Good morning, good afternoon, welcome to the capital markets update of MoonLake Immunotherapeutics. My name is Matthias Bodenstedt, I'm the Chief Financial Officer of the company. With me here today, our CEO and co-founder, Jorge Santos da Silva, and our CSO and co-founder, Professor Kristian Reich. It's our pleasure to have you here today for the capital markets update. We have a very exciting agenda. We will provide a couple of updates. You will see it here on the agenda slide. Jorge will start with a short introduction about MoonLake, about the molecule, about key points for the session, and then Kristian will walk you through the, yeah, highly, highly expected baseline characteristics of our VELA program, the phase III program in Hidradenitis Suppurativa. We will then also look into providing more narrowed guidance on the timing of the readout of the primary endpoint of this study. We'll talk about potential differentiation, a recap of what we see as the opportunity for MoonLake's Sonelokimab, and then Jorge will provide an update on the competitive dynamics in the HS market. Also very exciting, we will have a session on PPP, palmoplantar pustulosis, where we will provide an interim read of the data, of our phase II data, the LEDA study, and in the end, I will provide a brief update from the financial side before we get to closing remarks and Q&A. Here you see the disclaimer on forward-looking statements. Please take note of that. Here on this page, you see some instructions for the sessions. If you do have any questions, we have here the equity analysts in the room, and if you do have any questions viewing the session online, please feel free to submit them through the Q&A function. We will try to address as many questions as time allows. Now, with that, I'll hand over to Jorge. Thank you, Matthias, from my side. Good morning, good afternoon, and also welcome to the capital markets update. I'm going to spend the next couple of minutes, for those that are less familiar with the MoonLake story, sharing a little bit about the company and where we stand, and then, as Matthias mentioned, I will then do a brief summary of all the key points that we're going to go through today. Again, for those less familiar with our story, MoonLake was founded in 2021 in Switzerland, essentially on the back of a license agreement with Merck KGaA in Germany that gave us access to a platform that we're very excited about, the Nanobody platform, which I will talk more about, but more importantly, it gave us worldwide rights, full rights to a molecule that we're very excited about called sonelokimab, or SLK. Why are we excited about it? This is a very unique technology, as I mentioned, a tri-specific binder Nanobody, but also a molecule that targets a mechanism of action that we think is really proving to be very, very exciting in the I&I space, which obviously opens very large opportunities in terms of market. The company went public in 2022 at Nasdaq, and since then, we've raised through equity about $750 million, and very recently announced what we think is a really exciting facility, non-dilutive facility of about half a billion dollars that Matthias will tell you a little bit more about. We're a clinical phase company. As you know, we finished on our side the psoriasis phase II-B, which is a very large trial. We then proceeded to do our own clinical phase II-Bs in other indications like hidradenitis suppurativa, psoriatic arthritis, and last year saw us moving into the phase III, which we're really excited about, and obviously here on our phase III list is where we have our VELA program, which obviously is what's really driving a lot of the interest in the company today. We believe that the team has delivered quite on time and on quality, and I think you'll see more of that today, and obviously we're really trying to open here the pipeline and the product, as we call it, for SLK, a molecule that is showing really, really exciting clinical results in a plethora of indications. Again, for those less familiar with nanobodies and the MOA, what is a Nanobody? It's what we believe to be a next-generation biologic. What are they and where do they come from? As you can see there on the screen, you have your conventional monoclonal antibodies. These are the large molecules we all come to love and have changed the face of medicine in many, many ways, but obviously limited molecules in the fact that they're very large and they typically only bind one epitope. Fortunately, nature, through camelid, sharks, etc., gave us another version of these antibodies, which is much simpler. It only has the heavy chain, so the variable region essentially becomes a single chain, and that variable region, called the VHH there in dark blue, is what a Nanobody actually is, and we're very excited about it because it's really the smallest biological molecule that retains all the characteristics that we love about these very large monoclonal antibodies, but it's much, much smaller. It is not only smaller, which is excellent if you want to penetrate tissues, etc., but it is also amenable to come together as a multimeric molecule, and in fact, if you will, sonelokimab is actually three nanobodies put together. As you see there on the right side of the page, we have three domains. We have one domain that binds IL-17F, specifically it is a very unique epitope that we are not aware anybody binds to. We also bind to a common epitope between IL-17A and F. These are molecules that share 50% homology, again a unique epitope that nobody binds to, and we have this third domain here in gray, which binds albumin, which in our case has two effects. One is to prolong the half-life of what is a smaller molecule, but at the same time, it allows us to target sites of inflammation because those are very rich in albumin. Sonelokimab, even if you put these three domains together, is still just a third of the size of a monoclonal antibody, which is excellent when it comes to penetration, and we've shown several pieces of data for that. As I said, we can have different devices that monoclonal antibodies don't have. In our case, or in the case of sonelokimab, albumin is a targeting device. The molecule is relatively easy to produce, relatively easy to manufacture, very resistant in terms of temperature, etc., but also, as happens with many nanobodies, the solutions that we can produce through manufacturing have very, very low viscosity, so they're very amenable to very fast, thin-needle type of injections, and that's what we do subcutaneously with maintenance doses that typically are once a month, which is obviously very convenient for patients. The fact that we bind different domains, the fact that we penetrate more, is probably behind all that we see in terms of clinical responses, and I think one of the things that we always like to highlight is when you're inhibiting IL-17A and F, you really have to inhibit both NF and the dimers that they form, and our molecule, probably because of the way that it's constructed, is very unique in that it binds all these dimers, all these A and F dimers, with equal affinity and very high affinity, which is very unique. We've shown the comparisons between us and our competitors. It really is a molecule that is very, very, very efficient at inhibiting IL-17A and F. The company has really focused on two big areas of I&I: dermatology and rheumatology, and what we're showing you here is a little bit more detail on all the programs that we're running. As you can see, we try to keep ourselves busy. We run many, many trials, but also you see that we have now a very healthy mixture of phase III trials and phase II trials. Let me just quickly take you through it. On the dermatology side, our lead indication is hidradenitis suppurativa. We'll talk about VELA today. That's definitely a focus. Also, a phase III called Velatine, which we run in adolescent patients, which is a very unique trial. Today, you'll start hearing data about our second dermatology indication in PPP through our program called LEDA, which, again, will be a focus for today. We think this is very exciting because not only we're opening another market, if you will, and addressing pretty severe unmet needs, but at the same time, we think that this is all continuing to build that story of pipeline in a product and definitely de-risking further our molecule. On the rheumatology side, which, as you see here from the dates, will be really a focus of ours maybe towards the end of the year and into 2026, we have obviously psoriatic arthritis, our ISAR program, which we're really excited about. Today, we're not going to deep dive on that, but obviously very happy to talk about that anytime, and our Polaris trial, which is another phase II in PsA with imaging, and then our move into axSpA, second indication in rheumatology through our trial called S-OLARIS. Quite a busy calendar that we keep for ourselves, and today we're really going to focus on the derm side, and we're really going to focus on the VELA and the LEDA side. Before