Good morning, good afternoon. Thank you so much for joining our Investor Day today, MoonLake Immunotherapeutics. My name is Matthias Bodenstedt. I'm the CFO of the company, and I'm sitting here on the right, Dr. Jorge Santos da Silva, our Chief Executive Officer, and Professor Kristian Reich, our Chief Scientific Officer. Together, we are very excited to walk you through a number of updates about the company. I will start with a very brief introduction, then Kristian will present our Phase 2 data from the S-OLARIS study in axial spondyloarthritis. After that, Jorge will provide an update on the hidradenitis suppurativa front. He will, on the one hand, summarize the feedback of our regulatory interactions with the FDA, but he will also provide an interim read of the long-term data from our VELA program. The 52 weeks data from our VELA studies in adult HS patients, but also an interim read from the VELA-TEEN study in adolescent HS patients. After that, we will provide also a brief update on the PPP program, on the PsA program, and on the financials of the company. At the end of this session, we will open up for a Q&A. Please take note of our disclaimers. Another word up front, a replay of this session will be made available on our IR website, and you will also find the presentation document uploaded there. If you do have any questions, you can submit them through the Q&A function in your web browser. Now, before we get to the main content of this session, very brief recap for those that are more, more new to the story of MoonLake. Who are we? We are a company that was founded in 2021 in Switzerland, and we are focused on the development and eventual commercialization of a molecule that is called sonelokimab, or SLK, as we call it. It's a tri-specific IL-17A and IL-17F inhibiting nanobody, and it addresses multiple, very large indications in inflammation. We are public on Nasdaq, went public in April 2022, and are well-funded with a balance sheet that supports the ongoing studies, provides cash runway into the second half of 2027, and on top of that, we have access to a debt facility, providing additional funding of up to $400 million. We will talk a little bit more about this towards the end of the session. We have now conducted with our molecule, sonelokimab, Phase 2 and Phase 3 studies in five large indications across dermatology and rheumatology. Also here, we will provide more details during the session. We're planning to submit the BLA for SLK in the second half of this year, with then a potential first approval in the U.S. in the second half of next year. Now, what is SLK? You can see it here. SLK is a nanobody, and a nanobody is the variable region of a heavy-chain only antibody. You see it depicted here on the left-hand side. You know the traditional antibodies, then you have heavy-chain only antibodies, and a nanobody is the variable region, the VHH of a heavy-chain only antibody. sonelokimab are three of these VHHs covalently linked, with the one that you see on the right-hand side, the ones depicted in dark blue. We bind to IL-17A and IL-17F, and then in the middle, you see also a third VHH, with which we bind to human albumin. This is meant to extend the half-life, but there's also a lot of evidence that supports that this albumin binding helps us to accumulate the drug at sites of inflammation. Now, this whole construct that you see on the right-hand side together is only 40 kDa, so a lot smaller than the traditional antibodies that are around 140, 150 kDa. We are also unique in a way that we are not only a Nanobody instead of an antibody, but also in a way that we inhibit all three IL-17A and IL-17F containing dimers with the same affinity. This whole construct that we, that we have is administered subcutaneously, for commercial through an auto-injector with a monthly dosing of 1 mL. What does that translate to when we look at our clinical study data? We see a leading profile now across multiple indications. Not one or two, but really, as I said earlier, we have now tested this drug across five indications across dermatology and rheumatology. On the dermatology side, you see HS, PPP, and PsO psoriasis. On the rheumatology side, psoriatic arthritis and axSpA. Across all of these indications, you see a leading profile. Those are very large indications. You see our estimates in terms of market size in US dollars here, and you see here the response rate that are really the leading ones or among the leading ones across all of these indications. Not only do we show leading response rates, also in our trials, we aim to elevate the response, the care for the patients, by introducing novel elements. For example, in HS, we've been the very first company in the very first trial to use HiSCR75 as a primary endpoint. We've been the first company, to our knowledge, that uses the highest hidradenitis suppurativa specific quality of life instrument, this HiSCR, in the hierarchy as a key secondary endpoint. Other examples here, you will hear Kristian talk a lot about it today. For example, on the axSpA side, we conducted our study with a lot of imaging, PET imaging, MRI imaging, Kristian will share more on this a little bit later. Psoriatic arthritis, we emphasize a lot, the very deep responses, this ACR70, is something that you typically do not see reported by our competitors, because we believe that sonelokimab has the opportunity to truly elevate care for patients in need. You also see here in the bottom that we believe that sonelokimab provides a leading benefit risk profile. Overall, we think that the safety profile looks very good, and in particular, we do see no signals of events of interest that you see with other IL-17A and IL-17F inhibitors or with other MOAs that are relevant in these diseases. Last but not least, we believe that our posology, the administration of the drug, is very convenient. I mentioned it before, the Nanobody allows us to administer sonelokimab in 1 mL only, even in these indications where we use a higher dose, 1 mL only, and in maintenance, one shot every four weeks, and typically also a shorter induction period than what we see with other drugs. Today, we will talk about primarily the data on the right-hand side, the axSpA data, the S-OLARIS program that we've been running, and on the left-hand side, as I mentioned earlier, we will also talk about the HS program with the new data read of the interim data of the 52 weeks in VELA and the interim data from the VELA-TEEN study, the adolescent HS study. Before I hand over to Kristian, here's a little summary of our catalyst calendar this year. I will not get into any detail here. Jorge will cover it a little bit later, but enough to be said here, we have a lot of data reads this year, and very importantly, this is also the year where we expect to submit our BLA with the U.S. Food and Drug Administration, and then also 60 days later, the acceptance of this BLA. With that, over to you, Kristian. Thank you, Matthias. Very warm welcome also from my side. Excited to speak to you today about our second rheumatology indication after psoriatic arthritis, the results from our S-OLARIS trial. A small trial, but I think a diamond that really shines with regard to many outcomes, and I'm very happy to walk you through this. To give you a little bit of orientation, if you look into the bucket of the so-called seronegative spondyloarthropathies, you see two main diseases. One is psoriatic arthritis, where we think we have already shown very exciting data, especially when you look at these high levels of response, the minimal disease activity or MDA, the combination of ACR70 + PASI 100, what Matthias was talking about. This is the second biggest diagnosis in this bucket, the axial