Hello, and thank you for standing by. My name is Regina, and I will be your conference operator today. At this time, I would like to welcome everyone to the call. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question-and-answer session. If you'd like to ask a question during this time, simply press star, then the number one on your telephone keypad. To withdraw your question, press star one again. I'd now like to turn the conference over to Beth DelGiacco, Vice President of Corporate Communications and Investor Relations. Please go ahead. Thank you, and to everyone for joining us today. A press release was issued this morning with the top line results from the ADDRESS study of efgartigimod subQ in pemphigus. We have a short slide deck to accompany our remarks this morning, which is also available on the investor section of our website for your reference. Before we begin, I'd like to remind you on slide two that forward-looking statements may be presented during this call. These may include statements about our future expectations, clinical developments, regulatory timelines, the potential success of our product candidates, financial projections, and upcoming milestones. Actual results may differ materially from those indicated by these statements. argenx is not under any obligation to update statements regarding the future or to conform these statements in relation to actual results unless required by law. I'm joined on the call today by Tim Van Hauwermeiren, Chief Executive Officer, and Luc Truyen, Chief Medical Officer. Peter Ulrichts and Karen Massey will be available during Q&A. I'll now turn the call over to Tim. Thank you, Beth, and thank you all for joining us. As you saw from our press release this morning, the ADDRESS study evaluating efgartigimod subQ in pemphigus did not meet its primary endpoint. We are very disappointed by these results, particularly because we have been working closely with the pemphigus community for many years and hope deeply to be able to deliver a new treatment option to patients who have had little innovation in the space. We also hope to share better news with our shareholders to build on the momentum in what has been a remarkable year for argenx. We are facing a situation where even with strong scientific hypotheses and well-executed trial, we encountered the unknown unknown. The outcome of the study was surprising, but the path forward is clear from an opportunity perspective, and we will not be continuing development in pemphigus. Next slide. I want to start with this important visual up front, so that you can follow our decision to stop development based on the unexpected pharmacodynamic effects observed for corticosteroids in the ADDRESS study. First, efgartigimod behaved exactly as it typically does, showing a fast, deep, and sustained IgG reduction up to 75%. In the literature, steroids reduce total IgG by about 10%, and this is also what we see on the upper left. But surprisingly, in pemphigus, steroids reduced anti-DSG-1 and DSG-3 autoantibodies by 60%-70%. This level of reduction was clearly effective in improving clinical outcomes, as reflected in the PDAI score on the lower right, leaving little room for efgartigimod to drive further clinical benefit. This finding has not been documented in the literature and was particularly surprising to our global panel of pemphigus experts, given we used a low starting dose for steroids, approximately one-third to half of the recommended dose in the treatment guidelines. We are a data-based company and recognize our important role as leaders in this new field of medicine. With each trial, success or failure, we use the results to inform our future strategy as we deepen our understanding of FcRn and its role in autoimmunity. And you can trust that we are taking this moment seriously to reflect, double-clicking on all ongoing and future indications, to make sure we reapply this learning in both our indication, selection, and trial design. Before I turn the call over to Luc, I would like to zoom out to discuss the results in the broader context of our efgartigimod strategy and where we are today. We are in the business of transformation, providing solutions that raise the bar on what patients expect from their treatments. We've seen the VYVGART results in MG and CIDP, and we hear from patients and physicians about what transformation looks like. We have too much opportunity before us to invest in incremental benefits, and the data demonstrates that there is little room for us to provide additional benefits over standard of care in pemphigus. We have built a portfolio of indications with VYVGART and our earlier pipeline candidates that allows us to be uncompromising in our prioritization. The most important thing we can do is to look forward and double down on the breadth of indications we have today, and we will let the data guide us to uncover what the strongest opportunities will be amongst the many efgartigimod indications we have currently prioritized. I will now turn the call over to Luc to walk through