I hand it over to Kristian, a few messages for today that I think continue to highlight the fact that we're really building a leadership position here in I&I. I think what you'll see today is that we continue to execute at speed and at quality. When we say that we do something, we actually kind of do it, and it typically is in good quality, and I think you'll see that through the baseline characteristics in a week where we're celebrating our fourth anniversary, so it's quite momentous for us. In terms of the VELA phase III, the trial has finished recruitment as planned, and we've done it in twice the speed as all our competitors in HS. Kristian will take us through that data, so we're very happy about the level of ambition that we put and how we delivered. You will see that VELA is a high-quality trial. We essentially have replicated the baseline of MIRA to a degree that I think you will find quite exciting. You will also see that our VELA-1 and VELA- 2 trials are very close to each other, exquisitely close in terms of baseline, certainly compared to our competitors, so I really think that we've delivered on replicating the trial and on creating a situation where it will be very easy for everybody to make comparisons where, of course, we don't have head-to-heads. The dropout rates continue to be very low. We continue to operate in the single-digit dropout rates, which has been a characteristic for SLK across every trial. This is a very salient point because obviously patients leave trials for many reasons, but we continue to operate well below what you would expect from others, and we can tell you that now that we have all the data in our hands, the data will reach within Q3, around September. The specific data, obviously, will be to our choice, but it will be in Q3, and as you can see, it follows the timeline that we've previously discussed. I think I will also do a very quick update on the HS market. I think it's very important to understand and contextualize where we're going to be positioning this molecule, and I still believe that there are areas of the market that are not fully understood, and it's part of our mission to make sure that we continue shedding that light and how we can be the gold standard here. On the LEDA side, we're obviously very happy, and I think another indication of the quality, the excitement of physicians and patients with our molecule, the PPP trial recruited much faster than expected. We were expecting to start looking at interim data end of Q3 and into Q4, but I can tell you today the trial is already recruited, which even for us was a very positive surprise, and we will start sharing with you interim data. We really are a whole class above any of the data that is out there. This is very important for us because obviously PPP continues; it's another indication, another market, another source of value, but obviously it continues de-risking SLK if ever anybody has any doubt about what the molecule can do. Last but not least, and I think in the current situation, this is particularly interesting, MoonLake continues innovating in different directions, but also financially we innovated. I think we built a very, very unique facility with the colleagues from Hercules Capital, and this comes at a time where we wanted to gain optionality, where we wanted to have a bit of control how we tap the equity market. We only tap the equity market if it's convenient for us, and to create that runway into commercialization that removes overhangs that some folk might have, right? Again, innovation in many different directions. That's the messages for today. We'll now go through each of these in detail, and we'll start with the VELA program, and over to you, Kristian. Thank you very much. Also, very warm welcome from my side. I have to say, I look outside of the window here; it's a completely perfect blue sky. I overlook Park Avenue, I see Central Park. What a nice reflection of the mood I'm in, right? I hope you are as well. VELA, I remind you of the phase II trial. I think we have all learned that it's super important to do your phase II trials in a way what we call pivotal-like, that you have a chance to replicate them. You see the design here. We clearly identified the 120 mg as the dose with the optimal benefit-risk. That is the dose we took forward. This study was already pretty healthy in size. Again, compare this to recent releases on HS phase II programs. We had 234 patients randomized in North America and in Europe. HiSCR75 as the primary endpoint. We did a super conservative analysis, ITT-NRI. I think we handled antibiotic use in the way it should be handled, which is if you start antibiotic for HS, you're a non-responder. If you start an antibiotic because you have an aching tooth, then for God's sake, include it in your data, right? Just reminding you that the guidelines tell you give antibiotics for 8-12 weeks to see a response in HS, so don't think that an antibiotic that you give for other reasons for three days has any impact on the disease. We had a stratification for early stage and previous biologic use because we think that of all the different characteristics, those are probably those that have a trend to influence data more than other factors. What could we see? We will talk a little bit about comparisons throughout the presentation. I will comment here that what you see on the left-hand side are the results of the phase III programs that Humira, secukinumab, and bimekizumab conducted. What you see with the gray shade is our phase II sonelokimab program, right? Of course, all the cross-study comparisons come with limitations, but what you can clearly see is when you look at delta, HiSCR75 to placebo, we showed the best data, right? 29% at week 12. I remind you that the other studies had week 16 at the primary endpoint. By the way, we saw a continuous increase of the response over time. We now hear that some are better at week 12, but they're not so good at week 16. What does it mean for patients? They should stop at week two. I don't know what it means, right? Obviously, what you want to see is a continuous improvement. That's what we saw, so I can already share with you. We kept almost everything the same in our phase III. If you start to ask yourself, what's the risk that these guys compress? What's the probability that they will replicate what they showed in phase II? First of all, the study design is almost the same. Yes, we do week 16 instead of week 12. That should, in my eyes, if anything, elevate our chance to show better responses, and we changed a little bit the statistical analysis. If you have missing data for a reason that is unrelated to efficacy and safety, you will now be imputed by multiple imputation, which is what everybody else has been doing, right? We are a little bit less conservative in the statistical analysis compared to phase II. Anything else? The location, the inclusion-exclusion criteria, the remaining statistics, everything else remains the same, right? Now, this is a, we call it a cheat sheet. It is not so much a cheat sheet; it is just the facts. These are the data from the week 24, and just to share with you again where a lot of the excitement is coming from, because when you look at these high levels of response in HS, and this is the 24-week data, as I said, I think this is a little bit unheard of, right? I point out not only the HiSCR75 approaching 60%, but my favorite number of all these numbers is the IHS4-100. You are all aware that HiSCR quantifies abscesses and nodules. It does not quantify draining tunnels, although draining tunnels is for the patient a major phenotype of the disease. The IHS4 quantifies nodules and abscesses and draining tunnels. IHS4-100 means you have none of those phenotypes, what we have been calling inflammatory remission. One out of four, I think this is, if you think about that inflammatory lesions in this disease convert to irreversible tissue damage, that's what you want to achieve, and to already see it after 24 weeks in one out of four patients, that gave us real hope that we are not doing a me-too thing, but we are really up to something very different here. We presented, of course, the results of our pivotal phase II, pivotal-like phase II to the regulatory agencies. My sense is, and you can read it from their feedback, they acknowledged heavily that we did the study pivotal-like. We only had to do, we were asked to do 800 patients in our phase III program. Compare this to the numbers that others had to do in their phase III program. They clearly shared our view that the 120 milligram is the dose with the optimal benefit-risk ratio. I see some folks now calculating like an average between 120 and, that's all nonsense, right? We have clearly identified the key dose, and the agencies agreed, so this has turned into a straight shootout. As I said, week 16 now for primary endpoint, and then after week 16, every patient is on drug. The parental trial runs until one year. This is the data package we will submit for the BLA, but I can share