spondyloarthritis disease. You have it non-radiographic and radiographic. Many would think that these are two ends of the spectrum, that this is a disease that starts without ossification, if not treated well, and this is important, progresses to irreversible ossification, with irreversible ossification comes irreversible limitations in your mobility. I think it's an important dimension of the disease that you somehow therapeutically stop the ossification. I will come to this as I move you through the slides. You see that the prevalence is as high as psoriatic arthritis, around 1%. You see, as you see it with all I&I indications, that physicians and patients are more aware. You see more patients being diagnosed with this disease, axSpA every year, approximately 120,000 net patients newly diagnosed in the U.S., if you look into the claims database. If you compare to PsA, you also see some important differences. One is there's a lower use of biologics. You see here that although there is a 12% increase in the use of biologics per year in patients with a diagnosis of axSpA, you see that we still talk about below 15%, which is a lot higher in PsA. Even if you assume a very conservative growth rate of the use of biologics in axSpA, you see that by 2038 you get to a very healthy market size of $10 billion-$15 billion. What did we do to address this, and what is different in axSpA compared to psoriatic arthritis? As I said, small study, but really a diamond. Why? Because in this trial, we not only apply the typical clinical outcomes like ASAS40, a score that primarily looks into function and symptoms, it's a patient questionnaire, if you will, but also using ASDAS-CRP, a score that many KOLs would think is becoming the more important because it starts to look into the depth of inflammation and disease control. Then really taking it beyond, doing MRI to measure inflammation in the affected bone. Doing PET imaging, innovative PET imaging, that allows us to measure what sits in the core of axSpA, which is ossification. Using an imaging technique that shows you where you have increased osteoblast activity in patients, and what is your treatment doing with this? Then last but not least, really looking at biomarkers, an objective outcome to validate the findings, and again, I will walk you through this. The trial went on for 12 weeks. We know that we have a fast-acting drug. We already saw this in psoriatic arthritis, and I will present you the data from this 12-week period. As I said, if you look into PsA, what are the difference? A, there's a, there's a there are less drugs available. Just give you one example, the IL-23s that work in psoriasis, that work in psoriatic arthritis, they do not work in axSpA, so this whole MOA goes. You basically are down to TNF 17 and more recently, the Janus kinase inhibitors. If you look into this clinical score that is used in many trials, and I should say the more modern trials, the ASAS40, originally the TNFs, they only used ASAS20 as the primary endpoint. Now, we use ASAS40... But again, this is a score that looks into function and symptoms. Patients are asked, you see placebo responses, and you see that approximately 50% ±, using the available therapies of patients achieve this ASAS40 response, and at least 40% reduction in these patient-related questions related to function and symptoms. If you look at the ASDAS clinically important improvement, I will not go through the details here, but let's say these are patients that have a meaningful improvement of their inflammatory activity, of their disease control as per ASDAS-CRP. You see that the highest numbers are achieved with a more powerful IL-17 inhibitors, and you, you talked about 60%. Companies are becoming aware that these clinical outcomes have limitations, that they do not really allow you to address the question, what is the therapy doing with the main disease pathway, the ossification? We see that the first drugs try to generate data on this using PET imaging, and this was, of course, a focus of our study, and I will show you the data as we move along. ASAS40 responders, this study was an open-label study. You see that very rapidly, we see a high percentage of patients treated with sonelokimab achieving an ASAS40 response. For reference, we have been putting data that competitors were able to achieve in there with this gray bar. You see that the numbers are really high numbers. Now, you could say yes, but the numbers from the competitors, they partially come from placebo-controlled trials. We also give you here their open-label results achieved after every patient in their trials switched from placebo-controlled to only drugs. This would be the week 60 number, the week 52 number. This is the open label, non-placebo-controlled parts of their trial, and even if you take a very unconservative view, you look at the as observed data, you see that the numbers generated with sonelokimab early on remain very impressive numbers when it comes to ASAS40, with more than 80% of patients already achieving this by week eight and then maintaining by week 12. That is the traditional outcome. This is function symptoms. Let's do the next step, inflammation control, disease control, using the ASDAS-CRP. And again, surprisingly, I have to say high numbers already achieved early on at week four. These are patients that achieve an absolute disease stage axSpA of inactive or low disease. This is what the KOLs like, because similar to the MDA concept in PsA, this will be the treat to target, which the ASAS40 is not really. We see again that 80% of the patient achieve this high level of this deep in control of the inflammation. If you look at the relative improvement using the same score, Asking the question, what% of patients achieves a clinically important improvement, clinically meaningful improvement? You see a picture that's not too dissimilar from what I showed you with ASAS40, That 80%+ of the patients early on achieve this high level of response. Compare it to what you see with the competitors. I should point out that what is not shown here in the graph, but what you can see in the clinical trials, if you again, look at the one year plus open label part of competitor trials, you see numbers that go to 60%. These early numbers of 80% plus still make sonelokimab look extremely good when it comes to the comparison to other trials. These were the clinical outcomes and the outcomes with related to inflammation control. Now, I will build the story step by step. Let's now use MRI as a first objective measure of what is going on with the inflammation in the sacroiliac joints, which are the main area that are affected by the disease. This SPARCC score, M-- SPARCC MRI score is the established, objective, quantitative, semi-quantitative measure of bone inflammation in axSpA, primarily looking at bone marrow edema. I have to say again, a surprisingly high reduction already at week 12. Just to give you one number, if you look at all the competitor trials, you would say anything above an absolute reduction of -8 or -10 would be best in class, and the highest number is still being seen with regard to this score, delivered by the anti-TNFs. Here, we clearly go over. A more than 80% reduction of the absolute SPARCC MRI score and 90% of the patients achieving a reduction in the MRI measurement of bone inflammation. As I told you, we really want to use the Nanobody molecule, especially in rheumatology, to move away from symptom-only driven scores to scores that attack the core of the diseases. MDA in psoriatic arthritis, really showing that we stop radiographic progression in PsA, and you know that our Phase 3 study is in full swing as we speak. To really measure ossification in axSpA, you can apply a