the trial design and results. Luc? Thank you, Tim. I want to share my gratitude to the pemphigus patients and our investigators for their support with this trial. This was the largest pemphigus trial of its kind, enrolling 222 patients, and we would not have been able to run such a trial without the support of this community. Next slide. We also need to applaud the internal team for executing on a very high-quality study. It was grounded in strong science and designed based on the results of our phase II study, in close alignment with regulators, current treatment guidelines, and our partnership with the leading experts in the field. Pemphigus is well characterized as an IgG-mediated disease, which is one of the reasons we selected it early in the development of efgartigimod. IgG autoantibodies bind to desmogleins DSG-1 and DSG-3, driving a loss of cohesion in the skin. The detection of these autoantibodies in patients is part of the diagnostic criteria, and autoantibody titers correlate to disease severity. The second reason we selected pemphigus is the tight correlation between this IgG reduction and PDAI, which we confirmed in our phase II study, even on efgartigimod monotherapy. This gave us the confidence to move forward quickly into phase III. ADDRESS was a double-blind, placebo-controlled trial evaluating efgartigimod SC in newly diagnosed and relapsing moderate to severe pemphigus vulgaris and foliaceus patients. After two-week induction, all patients received 1,000 mg weekly subcutaneous dose over the 30-week study period until they achieved the primary endpoint. Importantly, both treated and placebo patients were dosed on a background of corticosteroids. Current treatment guidelines recommend a starting dose of 1-1.5 mg per kg. We were comfortable that starting at a dose deemed insufficient by guidelines would create enough room for efgartigimod to meaningfully contribute to the effect, especially by incorporating a strict tapering protocol. The primary endpoint of the study was the proportion of patients who achieved complete clinical remission for eight consecutive weeks on a minimal dose of steroids, CRmin. In this study, a minimal dose was defined as 10 mg per day. We also included a double-blind, eight-week follow-up as part of the open-label extension, to evaluate if responders could maintain CRmin off treatment. Next slide. We did not see a significant result on the primary endpoint. In total, 35% of efgartigimod-treated patients achieved sustained complete remission on a minimal dose of steroids within 30 weeks. This compared to 30% of placebo patients on standard of care. These responses were consistent across patient subgroups, including both newly diagnosed and relapsing patients, moderate and severe patients, and across multiple geographic regions. The new learning from the study, and surprise to us, was that even at a dose 1/2 to 1/3 that of the recommended treatment guidelines, steroids can deeply drive down pemphigus autoantibodies DSG-1 and DSG-3. It was, therefore, difficult for efgartigimod to drive additional benefit on top of steroids in PV. This was a surprising finding relating to the autoantibodies and dissociated from the known effect that steroids can have on total IgG, which were observed to be reduced by about 10%. Understandably, we did not achieve significance in the secondary endpoints either. The safety and tolerability profile looked consistent with previous clinical trials and with a confirmed safety profile of VYVGART and VYVGART Hytrulo. This is a learning moment for argenx. In order to become leaders in immunology, we recognize the need to embrace these teachable moments to set ourselves up for long-term success, and this is exactly what we're going to do. My team is committed to systematically applying the learnings from this study across our ongoing or future trials. The first example of this will be in the BALLAD study of efgartigimod in bullous pemphigoid. We had planned for a go/no-go decision after an interim analysis of the first 40 patients to complete the study. With these ADDRESS results and knowing the similar biology and trial design between the two indications, we are adapting our BP clinical strategy. We have gained significant learnings on autoimmune skin blistering diseases, and we will reapply these learnings to set the drug up for success. With that, I will now turn the call back to Tim. Thanks, Luc. With this news, we are not ending 2023 in the way we had hoped, especially at the end of what has been a phenomenal year for the company and for autoimmune patients. But 2024 provides us a momentum shift, and we are committed to doubling down on the execution of our ambitious business plan. Looking at the bigger picture of where we are today, the fundamentals of our business are incredibly strong. We continue to pioneer efgartigimod as a pipeline and a product while progressing our earlier-stage programs. We are preparing for our third launch in three years with CIDP, and this is a space where we have the potential to truly disrupt