with you there's a two-year open label extension because we intend to generate long-term data as early as possible. VELA- 1 and VELA- 2, of course, identical protocols, right? It's basically the same study. Big news, we said we would do the, we would recruit the study in a year, and we did. We started in May last year, and we sit here today and say enrollment recruitment in the study is finished. Almost 100% of the patients are already also randomized, so we delivered, right? The study is fully recruited. Yes, we are proud. We continue to believe that we do our clinical development a little bit better than others, leaner, faster, cleverer, higher quality. Just to put some numbers to it, you see on the upper right the recruitment in phase III programs, patients per month. You saw what we did in MIRA. We were not crazy to say we do it in a year. We did not even expect to replicate the MIRA enrollment. Of course, now you have 180 sites and no longer 60. It's a big phase III. You have to go to more sites, but you can clearly see that we are well above the industry benchmark, and what for me is more important is the lower right. This is the start of the study until the last patient is randomized. That's what matters for time to data, and you see that indeed we did it in almost half the time compared to others. You see the recent phase III programs here. What is also important, and Josh talked about it, we continue to see a very low dropout rate. We say here less than 10%. It currently stands at 6% across the two studies, and I think it speaks about the safety and the tolerability to our drug. We continue to see a very favorable safety and tolerability profile, and of course, this helps us to generate very valid data. Now, the big moment, right? The study design is the same. The inclusion-exclusion criteria are the same. The statistics are identical, if anything, having a chance to show someone better. The next big variable that you have in your equation is what does your patient characteristics look like? We all know that patient characteristics influence outcome, so the key thing here is what you see in this gray box, right? That is combined VELA- 1 and VELA- 2, and again, we are talking about 800 randomized patients here, and you see MIRA. You can go through the numbers. I have to say I couldn't have dreamed this up any better, right? I think that's the big news, and you cannot plan for this, right? You can plan for having high-quality sites. You can train them. You can get your protocols right, but ultimately it needs to convert into the real numbers. If you look at early stage, previous biologic use, smoking, duration of HS, all those important characteristics very similar between the combined VELA and the MIRA program. For those that believe that GLP-1s will be the solution to everything, we always said they won't, and one reason why they won't is they're not really being used. You see that we had 6% in MIRA. We have currently 3% in VELA, right? I give you as an immunologist, really the comorbidity, the metabolic comorbidity in chronic inflammatory diseases has a different pathophysiology than being obese and not having a chronic inflammatory disease. What you also see, that's the second important message on the slide, that the VELA- 1 and VELA- 2 are very similar in my eyes relative to the differences we saw. Everybody is doing two phase IIIs. What you see on the right part of this table is the range, in other words, the differences between the two phase III programs that the other drugs had, and you see quite a range, right? Meaning that they saw some differences in important characteristics. I look at the BHERT program. You see early stage 3, it's 38% in one, it's 53% in the other, right? That's very different, and again, we managed to keep our VELA- 1 and VELA-a 2 very close to each other. I am absolutely happy with the baseline characteristics of the patients that we have enrolled, and I think again it ticks another box that should increase the probability that we will be able to absolutely replicate the findings that we had in MIRA. We talked, we always said we will be able to talk about the primary endpoint data as of middle of this year. Why were we vague? Because you cannot plan for a single day that two 400-patient studies finish at the same time, and what you see here, they do not, right? It took a little bit longer to, despite the amazing speed, to fully recruit VELA- 1. You can do the maths. It is 16 weeks to primary endpoint. You need to lock your database. You need to do some quality controls, so obviously we will have primary completion of the whole VELA program in August, right? Give us some weeks to then do our quality work, and we will then really share with the world around September the readout of the primary endpoint. We have a chance to show primary endpoint and key secondary endpoints. You saw from the design that everybody after the primary endpoint is on active drug. Super happy to go into more details. We will not just say primary endpoint met, see you in nine months, right? We will be able to share more details, just so that we are all clear and absolutely aligned. Forgive me to bring out the scientists for a minute. I'm always surprised what is happening in the market, right? You see comparisons that are just crazy. Oh, let's take one arm from one study. Let's only look at those that have brown hair, and let's compare it to both arms in the other study, but only those that have a zip code that starts with one. It does not make sense, guys, right? It does not make sense. If you ask me what comparisons do make sense, I can come up with two things. One is the scientifically most correct way. This is called a network meta-analysis. This is a complicated statistical procedure where you really try to account for all the confounding factors, even differences in the patient baseline characteristics, differences in the statistics, differences in the readout by using a joint anchor arm between the studies. There is a network meta-analysis that MoonLake has nothing to do with it. That was shown at a meeting of the USHS Foundation in autumn last year. I'm going to share it with you in a minute. That for me is one way of doing it, and that's a cross-study comparison that is scientifically sound in the absence of a true head-to-head. The other is every company goes to the regulatory authorities and agrees with the regulatory authority. How will I generate my data, right? That's what you do. It's not the FDA that forces you to use a certain rule on antibiotics or statistical methods, so whatever you think gives your drug the best data, that's what you try to negotiate with the regulatory authorities, and that's what you get, guys, right? I call it the strategically correct way, and you know what? You find this number in the label. It's not a number that analysts come up with, right? It is what you negotiate with the FDA, how you generated your data. That's what you get in the label, and again, I show you an example for this in a minute. Anything else in my eyes is super questionable. It's probably more artifact than anything real. This is Amit Garg. That's one of the key KOLs on HS in the US. Again, we had nothing to do with this. I was sitting in the room when Amit presented the data. This is a result from a properly done network meta-analysis. We like it not only because it shows sonelokimab on top, but also because it includes all approved and all drugs currently in development as much as possible. This is a forest plot. This is calculated against adalimumab, so where you see the vertical line, the one, this is adalimumab, and you know how forest plots work. The more to the right you are of this line, the better is the efficacy of your drug. The more to the left of the line, the lower is the efficacy of your drug, and this HiSCR50. This is what Amit chose to use, and I can tell you why, because this is what every study shows, right? You can only use the. This is a network meta-analysis, and the results clearly indicate that the 120 milligram comes out on top. Now, the other way of doing it is just opening the label, and we open here together with you the label for bimekizumab. And very interestingly, although BE HEARD 1 and 2 had HiSCR50 as the primary endpoint, our study is HiSCR75. We continue to really honestly shoot for higher levels of response. The FDA made them put their HiSCR75 data in the label, interestingly, and here it is, right? It is in one study 15% delta to placebo, and in the other study it is 20%. You can run around naked with your nose painted green, but the data that you have is 17.5% HiSCR75 delta to placebo, right? Because that is what you negotiated with the regulatory authorities. That is the data that your folks, your sales rep have to run around in the country with, right? By the way, we always talk about this that we already have some key differentiations in the pocket. One is it takes bimekizumab 18 shots to get to maintenance. It takes us five shots to get to maintenance, right? There are massive