so-called 18F-NaF PET imaging. This will show you the regions where you have an increased osteoblast activity. It will show you the region where really in patients, increased ossification is going on as we speak. You see here two things. You see an example on the right-hand side. Everything that is highlighted in yellow means there is ossification, exaggerated ossification going on before treatment, and you can really see that already within 12 weeks, SLK cools these areas off. It stops increased osteoblast activity. It takes away the risk of increased ossification, and we would allow ourselves to call this disease modification.... we don't have really a good treat to target in axSpA. We don't have the concept of disease modification in axSpA yet. We have it in PsA. We want to use the Nanobody technology to really show disease modification in axSpA. We think this is an important step. You see on the right-hand side, if you look at this from all patients, you really measure this, we can see already within 12 weeks, overall patients, over all sacroiliac joint quadrants evaluated, we can see a more than 40% reduction of osteoblast activity. I told you that we did extensive biomarker work. We did this in the peripheral blood, and we did this in the tissue. Today, I will share with you as a first piece, the peripheral blood data. I have to say, as a scientist and physician, this data was truly unexpected and amazing. We did this non-supervised. We just asked the question: Do we find markers in the peripheral blood that correlate with the individual clinical response? Really showing that it's our therapy that drives these changes in the biomarkers. The biomarkers that we found, you see the names here depicted on the Y-axis, they all sit at the heart of ossification. These are markers that are known to reflect increased osteoblast activity. They are known to link inflammation with angiogenesis and increased mesenchymal activity and ossification, and ultimately, APCS, probably the best marker to reflect overall control of this whole process. This quartet of markers that I show you here, what you see on the X-axis is the degree of correlation of the reduction of these markers with treatment to, with SLK, measured as the individual clinical response to treatment with SLK. You see very high correlation levels, 0.5, 0.8. This reduction of this quartet indicates to us that SLK really treats structural damage. You see now, this is a completely different level to just measuring function and pain. If you look at the combination, the package that I showed you, MRI, structural damage, PET imaging to really show control of ossification, then completed by biomarkers, we think that this validates the clinical findings a lot more than any placebo control could have done it. You may see a placebo response in a patient questionnaire. You will not see a placebo response in structural damage, PET imaging, or these biomarkers. This is why we designed the study in the way we designed it. Safety profile. Not much to say other than we continue to see a very clean safety profile, especially in rheumatology, I should say. We know that even the Candida signal is shown here is very low. It's all very much in line compared to what we saw in our other seronegative spondyloarthropathy indication, psoriatic arthritis, and we continue to see a potential to differentiate on the safety side from competitors. To summarize, I hope you see my excitement, as I said, a diamond study that really links clinical outcomes in a degree that we have not seen with competitors, but really validates these findings by what we think is the next level of what a therapy should do, and that is control structural damage, become a disease-modifying drug in axSpA, prevent ossification and irreversible restriction of mobility. Jorge, is there any news in HS, regulatory? Thank you so much, Kristian. Also, from my side to all of those joining the session today, good morning, good afternoon, good evening. It's a pleasure to be here, again, reporting on some really exciting data. Again, thank you, Kristian, for that. We know that the S-OLARIS data was something that many of the stakeholders, many of the communities, including the street, were looking forward to, and we think the data is really, is really, really very strong. Obviously, the other question that is very dear to many of you watching today, is the trajectory and the path for HS, especially the BLA submission, and how, how will that result in a label that might be competitive and leading to reflect all the data that we see with SLK across different indications? What we wanna do today in this section is really discuss with you how we are building the BLA, and therefore, the label that will result, that will eventually drive our, our commercial approach. We are certain that conversations like those today will continue to bring clarity on, A, how narrow and clear the path is now that we've had the opportunity to discuss with the regulator on what happens next, and the regulator has given us the guidance on what to do next. Also how that very clear and very narrow path can actually result in a label that we believe is gonna be extremely competitive. I will start by reviewing the FDA feedback that we got in December and January. I will then really step by step, take you through how this very, very focused guidance results in scenarios for our label that we think are very advantageous for us. I will take also the opportunity to show you how, as of today, the long-term data looks like in VELA. I I will also show you a bit of VELA-TEEN. I will just finish off with a timeline of the regulatory steps on HS, which you will see will make a lot of sense versus the catalyst flow that Matthias started with. Let's start with what we heard from the FDA. One thing that I would like to highlight, especially to all the investors in the street, is really starting on the left side. Just want to remind everybody that obviously the, the, the interactions, and the type, especially the Type B interaction that we have with the FDA following the VELA primary endpoint readout, is obviously not just a meeting. It's very important that everybody bears in mind that, of course, there was a lot of preparation. There was a briefing book that was created. This briefing book had literally hundreds of pages, including detailed analysis of what happened in VELA, including VELA-2. So obviously, it's very important that you assume that both the team here and both the regulator are very aware of a lot of detail that perhaps the street or for sure, the street is not, not aware of, but that goes into the context of these conversations. Of course, again, a lot of those analyses, including a lot of VELA-2, including VELA-2 placebo analysis. Obviously, as we've informed the market, all the richness and the guidance that came out of this discussion and the analysis of this briefing book is already, already fully in our hands since we announced it on January 8. That's an important context element that I think is very important for people to bear in mind. What you see on the right side of the page is what results from the guidance. For those of you that have been closer to our story, you remember there was a lot of questions late last year: Will this all be sufficient? I think it's very clear to us now that for the bar of having two proper, well-controlled trials to submit and support the BLA, we obviously have that with VELA-1, VELA-2, and with MIRA, and I'll come to MIRA in a second. No additional clinical trials are required. If you hear some analysts asking: Is it submittable? Can we put this forward to the FDA for approvability? The answer is, is very clear. We have enough material to submit a