the current treatment paradigm, similar to what we are targeting in MG. We have established an impressive track record of success and are confident in the opportunities set in front of us. Next slide. I want to thank our internal team for all their hard work. When you're innovating a new class of medicines, failures will happen, but what is most important is that we learn from these setbacks. Core to our mission as innovators, we must maintain our entrepreneurial spirit and continue taking calculated risks to advance our novel science on behalf of patients.... We will begin the new year with the same ambition level as we did in 2023, and we look forward to kicking off our 2024 strategy with all of you at JP Morgan in San Francisco. Thank you again for your time today, and we will now open the call for your questions. At this time, if you'd like to ask a question, press star, then the number one on your telephone keypad. We ask that you please limit yourself to one question, then rejoin the queue for any additional questions that you might have. Our first question will come from the line of Tazeen Ahmad with Bank of America. Please go ahead. Hi, good morning. Thanks for taking my question. Sorry to hear about the disappointing data this morning, but Tim, I had a sort of big-picture question. I think people are looking at their models and trying to figure out what the size of the FcRn market overall could be, because I think the popular view is that if argenx can't design a trial to work, who really can? So as you think about the 13 or so programs that you're currently pursuing with ambitions to do more, are you going to be reevaluating, based on now two studies that didn't work, which of those programs might be less likely to work, and should we expect an update on that view at JP Morgan? Thanks. No, thank you, Tazeen. So as Luc explained in the call, we will basically double-check each ongoing and future study to really make sure that, you know, we don't run again into this unknown unknown. So understand the activity of the control arm or potential activity of the control arm on autoantibodies on the one hand, and make sure that, you know, patients are on a stable dose of medication and are still symptomatic. I think of all the ongoing and future trials that either properly placebo-controlled or they have a go-no-go decision point built in. So I think we're very well equipped from a risk mitigation point of view, but nevertheless, we're going to double-click on every study and provide you an update, you know, in the new year. Thanks for your question. Uh, maybe- Yes, Tazeen, go ahead. Do you have? Yeah, sorry, just to clarify, because these two indications were not related in terms of patient populations, how challenging does that make it to look at the rest of your indications to get a sense, for example, if, if placebo would be too hard to control for? Because, you know, pemphigus is a skin indication, ITP was with hematology. So if you have any color on that, that would be helpful. Thanks. Yeah, that's a great question. I think we have two distinctly different situations. What we know for ITP, by the way, is that that's not a failed indication, right? I mean, the first trial was, I think, a clear success, and we presented pretty strong data again from that trial recently at ASH. We're also continuing to collect translational data, really proving how we have fundamentally changed the disease biology in that study. The reason that the second trial failed is subject to further investigation, but clearly, you know, a confounding factor is the use of the concomitant medication. So that's one variable we need to further understand. I think in pemphigus, it's a totally different aspect. This is basically revealing an unknown effect of the active in the control arm, a suboptimal dose of steroids on autoantibody levels. That's a problem we run into in this study, which we should be able to avoid in each and any of the future studies. So I think they're two distinctly different stories. I think pemphigus, there is no room for improvement left. For ITP, I think the analysis continues, and I think we'll unravel interesting findings. Thanks for that extra question, Tazeen. Your next question will come from the line of Alex Thompson with Stifel. Please go ahead. Great, thanks for taking our questions. I guess, you know, thinking about 2024, can you talk, I guess, a little bit more specifically around your confidence in some of the proof-of-concept readouts for next year, like COVID, POTS, Sjögren's, and myositis? That would be great. Thank you. Yeah, thank you for the question. I mean, the call today is really focused on pemphigus and helping our audience to understand exactly what happened, because we think we understand exactly what happened. We will be talking at the JP Morgan conference about the strategic agenda for 2024. A proof of concept, by definition, is a proof of concept. So it serves to de-risk biology, establish a clear signal based on which you can lay the foundation for further clinical