convenience differences. We have already talked about this, and if you just open the label, you see it all. We want to win on efficacy, but you are aware that bimekizumab has some warnings in the label that worry some dermatologists. There is a warning on liver. There is a warning on suicidal ideation behavior. These warnings could be driven by, could be driven, we do not know, by a higher systemic exposure that they have to give to the patients in order to see some efficacy in HS. We do not need to overdose our patients. We are optimal already with the psoriasis dose, so we see this as a potential area of further differentiation. Jorge, what does good look like? Exactly, and I think this is a very good transition to some of the key messages on differentiation from our side, and then a contextualization of all these competitors in the market. We would like to reiterate what we feel is necessary to make SLK the gold standard drug in HS. What you see there in the table, you saw the 17.5 and the red nose or green nose analogy. That is the first line on that table. We did not show you the label, but you can consult it yourselves for two other competitors. Those are the numbers on HiSCR75. I remind everybody that no one has HiSCR75 as a primary endpoint. We are differentiated by nature, but even if you take a secondary endpoint from competitors and compare it with our primary, I think the table really shows you that in a market that has very, very limited competition, it is very few products that really can compete, and in a market that, as I will reiterate again, is very large, a numerical difference makes all the difference. We feel that considering where our competitors are, for us to become the gold standard drug, our delta HiSCR75 to placebo at week 16 needs to start with a two, okay? Now, what Kristian also mentioned, he reminded you of the data that we saw with MIRA, our phase II our pivotal-like phase II, which was 29 at week 12. Obviously, we're as ambitious as any other biotech company, and we obviously aspire for that number to be bigger, but to be gold standard, what we need is to start with a 2. Obviously, we have a lot of space based on the data, based on the baseline that you just saw, which is extremely comparable, so we believe that there's opportunity here, but that's what's required to become the gold standard. As many of you know, we've done the work with the US HCPs. By the way, with all due respect, this is not two or three interviews with KOLs. As you know, often KOLs know a lot about the science and the patients, but they prescribe very little. This is actually a list that includes both those types of KOLs and non-KOLs. What matters here is the big prescribers, the top 150 prescribers, which, by the way, really cover a vast percentage of the market, as we've discussed before, and they were very clear to us, right? We know what the other drugs do. What we need to see is a numerical advantage. Show us one more point, and what you see with bimekizumab and everything else being equal, you're already the gold standard. We reiterate that to be gold standard in HS, what matters is that our delta starts with a 2. This builds to the story of how can we differentiate? What are the cards that we're playing? What are the opportunities that we have to differentiate? Obviously, this is the big question coming into Q3. I think we have ever more reason to believe that we will probably have an elevated efficacy when it comes to comparisons. Obviously, we're using HiSCR75. We're talking about IHS4-100, which obviously our competitors hesitated for two years to talk about, and now we know our numbers continue to be larger than theirs if we compare across phases. These are the two big cards that we're going to look to play in the summer. Obviously, we cannot disclose too much on safety, but you've heard the comments from Christian that also on the benefit ratio, we expect things to be on the good news side. There's a card that I think we already have. This is celebrated in the label, celebrated in the protocols that we run. It takes our main competitor, the only other IL-17A/F molecule out there, 16 weeks to finish their induction. It takes us eight weeks. It takes them 18 injections. It takes us five. I mean, if you think of yourselves as doctors trying to talk to a patient, I think it's pretty clear which ones the patients would want. Obviously, we're also playing a card that we feel is quite unique to us, which is the Velatine trial, with the idea of within the same BLA time at the adolescent patients. Obviously, as you know, it's very important that the prescribers and the KOLs and everyone understands why are these differences there? Why do we have these clinical responses that seem to be differentiated? That is obviously because we have a very unique molecule, and I think the more you speak to future prescribers and KOLs, the more you start hearing about how interesting this angle is versus a more traditional monoclonal antibody. These are important potential ways to differentiate, even if when we really look at the market, we truly believe that there is really space for a lot of players. What you see in this trial, you have seen this chart from us before. Very happy. I used to feel that I was the guy running in the street with a green nose trying to tell people it's a very, very big market, and everybody looked at us a bit like, "Okay, what are they talking about?" Of course, the big number you see on the circle here is a number that you now start seeing from different banks, from different analysts, from our competitors. It's always the same Kegers, and it's always the same sizes, right? We truly are looking at a very large market here, but as you can already see in the bottom, a market that is interesting in the sense that there's not a lot of competition. There's not a lot of competition. We don't have 20 drugs that can do more or less the same. Not at all. You have Humira, which obviously got the market going, but as you know, it's very limited. Only works 50% of the times. It only improves you 50%, and after 10 to 11 months, the effect is gone. COSENTYX launched to great success. We'll see the latest numbers in a second. Even as you saw in the previous table, it's very marginal in terms of efficacy, but of course, adds response and adds another opportunity. Bimekizumab launched late last year. We'll show you the first numbers. It basically is following the same exciting trajectory that COSENTYX has been following, and obviously, that's us, right? Of course, you have other molecules that you hear about, a lot of failures, a lot of things that are not interesting typically in HS, but clearly, we are the big drug coming. JAK inhibitors, you've also heard about it, but the results are very strong, let me put it that way, as we saw recently. By launching SLK, we're really trying to bring this logic of the MOA. We know from bimekizumab that this is the MOA that is probably going to change things, but also a best of both worlds play. It's not just the MOA, but it's also the way that we bind the molecule. It's our low immunogenicity. It's our low dose. It's our easy, convenient injections. It's all these things put together in what we think is a rather unique molecule. Now, I think we still get the question, why is this market so big? Of course, why did we miss it, right? I think there's two fundamental dimensions that are always important to remind everyone on. One is that from a prevalence perspective, which you see here in the x-axis, this is of course something that I think we've made some good progress in the last couple of years in explaining to the market the prevalence is really around the 2%, right? We now know this. As I said, several folk have reached the same conclusion. You see it on the real-world data. We really have a very high prevalence disease, but the other dimension is really this y-axis. I know it's a simple fact. Many people here in the room might find this very simple, but we find that actually out there, it's actually not very simple. You have to remember that the price point for HS patients is double the price of psoriasis, right? This is really important because we feel that prevalence, as is seen today, is probably even conservative. Imagine the patients that we're not seeing in the real-world data that have not been diagnosed, that are not being paid for in terms of their therapy. There's obviously probably even a bit of ceiling space here on the prevalence side, but also the penetration of biologics continues to be really low, right? There's a lot of opportunity to grow here. It's really about figuring out the fact that prevalence is very large and patients are largely untreated. This is a huge naive market, if you want, and that's a unique element that I think is important to stress. As I said, the price value. Just think about the price values, and we notice here some of the more recent prices. Everything you see for psoriasis is always double the price in HS, and that's of course one of the things that drives