BLA. To establish something that I think is always important for us to bring to you in terms of the wording and what it means, to establish what we call and what the FDA calls substantial evidence of effica- of effectiveness, SEE. For short, if you allow me the, the more colloquial language, this means establishing efficacy. In a regulatory language, you, you refer to it as substantial evidence of effectiveness, SEE, and you will see this through, through the presentation. No additional trials are required to establish SEE. Second very important guidance, VELA-1 and MIRA. VELA-1 and MIRA are to be submitted to establish efficacy, to establish SEE, and to support safety as part of the BLA and as part of our request for approval. Very clearly, VELA-2 is to be submitted to support safety, i.e., we do not need more trials also to create the safety database. The question of whether VELA-2 will be used for SEE, for efficacy, is an open question to discuss with the FDA. As I take you through the label, you will realize that the impact on our label is either neutral or actually positive, I will come to this. Again, very clearly, VELA-1 and MIRA to support efficacy and safety, VELA-2 to support safety, VELA-2 participation in the, in establishing efficacy to be discussed. What I think is also very important in these cases is what was clearly excluded by the regulator. First, because again, it narrows the path. I've referred to this path as a very narrow, very clear path. It's important that people exclude things so that the path is narrow. It also tells you that there's a very clear, specific guidance that is being given to us, not some, some general statements. Those exclusions are, as you see there, on the 5th and the 6th bullet point. Supporting the BLA with 1 trial, using some of the recent ideas and guidance that is being given by the FDA, is to be excluded from our process, and that's simply because we have three well-controlled trials. No point in focusing in one trial when, of course, we can submit three. Very clear guidance, don't go down this path. And obviously, some suggestions and some clarity that VELA-1 and VELA-2 alone could create a question around SEE, again, because we have to discuss whether VELA-2 is included or not. Really, the scenario in which we submit and establish substantial evidence of effectiveness without MIRA is also to be excluded. Again, this gives us a very, very narrow path to operate. Also, to clarify, a, an, another important element in that penultimate bullet point there, to clarify to investors in the street, when we talk about submitting VELA-1 and MIRA and VELA-2, this does not mean that the whole BLA does not include all the data that we've generated. Clinically, pre-clinically, any data associated with SLK in HS, of course, will be submitted as part of the BLA. When we talk about this trial or that trial to establish SEE, efficacy, this is a pure BLA label element. Doesn't mean that we don't submit the whole package, doesn't mean that VELA-2 is not there in full. It just means that certain pieces of data, together with the regulator, are used to establish certain elements of the label. The last bullet point here is, of course, coming out of this FDA feedback, what is very clear is that we are completely back on track when it comes to timelines. We are now about to start the more technical meetings associated with the BLA submission. We intend to submit the BLA towards the end of Q3, obviously, we intend to hopefully get it accepted within 60 days after the submission. What's important also for the street is that the timelines are as they were already last year. Hopefully, that brings, yet again, a bit of clarity about what the BLA process is, what we've gotten in terms of guidance, and what we plan to do next. Another question that comes is: Why does MIRA matter? I-- we understand that this, for some investors, and certainly for some analysts, creates some confusion. We thought that putting side by side what has been happening in HS, among the various Phase 2s, can shed a little bit of light on this. On the r-- on the left side of the page, you see what we've done. You see MIRA, you see VELA. One of the things that you see with MIRA is that if you compare it with the right side of the page, where other IL-17s have done some work before they started their Phase 3, you see a very, very different story. What you can see with MIRA is that we have a large clinical trial, very similar in design to what we actually ended up doing in Phase 3, it's an adequate and well-controlled trial. It's controlled with placebo. It's also controlled with the standard of care. What you see is a very high number of patients, 234 at the end of the day, in a, in a study that in its, in its completion, actually took six months. What you can see on the right side of the page is, obviously, as I said, a very, very different picture. Either the doses were not really tested, or the number of patients were lower, or we used different statistical artificial methods to analyze the placebo, or we didn't even do much, if I may say it like this. When you think of MIRA from a regulatory perspective, and you put it in the context of VELA-1 and 2, what you have here is what we have tried to transmit several times, and it comes out in the regulatory guidance in the sense that we have three well-controlled and adequate trials for submission, and that's very different from what's happening in other with other drugs out there. I can think of one or two analysts that are gonna say, "Well, but this is a Phase 2. Phase 2s don't go into the label." That is just wrong. That is just wrong. If you search, you will see that there are many indications, there are many drugs that have been approved with Phase 3 and Phase 2 packages, including in immunology. We have three well-controlled trials. We've got very clear guidance. You see the structure of MIRA. You see the consistency that follows from MIRA to Phase 3. It's very important for us that the street and some analysts understand that MIRA is a perfectly plausible trial to make a BLA with, but also to try to establish that substantial evidence of effectiveness and safety, specifically in the label. Now, what does it all mean? What are we gonna submit in terms of BLA so that it drives, the label that we're expecting to drive? These two very quick charts, we just put a picture here of any label that any of you watching the, the session today can go into the internet and download and see. This is what a label looks like, and this is what allows us to do some, some things commercially. I think here we have the secukinumab example, just to keep it in the, keep it in the family of molecules. You, of course, in a label, you have several sections. We're highlighting three sections here. Why do we highlight these? Because as you start thinking, how does a drug establish the information that can be shared with patients and physicians to drive a commercial strategy to differentiate itself from others, okay? Those three sections that we're calling out here are Section 14. That's where all the work in establishing that substantial evidence of effectiveness, the efficacy, comes to fruition. You have tables with numbers, you have sentences that tell you, "This is how efficacy is driving for this drug." That's a really important element to think about and to compare ourselves when we're building the label for the BLA submission, but also for all of you out there to make those comparisons. There are two other sections that I think are important. Section 5, this is where you have all your warnings and precautions. Where, if you allow me my language, where all the things that you find on safety really come to bear, where, where rubber