stable dose of background medication, and double-check in phase 2 what that background medication is really doing to the disease. That's it in a nutshell. One question I've had has been about some of the early pipeline you talked about for the first time today, and there were two new things there. One was a next-generation FcRn, and you also talked about an IL-6. So quick questions on the... One is, if VYVGART is great, why do we need another FcRn? What's the remaining unmet need?... And the other one was, has been IL-6. I think Roche have ENSPRYNG, which is also an IL-6. Does the fact that you're going for an IL-6 mean you think that looks like a big competitor? Is it a defensive move, or why go for an IL-6 now? No, I think these are two great questions. So look, VYVGART is an incredible molecule. I think the clinical profile is best in class. We're trying to create as much area under the curve as we can by going for 15 indications by 2025. But nevertheless, that molecule has its limitations in terms of patent life and the IRA clock ticking. So there's an abundance of opportunity which cannot be tied by just one molecule, and that's why we feel the pressing need to bring a second molecule online, not necessarily to improve upon VYVGART, but basically to take on the additional opportunity in front of us. So that is the logic behind having two molecules in the portfolio. Literally, James, every week we uncover new diseases which are IgG mediated. It's just mind-blowing how many things are being reclassified as actually an autoimmune disease, IgG driven. On IL-6, this is one of the first molecules which we've built. We out-licensed it in the days that we didn't have any money, and at a given point in time, we got a global rise to the molecule back, and the insights in IL-6 biology have evolved. So, I think there are new findings suggesting an important role of IL-6 in a number of orphan indications. So we think it's warranted to take that molecule forward into clinical development ourselves. We are redoing the homework because the original partner had a poor-performing cell line, a process which we didn't like, but stellar phase one data, so we know what this molecule will do in phase one. But we want to redo the homework by building our own cell bank and building our own process. That's in a nutshell, the situation on IL-6. Thanks. Is there areas where this IL-6 is different to other IL-6s that are out there? Well, we know it's best in class. I think it's unparalleled. This is a molecule with femtomolar potency. I mean, if you read textbooks of immunology, that should not be possible. Well, we did it. And it has an incredible half-life using the enhanced technology. So, I think it is a differentiated molecule. Thanks. One other update was EMPA, where we got data, detailed data for the first cohort today. So I believe that we've still got another cohort still to come before you make a decision on going into phase three. So what do we still need to find out? What's the second cohort gonna tell us? And is the idea that this is something that'd be more convenient than immune globulin in terms of the administration profile or might actually be more effective as well? Where would this be positioned? I like the question. So because we're pioneering a novel target, nobody knows how much target inhibition you need to have full effect, clinical effect in MMN. So as my colleague, head of the clinic, Luc, would say, for a novel drug, you know, dose finding is a very important question you need to address in phase two. That's what we're doing. So the end result of the phase two should be a robust PK/PD model, which allows us then to triangulate what is the dose and the dosing regimen for phase three. We know it works. The question is, what's the optimal dose and dosing cadence? So that will be answered in cohort two before then we move into phase three. By going with a precision tool, which is nailing the pathogenic mode of action of the IgM autoantibody, we should be able to do fundamentally better than IVIG, which probably has just an indirect effect on complement. So the idea is to raise the bar. Many MMN patients worsen in between IVIG cycles. Many IVIG patients still worsen overall, despite being on drug. Imagine, you know, we can regain function, or we can at least stabilize the disease and stop it from being progressive. I think that would be pretty transformative in MMN. Thank you. I've got one question through the interface here. You may have partially answered it already, but the question is: How do you propose to get round the issue of background medications skewing future trials? It seems insurmountable because you're asking patients for a high level of trust. Is there a way to break out what the background therapy is doing versus what your therapy is doing? I think this is a key development question, we're double-clicking on for each trial design. I think it's doable. We have done it in MG. We have certainly done it in CIDP. So with everything we know now, we need to just double-click on the study designs of the ongoing trials and the future planned trials and make sure we take this unknown unknown into account. So, we are marching based on a solid biology rationale, but now when we look at the clinical feasibility filter, which is our second filter for indication selection, we need to be absolutely sure we are embarking on an indication where you can disentangle the signal of the drug from the background medication. One other question I've had has been about BP. So PV and BP both being skin conditions, so PV wasn't successful and perhaps because of this issue of background medication. So is that gonna be exactly the same on... for BP? Is the trial design the same or are there important differences? And also just on BP, am I right that you've got some data in-house already that you're currently looking at? I think that's a great question. So just quickly recapping on pemphigus, what have we seen? We have seen VYVGART working really well in terms of PD effect. But if you have a control arm where you know 60% of patients go into CR very quickly on a low dose of steroids, there's little room for the drug to add something on top of it. So we immediately mobilized the BP team to look at the pemphigus data, also take their own internal look at the first 40 patients, and make sure they can integrate all these lessons learned in the thinking for BP, because both trial designs are very similar. We use also 0.5 mg per kg steroids for induction. We taper the steroids. We know that was very effective in pemphigus, so why would it not be effective in BP? So we need to rethink, you know, how we go forward with the BP study. We think that the unmet medical need in Bullous Pemphigoid is very significant. Steroid toxicity is not manageable for these elderly, fragile patients. It's a big market, much bigger than pemphigus. So we're giving the team the time to analyze the data, think them through, and come forward with a proposal on how to continue BP. So is that something you think you could still be in place to make a decision this year on? I hope we will be in a position to do that, but if and when we do so, we will communicate. Okay? We've probably got time for one more question. Maybe I'll ask just one more, which is ITP. So you had ITP in reference to Japan. So the confidence that there still is a market based on the positive study in Japan, when could you have a Japanese launch? Well, if the marketing authorization in Japan is approved, we are basically set up for launch because we already have a price. There's a price established for MG. You would not need to go through new price negotiations, so our organization is ready to launch. And of course, we did the homework. Yes, there is a market for an IV ITP product. It is a fact that there are some treatment options in the toolbox, but they're basically all doing the same. And we have shown, and again, we were at ASH, you know, a few weeks ago with very strong data, there is an unmet medical need in ITP, which we think we can address very well with VYVGART. Thank you. In that case, I think we're gonna wrap up there, so thank you very much for the presentation. James, thanks for having us. Thank you.