the size. In terms of the prevalence and why we think we're probably not even seeing the whole game, as you know, we continue focusing on looking at real-world data. We don't like to take 50 pharmacies and extrapolate or three prescribers and extrapolate. We just like to look at the real data, and I always tell you when we're looking at real data, what we're looking at is 80% of the U.S. population in a database with eight years of longitudinal data, okay? We are looking at patients that have been coded for HS, have been diagnosed, have been treated for HS, and for which some payer is actually paying for the treatment, right? These are absolutely bona fide patients. You remember beginning of last year, we started showing you these numbers back when we were at the AD, and these were very surprising to a lot of folk, but it really showed the size of the market and the size of the matter. Fast forward one year, and you just see these numbers growing higher and higher, okay? Right now, we can detect about 2.5 million patients in the United States alone. That is of course an increase on the already pretty fast growth in new patients that you see there in the second line. If anything, that is increasing. The whole baseline is actually increasing. Obviously, great to see the third line there, a strong growth in terms of biologics treatment, but obviously, we're talking about a really, really small base, right? You really need to understand this because what you're having here is a market that has a very, very large untreated population, although they're all diagnosed and in the system, but of course, where you have a very, very small base, it's great that we get 18% more in biologics treatment, but it's obviously still from a really, really, really small base. I really call attention to this number here. It's 80,000 patients out of 2.5 million, okay? This is a really, really bio-naive market. We typically show you more stuff, but today we wanted to keep it compressed, but I think this picture shows you a little bit of what's happening in the market. We're looking here until very recently, basically the middle of April data. What you can see here is obviously the growth of the market, as we discussed, in terms of biologics. You see that Cosentyx obviously started with around 5-6% in their first quarter of launch and obviously took quite a bit of the market, I think at the expense of Humira, which is here in this blue that I cannot describe, sort of electric blue. You obviously have your biosimilars, which are also present in the market, but really not dominating, right? It is really a change away from TNFs, and it is obviously early days, but this little line here on 5% is what we can see in our database for bimekizumab. Very similar to the 5-6% that we saw with COSENTYX in their first quarter of launch. All the indications that we see from the market, and hopefully the colleagues from UCB will say more, is that things are really picking up, even if the drug had some challenges in terms of formularies. As we explained before, from a payer perspective, formularies in HS mean very little. I can tell you that most of the sales that you have from COSENTYX are actually ex-formulary, so that does not really matter right now. It is obvious that it does not matter because you do not have a lot of competition. You have a huge unmet need. Remember, a payer either gets a solution for these patients or needs to do surgery, physiotherapy, opioids, steroids, whatever, a huge cost burden. The other thing that I would call attention to is the fact that obviously the growth of COSENTYX, it is really a lot of patients that are new to therapy, and I will come to that in a second because I think that is the next learning step in terms of HS. This is a bio-naive market. Forget about switches, as you know them, for other indications. As I said, biologics share continues to be extremely low, right? Even with COSENTYX making billions of dollars now in HS and obviously bimekizumab going in the same direction, we still have a biologics share that is embarrassing, I would say, if we look a patient in the eye. Obviously, if you start looking at other areas of I&I, of dermatology, you can see where this needs to go. This is the last point I want to make with regards to the market and this bio-naive point because I think there's some questions around, "Okay, but if you come two years later, won't the other people have taken the market?" Right? I think that's just, in part of the pun, it's a very naive view of the market. We just show you here where COSENTYX is getting its business from, right? As you can see, almost two-thirds of that is pure bio-naive patients because, again, only 80,000 are getting biologics, right? Most of those 2.5 million people have never seen a biologic, and about a third of their sales is coming from refractory patients, right? Refractory patients is essentially a patient that has had a biologic, has stopped taking a biologic for a few months, and now gets back to a biologic, in this case, COSENTYX, right? Pure switches, patients that are on one month being treated with something and then switch is a very, very, very small fraction. This is very important to remember because bio-naive patients are millions of patients. The refractory patients, if we look at the longitudinal data that we have, are hundreds of thousands of patients. The switch patients are single-digit thousands. You really have to work on these orders of magnitude to understand that the big potential of this market is not on switches. It's on getting the new patients into treatment. I remind you, these are 2.5 million people that are diagnosed, that are receiving treatment, and somebody's paying for them. It's not even all the other patients that probably are out there in the world, at least in the U.S. I'll conclude the very brief view on the market, just to let you know that the size is the size. I think we were right. We still have a long way to go in terms of the biologics share. The biggest driver of this market is naive patients, and in two years, believe me, neither UCB nor anybody else will be able to cover millions of patients. It just doesn't happen, right? The refractory patients are still a large pool, but it's not going to be a switch market. Remember, this is very limited competition. You saw the tofacitinib data. You saw amlatilimab. You saw the vague mentions of data when it comes to the TNF, OX40 ligand Nanobody. This is really not a lot of competition. We still see that ANF is the right MOA, and obviously, we haven't gone into it, but obviously, this is something from a payer perspective, as we've shared before, is not super closely managed because we really need to address the unmet needs of the patients. That's a very, very quick view of the market, and Novella, again, fantastic baseline. Data comes in September. The market is huge, and we have a lot of potential. Quickly to LEDA. Yeah, quickly to LEDA. I have to say what I, as a dermatologist, find most shocking is this below 3.5%, where it should be 35%. You have the most terrible skin disease where inflammatory lesions progress to irreversible tissue damage, and no one gets a biologic, right? I agree. I'll try to do this brief, although this is very, very close to my heart. This is actually the third derm indication after psoriasis and HS that we are addressing, palmoplantar pustulosis. It's a terrible skin condition. I do hope you can see the picture in the upper left. Patients have massively inflamed pustule-containing lesions on their palms and soles. They have a lot of pain. They can't walk. They can't use their hands. For me, it's another example of a dramatically underestimated disease. No treatment is approved east and west of the Atlantic, neither in the U.S. nor in Europe. You see this massive formation of pustules, sterile pustules, neutrophils infiltrating the epidermis is a hallmark of the disease, and you see this also in the histopathology. There are some similarities with psoriasis. Some have been calling this pustular palmar plantar psoriasis, but what I want to make 100% sure is that you don't confuse it with psoriasis vulgaris, pluck-type psoriasis. It's a different disease, right? You can see here that you can have also pluck-type psoriasis on your palms and soles, but it's a different disease, right? It's a completely different phenotype. Interestingly, again, when you see cumulative prevalence from 2016 to 2025, we are talking about 170,000 patients that have this code, palmar plantar pustular psoriasis, L40.3. Interestingly, again, you see 20,000 newly diagnosed patients being added per year, and of course, the disease is chronic, right? They are just added to the patients that currently have this diagnosis. We see a relatively low number of patients being treated with biologics. You can see this in the bar graph on the right, but we saw a healthy increase, so there is an attempt off-label to use biologics to treat PPP. You see also that even if you conservatively estimate a growth increase