hits the road when it comes to safety. Also Section 2, which reflects the dosing scheme that the patients will follow. Obviously, here, if there's anything about how you administer this drug, this obviously creates a potential for differentiation. I would say consult the labels, think about the labels, and specifically look at these three sections because we believe that's where a lot of this efficacy, safety conversation really comes to bear and gets written black and white. For those that will check this document later, we've, for your convenience, we included the elements here for two of the drugs that are competitive to us. I would just call quickly your attention because this is now important for the next part. For the pictures of the Section 14 of bimekizumab and secukinumab, you will see that in Section 14, the secukinumab table only contains HiSCR50, which was their primary endpoint, including a number that was not significant and didn't meet, just for everybody out there to remember this. As you can see more to the left, you see the bimekizumab label, which has HiSCR50, which is the primary endpoint of bimekizumab as well. It also starts including HiSCR75. You always see the absolute response to placebo, and you never see p-values, you see a confidence interval and a statement on significance. That's really the tables on Section 14 for a label with the FDA that are out there for our competitors. Then, of course, some important statements in Section 5 and Section 2. With this view of what really matters in a section, we thought, let's put on the screen what we believe is the structure of the BLA and the label that we are going to have to put forward based on the very narrow guidance that we got. That's illustrated here. Let me take you, let me take you through what we believe is the base scenario for Section 14. What we expect to see here is something very similar to what we see. Now, the drugs in for reference, on the right side of the page, we always have here, the IL-17A and F monoclonal antibody, so that you have a sense of reference. First and foremost, of course, there are no trial names. You just have HS Trial 1, HS Trial 2 or 3 or 4, depending on the trials that you have. That's what we expect to have. When it comes to efficacy data for Section 14, we expect HS Trial 1 and HS Trial 2 to be reflected, we expect Trial 1 to be VELA-1 and Trial 2 to be MIRA. What you see in this very base scenario is that we assume that we get a table that looks exactly in terms of its structure, exactly like, like we have seen for the IL-17A and F monoclonal. You see HiSCR50 in the second line because it's a secondary endpoint. In our case, HiSCR75 in the first line, because that's our primary endpoint, those are the numbers. Those are the numbers that we have seen in our clinical trials corresponding to the absolute response of HiSCR75 and HiSCR50. For your convenience, although this is not part of labels, we have the delta to placebo, which we know is very important for the street. As you can see in this base scenario, where we use the two trials that we were guided to include, the label looks very, very competitive. As you see on the right side of the, of the page for, for the IL-17A and IL-17F monoclonal antibody, apart from the table, you also have some statements. For example, that drug is a state on the improvement of the worst skin pain, which is also a metric that is really, really very important for physicians, perhaps even more sometimes than HiSCR. There's a statement about it. There's no numbers. Obviously, this, this particular metric did not meet stats, stat sig in one of the trials and or for one of the doses. The statements are still there, even when you don't meet statistical significance. What you do not see with that monoclonal antibody is statements on IHS4 or HiSCR, because those were not tested. Those were not tested. As you can see, back to our label here, we believe that our pain, our HiSCR, our IHS4, all these very important endpoints that we had, we believe they in our base scenario, they will not be in the table, but there will be text to reflect that these were important metrics and therefore can be used commercially. In the, in the simplest base scenario, you can see that the guidance that we're obtaining, gives us the very, very clear opportunity to have a very competitive label when it comes to HS. We believe there's a, a slight upside case, as, as we call it, wherein we are actually able to even spell out all the numbers, make it a bigger table that includes metrics like pain, HiSCR, IHS4. Why are we so keen on these metrics? Because these are the metrics that we know really drive the decision of prescription when a physician has a, has a patient in front of, of, of her or him in the practice. We would like to try to have this in the table so that we can always refer to these numbers if they're not in the text. That's what we call a, a, an upside case in which we can start evolving the, the, the table of Section 14 for HS drugs as we move forward, but also where we really bring the numbers for the physicians because we know how important they are, much more than perhaps I-score, I-score is. These are, these are really the scenarios we can operate in the guidance. You ask me, "So what about VELA-2? What do we do with VELA-2? If it's in safety, fine, but what happens with efficacy?" We believe that this is another, another element that we could add to the, to, to the, to the label. We're probably not gonna do it proactively, but as we said, this is a discussion that the FDA said we will have to, to take decisions based on a third trial, VELA-2. If VELA-2 would be included, the data would be either on the table or, which we think is more likely, if it gets included, referenced to in the text. Even if the data of VELA-2 is there, you can see that the absolute responses, as, as you saw us presenting the data in September, the absolute responses are similar to VELA-1. Even if you consider a nine or 10% delta to placebo, which again, is more of a metric for the street than for prescribers, you see that we continue to have a very, very competitive label that, in my mind, looks numerically higher than any of the competitors. Very, very clear path, very, very narrow path. Hopefully, through this step-by-step exercise, we've showed you that how it gets built, what we believe is the base scenario. As you can see, there's not a lot, there's not a lot of flexibility that we believe we can get from this guidance in terms of how we structure the BLA. Therefore, we believe that Section 14 of the label we're going to propose can be really a leading profile versus many of our competitors. We hope that brings a little bit of clarity on the efficacy side. I'm very briefly gonna talk about the other two sections. As I mentioned before, we have a Section 5 on warnings and precautions. We have a Section 2 on dosage administration. We will, of course, this, this document is available, let me just tell you that when it comes to warnings and precautions, especially as we see them applied to IL-17A and IL-17F monoclonal antibodies, suicidal ideation, infections, tuberculosis, liver, IBD, we did not detect those signals in VELA during our controlled Phase. Obviously, we think that there's a real opportunity here to differentiate, and we're, of course, gonna submit in that, in that direction. Also, when you look at dosage administration for an IL-17A or for an IL-17F, as depicted in the page, as we've said many times, our drug requires a lot less injections for that induction period. Our, our drug has a much shorter induction period, and in general, you're, you're, you're injecting very little volume. There's another element that we know is