development. So bear with us, we will talk about these POC studies, but they are POC studies. Thank you. Your next question will come from the line of Danielle Brill with Raymond James. Please go ahead. Hey, guys, good morning. Thanks for the question. I guess as a follow-up to Tazeen's question, Tim, can you elaborate further? Has this outcome shifted your thesis at all on FcRn's potential utility in any other planned indications? And I guess, for example, are you still planning to initiate a trial in TED? And then I have a quick follow-up specific to PV. Yeah, Danielle, I think this is a good question. Thank you. Look, our approach has not changed. You know how we select indications, and there is a universe of indications to choose from. The first filter is biology. I think every one of you would agree with us that in pemphigus, for example, the correlation between reduction in the titer of autoantibodies on the one hand, and improvement on the PDAI score on the other hand, that's a one-to-one correlation. So I think the homework on biology was done well. The second filter talks about clinical feasibility. And there we have mainly been studying, you know, the existence of clinical endpoints, approvable endpoints, enrollability of the study, et cetera. I think we're strengthening filter two in our indication selection, and that is understand the potential contribution and confounding factors introduced by your background medication. So we're adding that to filter two, and then, you know, that filter three all has to do with unmet medical need and our ability to transform a treatment paradigm. So I would say that the fundamentals of the strategy are intact. We will continue to navigate all that opportunity in front of us based on these filters. But I think based on this learning moment, we're strengthening filter number two. Okay? Great, yeah, thank you. And then just regarding the trial, I'm curious, was there a high percentage of treatment-naive patients that were enrolled, or maybe a high proportion of patients with more mild disease that might have explained the outperformance of steroids? Thank you. Yeah, thanks for that question, Luc here. So this trial enrolled about half of the patients who were newly diagnosed, and half of the patients had relapsing disease with a moderate to severe disease severity. So in that sense, yeah, quite a proportion of new patients, not previously exposed. We did not see, Danielle, any impact of time from diagnosis, disease severity, or other baseline characteristics on the end results. The end result is identical, no matter how you look at the study. Thanks for the question. As a reminder, we do ask that you limit your questions to one and rejoin the queue for any additional questions. Ensure that your phone is not on mute when asking your question. Your next question is from the line of Derek Archila with Wells Fargo. Please go ahead. Hey, good morning, and thanks for taking the questions. I guess first, on the pemphigus failure, I guess, what type of modifications from a trial perspective, you know, could you look to employ for bullous pemphigoid, you know, moving forward? I mean, is that something that obviously we probably learn afterwards, but, I mean, what do you think is most prominent from this data set for pemphigus that you would look to probably address in the bullous pemphigoid trial going forward? Thanks. So, I think we first have to really fully understand PV data because this is a top-line results only, and look at the dynamics of the BP trial before thinking about any particular modification, because you can go theoretically many directions, but I wouldn't speculate which it would be for now. Gotcha. All right, thank you. Your next question comes from the line of Yaron Werber with TD Cowen. Please go ahead. Great, thanks for taking my question. I guess, Tim, the decision to totally stop PV, I mean, this data is a little weird in the sense that it looks like steroids are only really reducing autoantibodies. They're not really leaving-- They're not changing total IgG. You really got to think that they got a very specific, you know, anti-inflammatory effect and not that pleiotropic. And this data is very different than historical data. So is there a chance it's a false negative? And what about running a study where the goal is to delay starting rituximab? That's what a lot of the KOLs like that trial design, where you start with VYVGART first, and then you layer on rituximab in PV. Any thoughts about that? Yeah, Yaron, I think your observation is spot on. I mean, we make the same observation. This was not obvious from literature, the disconnect between IgGs, and then specifically the auto IgGs. So that's a total surprise to us. Why that is the case is a scientific question we're going to drill deep into. I mean, who are these B cells? What are these B cells producing the auto IgGs, and why are they so sensitive to the steroids? I think that's an important question still to address. We have to believe the data point, Yaron, because this is the