in biologic use of just half of what we have observed, that by 2038, we have a very healthy market size in PPP of around $3 billion-$4 billion. Again, I'll try to be a little bit brief. You see the slides. Studies have been tried. Drugs have been tried. Most of them failed. We have looked into four studies that we thought make sense to be used as comparators here. Otezla is a study that actually I was involved in, smaller open-label trial, the same with guselkumab on the far right, spesolimab, the IL-36 receptor from Boehringer, and COSENTYX. They have been doing larger phase II trials, both of them failing, by the way. We saw some response with apremilast and guselkumab, but what we can do, we can look at these trials to get a feel for what would good look like, right? What is the outcome that we would want to see? By the way, we decided to do PPP because we were sensing that IL-17 again would be in the heart of this disease, another neutrophil-rich chronic inflammatory disease. We were sensing that one reason that antibodies have failed could be the limited tissue penetration because this is a disease that, in contrast to HS, that sits deep in the dermis, surrounded by scars. This disease sits up in the epidermis where you have no blood vessels. We decided to go there, and we decided to go there with a relatively small open-label proof of concept study, but with a lot of objective markers to control the outcome. I think we invented this. We now call this a biomarker control study. Don't tell me that doing eight or ten placebo patients and then two going up and down changes the results is telling you what's really going on. We took peripheral blood. We took biopsies. We used artificial intelligence to read out the photos to really get a clear objective view of what sonelokimab would do in this indication. You see the study design here. As I said, proof of concept, open-label. We started the study in Q3 last year. It's already fully enrolled. It's done, and we are beginning to use all these analyses that I'm showing you. You see when we take biomarkers, tissue biomarkers, you see when we take peripheral blood to do proteomics. This is all super important in the study, and I can only show you a sprinkle of the results today. Based on characteristics, it takes some time later to go through this, but again, we enroll the patients that are typically enrolled in such trials when it comes to age, gender, weight, smoking status, disease duration, prior biologic use. We think from a patient characteristic, we will get valid data from the study. Again, this is just a sprinkle, right? We used some of the best labs, Tissue Immune that sits in Erlangen with Georg Schetz Group. We use O-Link. We see for the first time really IL-17 disappearing in the tissue. You see A on the upper left, IL-17A and F dramatically upregulated in the disease as evidence that it's really driving, and we have a lot of functional data really driving the disease. On the lower left side, you see compared to healthy controls, always compared to healthy controls, that sonelokimab treatment makes 17 pathway disappear in the skin, right? This is very strongly correlated with a good clinical response that I will talk about in a minute. I'm already looking forward to do a really high-ranked publication out of this. Obviously, IL-17 induces in keratinocytes a second cytokine called IL-19. We'll talk about this at a later time point, but it's really this IL-17, IL-19 axis that drives the disease that leads to this chronic formation of pustules in the epidermis. What can I say? IL-19 is upregulated in the skin, is upregulated in the peripheral blood, and when we treat with sonelokimab, it disappears in this tissue, and it disappears in the peripheral blood. I have never seen a single biomarker in peripheral blood that correlates with a disease activity measured by palmoplantar pustulosis with 0.6 something, right? We really have even identified a biomarker that tells us what's going on. You see here that already after four weeks, IL-19 disappears in the peripheral blood. Just take a quick look. This is parental guidance advised, right? Because now we do what we always tell you to not do, which is putting different studies in one graph. We do this because this is all super preliminary. Some are open-label. Some are placebo control. It doesn't really matter, but what matters for us is that we have clear indication that this objective markers is one thing, but it converts. It correlates with the clinical response when we look at the main readouts, mean palmoplantar pathy and PPP pathy 75, so a high level of response. You can see what the others have produced. You can see what we see in the study. It really looks like we have another chance to really elevate outcomes in an important chronic condition. I'm a dermatologist, right? We are visual people, and this is just on the you see some examples, and you can always say, "Yeah, they picked the three best," right? What you also see in the graph is an artificial intelligence readout of the photos that were taken. Guys, I have to say when I saw this, when my friends saw this, we were absolutely excited. We have not even seen such responses with hydroxychloroquine, which we did out of desperation some years ago. You see here a biologic naive case. You see a biologic refractory case. It does not matter. You see a case that has less pustule, but it is more tissue damage. The tissue is healing, and this is all week eight already, right? Really an unexpectedly fantastic response, and of course, opening up for us the possibility to move to phase III relatively quickly, right? I think a small but very valid study showing a potentially leading role for sonelokimab in a third skin chronic disease, palmoplantar pustulosis. I'm already looking forward to debate with the FDA how we get a fast track designation for this or a breakthrough and really moving to having all the options on the table to move to phase III relatively quickly. Perfect. Thank you, Christian. Very briefly in the end, because we're running almost out of time, just an update on the financial side. Obviously, very notable is the facility that we entered into with Hercules Capital. You see it here on this page. On March 31st, we signed into an agreement, and pursuant to this agreement, we have access to up to $500 million in committed capital. It really provides us with a lot of optionality. It protects us from this volatile markets driven by a macro environment that is not very favorable for the biotech sector at the moment. You see the tranches listed out here. They really align very well with the needs that we have as the company to really drive the further drive the development, but also the commercialization of sonelokimab. You see it split here in five tranches. The first tranche is the one that we've drawn, the $75 million. The other four tranches are tranches that we can draw from, but there's also no commitment for us that we need to take the money. It provides us with a lot of optionality. That said, you see on the right-hand side at a very, very attractive cost of capital. You see here, 8.95% is the cash interest rate that even goes further down upon BLA acceptance by the FDA. It is really something that we are very excited about. If I had to summarize, what are the real advantages for MoonLake? On the one hand, it really strengthens further our cash position, and we're already coming from a position of strength here. You will see in a moment, but even before this facility, we were close to $500,000,000 in cash equivalents and short-term market securities. Now we are further adding to this, so really this puts us into a very, very strong position, eliminating in our view any potential perceived financing overhang as we get into the valor readout. It allows us to get into commercialization into 2028. Really, we have the opportunity here to weather any storm that might be out there. Obviously, we are not happy with where the share price is currently. We think it's completely undervaluing the real intrinsic value of the asset, and we are shareholders of the company, and we also, yeah, act in the interest of our shareholders, and we don't want to dilute any shareholder at these prices. Really, it's something that we are very excited about to have this non-dilutive facility available for us. I think also we talked about the competitive cost of capital. I mean, it's something that we are also very excited about that even almost makes it a no regret to rather use this facility than actually getting capital through higher cost of capital sources. Again, the flexibility I've highlighted. What does it allow us? I talked about it. It It allows us to extend cash runway, get into 2028 to support the commercialization of the drug. Also gives us some opportunity to now think of how do we ramp out manufacturing capacity. I mean, we do have capacity already to get into year two, year three of commercial, but obviously these times have long lead time. These matters have long lead time, so we are