important for the street and for many of the stakeholders out there, which is not necessarily reflected on any of these sections in the labels of our competitors. As we know, there are some questions around the usage of IL-17A and F monoclonal antibodies in terms of, especially when you uptitrate, causing eczema, dermatitis, etc. Again, as we've said in September, we don't, we don't really see a lot of signal in this area. I would like to remind you that because of our dosage, we're always injecting far less number of molecules into every patient to produce a similar or better result, as you just saw on the label. Obviously, this is what we believe can drive some of the differentiation in Section 5, warnings and precautions. We also believe that this particular dosage, our nanobody, the way it binds, the way it responds, the very few number of molecules we actually inject, will also drive additional differentiation in other elements, such as some elements of safety. I know I went step by step. I know I repeated myself a couple of times, but hopefully, this tells you exactly how narrow and clear our path is and how our label can look like, and what is the slight variations that could be there, and how they do not really impact us in terms of of differentiation, especially versus our main, main competitor. Obviously, let me shift gears to the long-term data so that you also see what's, what's going on in, on in the real world while we're hypothesizing and writing all these, all these papers for, for the regulator. Obviously, the long-term data will be a key supporter of the, of the submission. I would argue that our long-term data is looking quite good. A couple of things that I wanna call your attention to. We're comparing ourselves here with two other commercialized drugs. We're comparing ourselves to the level of HiSCR75 response, which was a secondary endpoint for these drugs, that they've reached at the end of their respective parental trials that supported their BLA submission. A couple of things that you can see that I think are important are, A, our long-term response at the end of the year, at the end of the parental trial, for both VELA-1 and VELA-2 is quite high, especially, compared to the values that were reached by other drugs, at the end of their year parental trials. That's one element that, of course, I would call attention to. I would also call attention to the N numbers here at the bottom. The numbers that you're seeing for sonelokimab, 104 patients for VELA-1, 123 patients for VELA-2. If you look at it, it's already the number of patients or above the number of patients that our competitors reached in their full parental trial. The results that we're seeing are actually quite interesting and quite significant because, of course, they already correspond to numbers of patients that are similar to our competitors. It also tells you, and something else, around the sheer size of each of these trials. For example, VELA-1, in that we're still kind of halfway through reaching the end of the parental trials, because in our dose arms, the number of patients is double that of our competitors. When people start wondering, "Is VELA-1 enough to submit something?" Always bear in mind that one of our dose arms is worth two of the dose arms in two trials from our competitors. That's an important point for folk to remember. We're obviously very happy with the direction of travel here with HiSCR data. HiSCR75, obviously. Just very briefly, because again, we always try to balance these two sides. HiSCR is interesting from a regulatory approval perspective and obviously for the street, but this is really the stuff that we think gives traction when it comes to commercial. Do the patients feel a lot less pain, and do they see improvement in quality of life? As you can see, the long-term data continues to look extremely promising for, for the both arms of SLK and also the transitions from placebo when it comes to VELA-1 and VELA-2. There's one particular thing that I would like to call you, because this is, this is really... we, we feel, quite impressive. If you look at the, at the middle panel on the quality of life, you've seen that not, not only we have a very, very strong response, but that response continues improving over time into the one-year mark. This, I would argue, is not, not usual to see in quality of life improvements. You typically see a first response, and then it sort of stays stable if, if, if everything is good. Here, we're really seeing a continuous improvement over time, which is very, very exciting to see, and I'm pretty sure physicians and patients will find very exciting as well. A brief note on VELA-TEEN. As you know, this, this is a, an open-label trial that we've been updating you all on as we go. The results continue to look extremely promising. If anything, the overall response, for example, in HiSCR 75, is really showing a lot of promise. Even HiSCR 100, even at six months, is already on the 1/3 mark, and if anything, HiSCR looks, looks, looks probably even better, than we've seen with MIRA and with VELA. So this is extremely exciting because you know how important it is that we start addressing the disease very early on in its onset, which is, at the end of the day, is adolescence. Quick update on the safety. Nothing to report. It looks clean as, as it does, and as it has, on the, on the VELA-TEEN trial. Again, for details, you can consult the deck that we share. I'm just gonna wrap up this part. I'm not gonna go through the details, but I wanted to make sure that we hit on a, on a few points. We have regulatory clarity. The guidance is, is quite complete and it very narrow. It doesn't allow us or, or any analyst or any investor to create all these, the all these very wide scenarios. We know what we need to establish SEE and safety. I think you're seeing all, all the data is suggesting that numerically, we're gonna have very, very, very exciting numbers also on efficacy and also on HiSCR. You see our attempt to continue including all the metrics that truly matter for patients. That, I think, is gonna be one of the biggest differentiations. Very importantly, I would say that we're back on track. We know exactly what we have to do. There's not a lot of things that we can change. I would argue that the risk profile of SLK being approved in HS is no different than that of a drug that has completed all its packages, and it's going through a BLA process. Obviously, BLA processes have a risk element to it, but I would say that there's no big difference between us and any other strong biotech product out there. I'm I'm just gonna tell you that obviously on the right side, you see all the detailed steps that we're gonna be following, leading to what Matthias mentioned at the beginning, is that submission at the end of Q3. Of course, this page will be available to you for perusal and for further questions. Hopefully that clarified a few things regarding HS. Hopefully, it clearly establishes the excitement that we have here. With that, I would move us to additional guidance and reporting on other indications and on financials, and I think the next is PPP, Kristian. It sure is. Thank you, Jorge. I'll make this brief. We've talked about this before. As a dermatologist, we talked a lot about the, the street. You talked about the street, Jorge. As a dermatologist, a little bit frustrating for me that obviously some analysts, the street, still do not understand that there is a psoriasis of the palms and soles, which is called palmoplantar psoriasis, and then there is PPP, right? It's a different disease. As reflected in the ICD coding, psoriasis being L40.0 and PPP being L40.3. For PPP, palmoplantar pustulosis, there is no drug approved, neither