biggest pemphigus trial ever on a global scale, which was executed with a meticulous quality. So this is a data point you cannot deny. I think it's a meaningful contribution to furthering the field and our understanding of the disease and impact of steroids. And look, we have been scenario planning the study design back and forth with the global community, the who's who in pemphigus, and this was a study design we all agreed on. So I think we gave it its best possible shot, and it makes you think twice if such a low dose of steroids has such an effect in pemphigus, whether there is actually an unmet need left for a drug like efgartigimod. But let's pause here and give us time to further dive into the details of the data now, okay? Your next question will come from the line of Yatin Suneja with Guggenheim Partners. Thank you for taking my question. Just a question on the BALLAD study. Like, what are the timelines now for BALLAD? Like, given similar pathogenesis to PV, what would you want to see in that study? This is an excellent question, but it's undecided. So the mandate we have given to the team is to basically understand the pemphigus data set. It's a big data set, merge it with our current understanding of the BP patients, and then think through the consequences and come back to management with a clear proposal on how to further navigate clinical development. So this is basically an opportunity to learn. I think that's important for this organization, learn, and then think how to reapply with everything we know, the lessons learned in BP. I would say that there's probably no other company on the planet which has now so much autoimmune disease expertise under one roof. So it's up to us to distill the learnings and apply them, but give us a bit of time, please. Your next question comes from the line of Matt Phipps with William Blair. Please go ahead. Thank you. Karl, I was wondering if you could maybe give us a sense at this point of how expenses look going forward, and whether the failure now of ITP and ADDRESS and, and sounds like a pushback in ADHERE kind of reduces burn over the next 12-18 months. So, I mean, Karl is not on, on the phone today. This is mainly an R&D call. I think that's a great question, by the way, for the JPMorgan meetings. But look, I mean, we focus on value creation, right? That's our role in the ecosystem. Our approach has not changed. The fundamentals are intact, and you know we're always disciplined in how we deploy capital, how we make capital allocations, and we will continue to do so. Okay? Thanks for the question. Your next question comes from the line of Joel Beatty with Baird. Please go ahead. Thanks for taking the question. On the autoantibody curves, it looks like the efgartigimod did have some greater reduction in those autoantibodies compared to the control arm, yet the PDAI total activity score curves completely overlapped. How come you think the reduction in autoantibodies did not translate into some improvement in PDAI score? There, this is, Peter. So there, I think what the, what the ongoing hypothesis was, was exactly what you were indicating, that that delta would drive, better or faster disease control, faster time to complete the mission, and then faster initiation of tapering. I think this is part of the surprise, which we, have seen today. And, and apparently, the, the drop in autoantibody reduced by steroids is sufficient to bring you as disease control and then use subsequent tests. Your next question comes from the line of Douglas Tsao, with H.C. Wainwright. Please go ahead. Hi, good morning. Thanks for taking the questions. Just maybe just a quick follow-up comment on... or a comment, follow-up on a comment you made, Tim. It sounds like you have potentially identified a path forward in ITP. When do you think you might be in position to further sort of elucidate that? Thank you. Yeah, so data analysis is still ongoing, and that's what I'm referring to. I was trying to make a clear distinction between the situation within pemphigus, where I think already today, we can show you exactly the reason why the study failed. While in ITP, we're facing one study which is very successful and one study which is flat, and we need to understand, you know, all the details. So that analysis ongoing. You know, we're a science-based company, so we're digging pretty deep into biomarker data, et cetera, and we start to see the first clues. So I would say stay tuned. It's too early, I think, to make any decision here, but for sure, you will hear about this, you know, in, in the years to come. So bear with us, please. Thank you. Your next question comes from the line of Joon Lee with Truist Securities. Please go ahead. Thanks for taking our questions. So just wanted to clarify, does the results of the ADDRESS study imply that low-dose steroid may be more effective in PV compared to standard, standard of care, high-dose steroid? And if so, you know, are you implying that low-dose steroid should now be the standard of care for PV? Yeah, thanks for that question. That