starting to think about now how do we add capacity beyond year three of launch. By the way, I just saw one question coming through the Q&A asking about where the product is manufactured. Right now, the drug substance is manufactured in Europe, but again, we're thinking about where do we add a second source of drug substance. I assume this question relates now to tariff discussions, etc. I think one of the benefits of our Nanobody sonelokimab is actually that we have a very, very attractive cost of goods sold. I think the manufacturing cost is really, really only a fraction, something that makes it very attractive for us, and that also makes the whole tariff discussion for us, if it's applied on the cost of goods sold, largely irrelevant. Again, the other advantage that we have is that we have the whole field in front of us. We can now take the next two years to really decide how do we add a second drug substance source, where do we fill, where do we do the auto injector assembly, etc. We do have a lot of opportunity that obviously companies that are already at commercial stage have a little bit more difficulties to adapt to the changing environment. I think very important the box in the bottom. There are some people that said, "Well, maybe these MoonLake guys, they see something. They're not too sure about their data anymore, and that's now why they are trying to hedge their bets and put in place such a facility." The answer is absolutely no. We started this process looking into the opportunity here. You see it on that page in October last year, and it's really something that we believe helps to keep the upside, the upside of the asset with the shareholders and not to unnecessarily dilute them. It's really nothing that we put in place now to, yeah, to hedge our bets because we see something bad and blind the data, rather the opposite. Now, if we go to the last page, this is a preliminary view on the financials. Obviously, you will see all the details in the forthcoming 10Q that will be filed in the beginning of May, but you can see that we really come from a position of strength. We ended March 31 now with $480.1 million in cash equivalents and short-term market of debt securities. Through the facility, we have access to up to $425 million more. It really gets us into commercial of sonelokimab. We do have full flexibility, optionality, and opportunity to drive what maximizes value for the shareholders. Perfect. I think we'll stop here and open for questions. We had prepared a few closing remarks, especially trying to take the bear view on our share just to try to understand how all the learnings from today get positioned. I think we touched on all these points as we went through, so I'll leave that on the screen and open here in the room and online for questions. Yatin. Thank you for the presentation. If you can keep it short and quick, that would be great. We'll do the same. On the placebo response, how should we think about placebo? You know, some You know, some mechanism that tends to work very well. You do have some biases. What that impact, how that impact the effect? The question that is being asked in the room is, what are our expectations in terms of placebo? Yeah. First of all, you have to do your study well, right? Train your sites, have your protocol right, all the things. When I say train, having Alexa Kimball and her team from Harvard really training every site, and before they have not fulfilled the training, they do not start. It is things like this and doing continuous quality control. In the end, I have to say I am not so nervous. If I look at every pivotal trial that talked about a placebo HiSCR75 response, I see a range of 13-18, right? What I liked about recent inside trial, not so much their delta, the delta that they created, but I liked the placebo response. One study was 13, the other was 16, right? Again, now we have all pivotal trials between 13 and 18. There's not so much evidence that placebo responses, when you look at the HiSCR outcome, that's important. Don't do HiSCR50. But when you look at HiSCR75, I think we're fine. Hi, thank you. Thanks for taking my question before the senior event. I just want to understand if you can provide a little more details on your commercial efforts, where you are and how you are thinking about it in the future, as well as how you're thinking about prioritizing some of the asset programs. I also want to understand that given that HS is a $10 billion-$15 billion market opportunity, are you thinking about any US, ex-US, or partnerships? The question is around our commercial plans, including US versus non-US. Matthias, do you want to take that? Yeah. I mean, first of all, starting with the last part of your question about partnerships, now is not the time for partnerships. The development, the speed, the quality of development that you saw Kristian talking about would be impossible if we had to entertain partnerships, development partnerships in parallel. We do not need the funds that would come from selling ex-US rights or Asia rights or certain Central Eastern Europe. We have a lot of interest. Lots of companies come to us. They want the rights for sonelokimab for certain regions. Now is not the time for that. We focus very much on the development for the US. We also work very closely with the EMA, so we also make sure that everything is set up well for FDA and EMA. Clearly, the commercial opportunity, the 70-75% is in the U.S. We're working very closely on starting all the payer research. We have a team in place that is now looking into what is needed from that side of things. Believe it or not, we already had to submit the brand name of the product because that's something that you need to do well in advance. We're building out all these things and are very, very confident where we stand from the partners that we work with, like specialty pharmacies, etc., third-party logistic providers. All of this is happening right now. We get the feedback that we're actually very, very well prepared. Also, we start the effort in thinking about what does the field look like. You may have seen in our 10K filing that we are planning to establish a presence in the U.S., a physical presence in the U.S. in the beginning of next year. Also, preparations for that are well underway. I think we're very well prepared when it comes to U.S. I think ex-US, we will need to see over the coming 12-18 months whether this is actually something for MoonLake to do or to do rather with a partner. I think there we want to keep for now all options open. Great. Prakar, I'll go in order. No worries. I'll get you all. Yeah. Thanks for sharing the baseline. It looks very good. Maybe if you can talk about the geography split of patients in the U.S. versus Europe or specifically Eastern Europe, and does the HiSCR75 responses vary by geography? I know this was a bit of an issue in the psoriatic arthritis trial as we think about the placebo response. Secondly, we have talked about differentiation on safety as well with the rucumab. Do you think you can differentiate on things like candidiasis or even lack of suicidal ideation warnings? Great. Kristian, you'll take this. The question here in the room is around the geographical distribution and any potential variations among that for high scores in HS and any concerns. Second question was? On safety. The safety, as much as we can. I'll try to be super brief. U.S. is approximately 40% of the patients. We don't have evidence for a big difference in response between geographies, but we have made geography a stratification factor, so we protect it against this. Safety, you heard me saying I don't want to win on safety, right? If I have a clever drug that I can give with lower doses, that because of the better penetration is doing the job, and I can limit my systemic exposure, and thereby I see somewhat less Candida, I don't get a liver warning, I don't get an SIB warning, would I and the prescribers be happy to have this leaner safety profile? Definitely yes. Back there. Yeah, Phil made up the panel. You talked about differentiation on efficacy. Skeptics point out that the bimekizumab HiSCR75 for the HS antibiotic use was 22.5%. Looks like you're using the 17.5% all antibiotic use. Why use the 17.5% not the 22.5%? What What do you do to compare between the sonelokimab data and bimekizumab? The question is, why not take the numbers from bimekizumab with their interesting antibiotic imputation? Maybe I'll take that question quickly. I think we were pretty clear on that. We can do whatever post-hoc analysis we want. I can do one after this meeting with you and come up with a number for SLK, but that does not matter because what you can promote, what you can discuss from a label perspective is the 17.5. When you look at those comparisons, Phil, as well, it is very important to notice that people only take one dose from bimekizumab and decide to average our two doses. To do this ludicrous, let me really call it like this, this ludicrous type of comparisons, I think it is just noise. I