in Europe nor in the US. It's a devastating condition. You see the clinical pictures on top. Yes, they are also red. They have some scales, but the, the clinically leading phenotype is that of pustules. You see this in the histological picture. It's a healthy market. We can see that out of desperation, biologics are already being used in increasing numbers, and I should say out of desperation, because most of the biologics that work in psoriasis do not work in PPP. That's why it's so important that we really do SLK development in PPP. As you've heard before, we have very exciting data from another small diamond study. We have been moving towards objective parameters to really validate a clinical response, to make sure that we understand what is SLK really doing in a disease. Similar to what I showed you for axial spondyloarthritis, the biomarker data, the clinical outcomes in PPP were really overwhelming in a sense that we, we are progressing now. We could show that the SLK not only controls the clinical outcomes, it actually controls all these molecular markers, again, that are established to define the core disease process in PPP. Very interesting molecular pattern being observed. Early with normalization of this pattern, together with a clinical response. We even went as far to subject the photos that were taken from these patients to an AI-based validity verification, but I have to say, the investigators did a really good job, and the objective assessment of the photos validated more or less what you see here, which is that 40% plus of the patients achieved very high levels of response. A palmoplantar PGA of zero or one, meaning clear or almost clear disease, is seen in more than 40% of the patients, very nicely correlating with 40%+ of the patients achieving at least 75% reduction if you use the palmoplantar PASI. For reference, on the right-hand side, you see how this compares to what competitors were able to show. By the way, these gray bars include placebo and non-placebo-controlled trials, so I think this is a fair, a fair comparison. A lot of excitement in PPP. No drug approved. For the first time, we see biomarker validation of a Phase 2 program in this indication. This opens the door for a more rapid development towards approval. We have already shared with the world that we received Fast Track designation. I think this reflects that the FDA sees this is a disease where that is terrible, and whereas there's no drug currently approved, we will have many interactions with the FDA. Our current thinking is that we want to create a very exciting Phase 3 program. We want to make use of the very fast onset of response that we seem to have, probably even faster than what we saw in HS, so with a 12-week induction period, using every other week dosing, and then actually testing our standard monthly maintenance versus a Q 2-week. You can ask me why? Because we have evidence that PPP is a tough nut to crack. Although we have this super strong drug that penetrates deep into the epidermis, has this molecular support, we want to leave nothing on the table. We want to make sure that we really exploit the dosing options that we have, and maybe even include a direct uptitration of patients that achieve no disease control with a Q4W maintenance. Making progress, using this, this outcome we had from our diamond Phase 2 and progressing towards Phase 3 as fast as possible. psoriatic arthritis. Yeah, maybe I'll, I'll do the quick, the quick update here on PsA. Just, just a couple of pages, in terms of guidance here. Guidance number one, it's, it's, it's important that folk reflect on, on what you see on this page. Psoriatic arthritis obviously has been around for a while. There are several drugs approved, but I think sometimes there's a bit of misconception that because several drugs are approved, this is a mature market where new drugs cannot be launched or where new drugs will have a very hard time succeeding. I think what you see in this picture is really a bit of an evolution, of, of the drugs that were introduced for PsA. We know the market has, has the potential to be also about $10 billion-$15 billion in size. These immunology markets tend to have a very similar size to each other. What you see is you can actually launch several drugs into this space, and they will all be commercially successful. I think that's, that's important that sonelokimab also it's given its, its, its value in terms of its potential just being part of a market where several drugs continue to succeed as they launch. As you can see, any class of this drug is actually quite successful. I mean, the, the commercial opportunity in any of these classes is very, very large. As you can see, that's the second point that I would want to make here. Not only that the market is big and can accommodate several drugs, including ours, but also that you have really seen this progression. ACR20 was the endpoint for the first drugs approved, then came ACR50. Then we started, of course, bringing some of the PsA PASI, some of the effect on the skin. Also, because with ACR, I remind everybody, we're measuring joint improvements for a disease that is not even PsA. This is originally a rheumatoid arthritis score. Then you started getting into the IL-17s that started marrying, to some extent, ACR50 responses together with PASI, because, of course, you not only need to improve the joint, you also need to improve the skin. In fact, you need to improve those two things and many, many more things. That's why we position ourselves, and we position IL-17A/F, really as the next generation drug, where you're not only trying to achieve an ACR, but really elevating that ACR well above 50, trying to reach PASI of full clearance, but all together in the same patient, and really moving to scores like MDA, which is really what you're trying to achieve as a, as a physician, and where you really start thinking that you're really controlling the disease. I want to establish a parallel here between PsA and what Kristian discussed for axSpA. In many ways, with these very basic scores, we're just seeing if the symptoms are improving to some extent, right? I think it's time that we understand that these diseases require us to improve the symptoms a lot more, but also that we really start modifying the disease, controlling the disease, going to that MDA, going to that very high ACR with PASI. That's why we believe that, yes, the market is large, but there's so much head space in terms of what you can achieve. If you're only improving 40%-50% of the patients on a 50% improvement of just the symptoms, aren't we missing a big opportunity? I think we are. That's why I believe that IL-17A/Fs and sonelokimab, in particular, have such potential here. That's why I and we would not subscribe to the thesis that this market has many drugs there, therefore, it's done. As you know, we've started a while back, our very large Phase 3 program with IZAR. Remind everybody that IZAR-1 is a biologic-naïve trial in biologic-naïve patients with radiographic in PsA. We have an IZAR-2, which is a trial that is conducted in patients that are biologic-experienced and where I think very interestingly, we use a standard of care reference, I mean, what today is the highest prescribed drug in PsA as we see it, which is risankizumab. IZAR-1 has recruited. We're done there. IZAR- 2 is recruiting, and we'll read out IZAR- 1 now in the cusp between Q2 and Q3 of 2026. IZAR- 2 will come later in the year. I wanna make sure that I share with you what you should expect to see for IZAR-1 and eventually for IZAR-2, but of course, first for IZAR-1 between Q2 and Q3. Obviously here, as with any other, any other reporting of our primary endpoints, we try to