is certainly a thought that is on my mind. Everybody knows the burden of high-dose steroids in patients. And this study, contrary to what the belief when this was started, did show that low-dose steroids with this regimen are able to effectively control disease. So I not to extend this data set beyond of what it could do, but it certainly gives food for thought that we might have been treating with two higher levels of steroids. Yeah, look, I think it's, from our point of view, it's a failed study. For the field and for the community, I think it's a very important insight, so we're furthering the understanding here. So good for the community, but, but not good for the company. But- Thanks for the question. This finding is actually... This, this is a medical breakthrough in terms of finding, no? Well, it's certainly something that took us by surprise and somewhat disbelief from others, that we were able to achieve this response in this trial. But it is what it is. It's a well-done, executed trial, and the data stands. Thank you. Your next question comes from the line of Suzanne van Voorthuizen with Kempen. Please go ahead. Hi, team, this is Suzanne. Thank you for taking my question. Can you elaborate a bit more on your thoughts on the biology that the low-dose steroids specifically reduce autoantibodies? What do you think is going on, and do you have any thoughts if and how this would relate to your earlier observation in phase II, where you also saw a long-term modification of the B-cell compartment with efgartigimod treatment? Thank you. I think that's an excellent question and something which we are going to investigate, obviously, on the sensitivity of these autoantibody-producing cells for corticosteroids. That's, again, something which we need to evaluate, and it's something different as compared to what we see in gMG. ... Your next question comes from the line of Samantha Semenkow with Citi. Please go ahead. Yeah, good morning. Thank you for taking the question. Just on the observation for the steroids driving the specific decrease in autoantibodies, is this something that you think could be applied to other indications you're pursuing? And how are you thinking about that? And then, additionally, did you observe any rebounds on an individual level in regards to the steroid tapering? I'm just curious. Obviously, if you taper the steroids, it doesn't seem that the autoantibodies are increasing, so any thoughts you could provide there would be helpful. I'm going to give the second question to Peter on potential rebound of autoantibodies and durability of the steroid effects. Well, it's a surprise because, as far as we could tell from the indications where we have been and have been successful, that is not the case in those indications. That is not reported, and that's also not our own findings. So this is the first time we're running into this observation, and as I said, it's a learning moment. So this is now begging the question for any and all of the future indications: is anything known in literature, and can we de-risk that unknown through experimentation? So I think that's an open question to be answered. Peter, would you mind quickly commenting on durability effects we have seen? Yeah, that I think a big part of that data is covered in the open-label extension. However, this is top-line data, so we need to further dig into that. But what we do see is, and that's known in the field, is that relapses and pregnancies are associated with an increase in autoantibodies. So this is something which we need to further evaluate in with open-label extension data. Thank you. Your next question comes from the line of Xian Deng with UBS. Please go ahead. Hi, thank you for taking my question. So sorry about the trial readout. But at least for what is worth, I think these data are just as valuable for scientists to understand the disease more in the future. So just one question, please. So my understanding is that you do like to bring innovation when it comes to trial design, you know, with a faster speed to readout whenever possible. So for example, the CIDP trial is very different from IVIG, and PV here is also quite different from the Rituxan previous trials. So just wondering, given the sort of results now, just wondering, are you intend to review other trials and potentially rethink this sort of innovative trial design strategy? Maybe some indications are a bit more sort of applicable, where some other indications probably better to stick with a sort of more, let's say, conventional trial design. Thank you very much. Yeah, it's a great question, and it's almost a philosophical question. I think the worst thing which can happen to this company is that we go risk-off, and then basically we, we become ultra-conservative in, in the way we innovate. That's not our role. I think we should make careful and thoughtful risk-rewards based decisions. And I think what we do here is we learn, because, yes, we want to go fast, and we want to go with innovative trial designs, but you'd better de-risk in a, in a