understand we have a very big short position. People tend to lose a lot of money. I understand that, right? Scientifically and fact-wise, it really has no bearing to reality. Tom? Thanks for putting together the event. Can you just elaborate on the multiple imputation that you're going to apply in VELA? And have you looked at the MIRA data set in that way? Can you just comment on what the MIRA? Sorry, just for those online questions in the room, is some more comments on our imputation for phase III versus phase II? Kristian? I'm happy to do an extra workshop. I love the imputation, right? Very brief. In MIRA, we did ITT NRI. Every missing data was imputed as a non-responder, right? In phase III, we do what everybody else is doing, which is if you have missing data because of an efficacy or safety problem, you remain a non-responder. If you have missing data leaving the study with IHS4-100 just because you fall in love and you move to Rome, you no longer come to my site, I impute you using multiple imputation. We have applied the MI to MIRA, but because we had almost no dropouts for MIRA, the ITT NRI and the ITT MI are almost the same. If anything, it should lift the delta a little bit. Brian. Obviously, great news that you had really rapid enrollment in the phase IIIs and had ended up with pretty similar baseline characteristics both across the two between the two studies and to the phase III. Can you talk about the relative contribution from sites that were in the phase II versus the phase III? What gives you confidence in the quality of the conduct of the study, things like assessment of endpoints, just given how rapidly you were able to relate to the study? Yeah. The question in the room is around the contribution of phase II sites to phase III and how have we kept quality. Let me very quickly answer that. It's about a third of the sites of phase III were the sites of phase II. We virtually converted all the sites. That already tells you something about the level of excitement, of course, and that's behind the recruitment rate. In terms of conduct, we basically learned everything on phase II and we just replicated it. Selection of sites, training of sites that Kristian has already mentioned. Control, as you know, we have a very exquisite level of control between us and our CRO on a daily basis on a single site level, on a single contract, single patient level, right? We kept all of that, Brian, and I think you're starting to see it, and you see it on how exquisite the delta is between VELA- 1 and VELA- 2. I mean, compare that to the width of the other trials and you really see the level of control that we have together with our sites. Maybe to the side of the table. Go ahead. Hi, Liam from Whitehorse. Looking at the baseline characteristics of the phase III study and looking at the AN number and the IHS4 scores, would you say that the phase III study maybe enrolled a little less severe patient as compared to the VELA-1 and 2? I know it's probably minor, just a numerical difference. Second question, what's your expectation on the IHS4-100? Because we heard that that's probably going to be the strongest differentiation in the question. The question in the room, and I think it goes to you, Kristian, is around potential elements on our baseline that should say that we have less severe patients. The second one, as you heard, is just go ahead. Yeah. Number one, if you cleverly design your phase III, you want to limit the early stage threes because these patients need surgery and they don't necessarily need an anti-inflammatory drug, right? We had a cap at 40%. This explains why we sit where we sit and should sit and why we're identical to MIRA and maybe deviate a little bit, for example, from a BHERT study that suddenly has above 50%, right? I remind you that in the real world, early stage three is 10-20% of the population of moderate to severe, right? There's an artificial enrichment of very severe patients because you don't design your study well. I don't think that there is any baseline characteristics that have an impact. I think we enrolled the same moderate to severe. If AN count is one up, one down, I think it really doesn't matter. I also remind you that in order to enroll in our study, you had to have five anti-inflammatory lesions at two anatomical sites. Others often use three. Also, the low hurdle for us is relatively high. I have to say when I look at the characteristics, that's the ideal reflection of a moderate to severe HS patient population that should receive a biologic. Two more questions before we close. One on Julian and then Rich, and maybe three if we do it quickly, if you guys can keep it quick. Otherwise, I get. Same question. I'm wondering maybe just reflecting on some early feedback from payers, any receptivity for efficacy endpoints beyond HiSCR. More broadly, how are you thinking about the potential plans on endpoints like IHS4, the potential data that. Julian, I'll take the question. The The question in the room is around how payers basically see our various endpoints, right? This is one of those questions where we will be a little bit more evasive, right? This is work that is ongoing. We actually have a team that is sitting with payers, third-party providers, all critical players of our supply chain as we speak. Obviously, this is very, very competitive. What I can say is that obviously, payers in our minds are talking to us about things that go well beyond HiSCR, right? I think that's the real important thing because I think HiSCR is just the primary metric. Things like IHS4-100, when you're really in remission, when you really avoid surgery, where all your painkillers and everything goes down, that's the kind of stuff that the payers are interested in. I think the message that we're getting is really these are patients with a huge burden also on the cost side. Let's not debate so much about formularies and first lines and second lines, etc. Let's just get to a price that is sustainable and makes sense from an economic perspective. That's a very interesting and new conversation for us that goes away from clinical data. That's as much as I can tell you, but I think this is a competitive advantage that I think we'll create in the next couple of months. Rich? Hi. Congrats on completing enrollment. Thank you. For you guys. What I asked is the question that was asked earlier in a different way. What increment of HiSCR75 difference would you consider to be clinically meaningful? I think we heard about maybe five would be considered clinically meaningful. If you add that to at least 0.5, you could still get that to 22.5. The question in the room from Rich is, what's the meaningful delta in HiSCR75 from a clinical perspective? And who better than the clinician? The answer that we gave you, you heard, right? We want to see a two as the first number. Let me quickly remind you of what we have been calling the gold medal concept. Put yourself for 30 seconds in the shoes of a KOL prescriber that sees thousands of patients with HS. Why do they come to you? Because they expect from you that you prescribe them the best drug out there. That's Usain Bolt. That's not beating everyone by 20%. That's the drug that you perceive as the drug that wins. When we asked high prescribers about it, they said, "Show us any number that's above the best number we have previously seen. Show us 18.5 or 19." We already said we want to see a two. Now, do we think, do we have the ambition that we can go way beyond this? Absolutely yes. Strategically, win the market, we want to be the gold medal drug. By the way, you see the relevance of this in the uptake of bimekizumab in the psoriasis market. Was it beating everybody else by 30%? No. It was perceived as the gold medal drug. And boy, did they have a good launch, right? It was a better launch than Skyrizi. That is what gold medal drug means for a prescriber. Very last question. Prior trials like bimekizumab and the drug I inhibitor, they both have a huge efficacy discount from phase II to phase III. We understand SLK has a pivotal line phase II. What else can make us confident that there will be less efficacy discount from phase II to phase III? The last question in the room is, and last question for this session is around the compression of phase II to phase III, Kristian? I'm a little bit frustrated because I thought we had given you the answer today. Use the same protocol. Use the same sites. Use the same quality. Use the same readouts. Show, and this is new, this is what we did today, that you actually enrolled these patients with the same characteristics than your phase II, right? These are all elements, and the big variable we discussed today, which we now clarified, which we took out of the equation, is the baseline characteristic. Great. I would like to thank everybody that joined us in the room and online. I think the questions we took in the room reflect the questions that were coming through the Q&A. Thank you, everybody, for joining and from us. Have a very great day. Thank you. Thank you.