reasonable, and responsible way. And I think that's exactly where we're double-clicking on the ongoing and the future trials. Knowing what we know today, let's pressure test what we're doing and make sure you know that our eagerness to go fast and be innovative is not running into these risks, which now we have made visible. So that's the work we're going through. Thank you. Thank you. Your next question comes from the line of Akash Tewari with Jefferies. Please go ahead. Hey, this is Amy on for Akash. Thanks so much for taking our question. So just wanted to get the company's internal early view on why your placebo ended up around 12% higher than what we saw with rilzabrutinib, you know, despite a potentially earlier endpoint. And then, I guess, in general to PV, what levers are you currently considering on how you could potentially modify the trial? Could you potentially go for a population that's, you know, refractory to steroids? And then in terms of endpoints and, you know, like, just timing cut off, love to hear, you know, kind of your early thoughts here. Yeah, thank you for the question. Maybe, Peter, you want to briefly comment on the rilzabrutinib trial, despite the fact there's not much known? Yeah, I think that is my main, main point there. There's very little data on how they specifically taper steroids. There's a difference in the timing of when they read out their endpoint, so it's very difficult to comment on that observation, yeah. Luc, do you want to comment on... It's probably premature. I don't know, you know, how we're considering changing certain variables in a future study? No, that is all predicated on the dynamics of the data we are still evaluating. And so I, as I said earlier, I wouldn't speculate on what it is, but we should be open to all options to maximize the ability for efgar to contrast and show where it can benefit. Now, Amy, these are top-line data, right? So we're under an obligation to disclose the negative trial results ASAP, because, of course, there's a ton of further data analysis going on and reflection from the team. So I think your question is a very valid one. Give us the time to do the homework, and we will be back to you, okay? Great. Your next question comes from the line of Thomas Smith with Leerink Partners. Please go ahead. Hey, good morning. Thanks for taking our questions. Apologies if I missed this, but I just wanted to clarify, has anything changed regarding your assessment of the thyroid eye disease opportunity? And, are you still committed to starting the phase III TED study by the end of this year? Yeah, thank you for the question, Thomas. I mean, as we always say, we see very little read-through into other indications. If I'm not mistaken, the biology in TED is pretty clear, but also there is already clinical proof of concept with an FcRn antagonist. So I think there has been some further de-risking done already. So I do not think that pemphigus data are going to influence this specific trial thinking. Thanks for the question. Our final question will come from the line of Thomas Vranken with KBC Securities. Please go ahead. Hi, thanks for taking my question. I just wanted to zoom in a little bit on the types of learnings that exactly you take with you for further trials. More specifically, I just wanted to ask, do you see an overall risk of using concomitant steroids in your trial designs across indications? So I think, a factor here is whether it's stable or non-stable doses of steroids. If people come on stable steroids with remaining symptomatology, we should be able to draw the contrast just as we've done in prior indications. If there's a tapering scenario, we need to understand the speed of tapering and so forth to see is there a dynamic where we might replicate what we see here, or not? And that is exactly the evaluations we're doing today, across our programs, are any of these situations present, and how can we mitigate them? Thank you. We do have our final question from the line of Vikram Purohit with Morgan Stanley. Please go ahead. Hi, good morning. Thanks for fitting us in. Just a quick question from our side. So I understood that you're going to be doing a comprehensive review of the indications under development for efgartigimod, but is this pipeline review going to include an evaluation of opportunities for 117 and 119? And should we expect to hear any potential updates for those two programs as well come next year? Thanks. Thank you for the question, and that's a great introduction to how we concluded the prepared remarks, right? So JP Morgan is going to be an important presentation for us. We typically show you the strategic agenda for the year, and boy, 117 and 119 are going to be part of that. 117 now well advanced in phase II, and then 119 coming out of phase I and getting ready for its first indications in phase II. So we will be talking about it, and I hope we will meet on that topic at JP Morgan. Ladies and gentlemen, that will conclude our call for today. We thank you all for joining, and you may now disconnect.