be very transparent with the, with, with everyone, with the street, and share it as quickly as possible. Obviously, we have to find regulatory guidance, as we always do. Considering the structure of the arms, we obviously have to always make sure that we are reading the primary endpoint, but also not risking any, any, any unblinding. This is, of course, a, a disclaimer that I have to make every time we talk about disclosures of primary endpoints. What you should see in that press release and probably in a session such as this, immediately after, you should see statements around us meeting or not meeting the statistical significance, both for the primary endpoint and the secondary endpoints in the hierarchy. We plan to share with the world SLK response levels for primary and secondary endpoints for both 60 mg and 120 mg, depending on the trial. This should give you a sense of what we expect to show you, especially for IZAR- 1, which is coming in a couple months' time. That's what you should expect to see. Obviously, in terms of response, you have our ARGO data in terms of the drug response versus others, and that should give you enough reference of what the competitors and ourselves have achieved and expect to achieve. Then I think we will wrap up with finance and then open for questions. Absolutely. Thank you, Jorge. Thank, thank you, Kristian, for walking us through some exciting data updates and also some very exciting label scenarios, I believe. From a cash position, we ended up December 31st, 2025, with $394 million on the balance sheet. That covers cash, cash equivalents, and short-term marketable debt securities, as you see on the page. That also included the $75 million offering that we made in November. With this cash that we have on the balance sheet, we expect to have runway into the second half of 2027. What you also see here on the page is that as a subsequent event, last Friday, we amended the Hercules Facility. We drew down another $25 million in debt, non-dilutive funds. We retain access to up to $400 million in additional non-dilutive funds to support future cash needs of the company. In terms of OpEx, you see it here on the page. Q4 OpEx were $65 million. You see a small decrease on the R&D side, from $60 million in the prior quarter, now to $56 million, reflecting that we are now past the peak of R&D expense. VELA-1 and VELA-2 are concluding very, very soon. The later study in PPP has been completed. S-OLARIS has also been completed. Yes, we're expecting to initiate the PPP Phase 3 study in the middle of this year, but in terms of overall size, we expect the Phase 3 study in PPP to be substantially smaller than the VELA program. On the G&A side, you could see also a reduction in the fourth quarter from $10.8 million - $9.2 million. That reflects some efficiency measures that we've implemented in the company in the end of last year. There will be some increases in 2026 as we ramp up for pre-commercial activities, but overall, we expect no material changes on the OpEx side. As I said before, we're very excited that we have amended our loan facility with Hercules Capital. Hercules Capital has proven to be a very reliable and supportive partner of the company. Reminder, we drew down at the closing of the facility in March last year, $75 million in debt, and on top of that, we had $425 million being available through a variety of milestones. Given the VELA readout last year, some of these milestones, the technical definition could no longer be met. We revised these milestones also to reflect revised needs and timing in terms of cash needs for the company, are now very happy that we drew down another $25 million. Not that we need it right now, obviously there's also some incentive for Hercules to earn some interest on it. Overall, we're very excited that we retain access to the full up to $400 million in additional funding capital. That will not only help us with the future development of sonidegib, but will then therefore and primarily also contribute to the commercial readiness, to the preparation of the commercial activities. You see on the right-hand side, in terms of cash interest rate, it's 8.45%. We retain full flexibility. There's no obligation for us to draw down any future tranches, we believe it's actually a very attractive cost of capital. It's something that we will very well consider, depending on the market conditions. With that, some closing remarks before- I mean, I, I will just quickly wrap, wrap here, Matthias, to allow maximal time for questions. I, I just wanna sort of take a step back. Today, you saw S-OLARIS, and as you saw on the page, we will of course, engage with the regulators now to think how do we move that the Oxba forward. Obviously, what comes after today, and it comes quick, is a lot of interactions regarding the derm side and with the FDA. Several pre-BLA meetings in April and May, which are technical meetings that happen in any process, but it's great to see them happening. It means that we're moving the ball forward. VELA team, readouts, meetings with the same division of the FDA around, around other elements. Obviously, the Fast Track designation for PPP allows us to continue the interactions on the derm side. As we sort of get into summer, some pretty big readouts, Phase 3 readouts, 52-week data on VELA. Obviously, quite exciting to see the results as they stand, very shortly thereafter, starting to read the Phase 3s on the rheum side. During the summer, we expect more news in PPP, obviously, we expect to be extremely busy and not on holiday.... while we're preparing the BLA submission. That should lead us into fall and early winter, where we obviously expect the HS BLA acceptance of the BLA. Obviously, then moving into the IZAR-2 and additional readings such as POLARIS, so that we finish the year with more readouts. If you just take a step back and look at this map, you realize how busy it's going to be, how many catalysts there are, how many inflection points there are, and really how MoonLake Immunotherapeutics is going well up beyond derm and establishing itself as a rheum player, but also really moving into the commercialization stages in the latest part of this year. Maybe I would leave it there, Matthias, and open for questions. Yeah, I mean, certainly we have many viewers and also quite a few questions, so trying to go through it quickly, and apologies if we cannot address all questions. Starting in terms of order of presentation, so with the S-OLARIS data, we have a question here from Thom Smith, Leerink: "Hi, team. Congrats on the strong axSpA data. Can you elaborate on the patient baseline characteristics in the study? How many were radiographic versus non-radiographic? Were there TNF or JAK-experienced patients in the study and study, and more broadly, how does the study compare to other studies in axSpA? Yeah, very happy to take this. It was a mixture of radiographic and non-radiographic patients, both almost equally sized, so a healthy proportion of each of these variants of axSpA. When it comes to disease duration, previous therapy, comparable in general to what others have been doing. I think the baseline characteristics are similar to what others have been studying, adding to the validity of what I tried to show. When you look at the outcomes, Matthias, just to quickly reflect on this, I hope I could really make this point clear. Yes, it's a small study. Yes, it's open label, it has elements that really validate the findings. When I showed the clinical outcomes that are always subject to placebo responses, because as, again, you ask patients, how much pain or morning stiffness do you have? Of course, there is a placebo response. There will be no placebo response with, with imaging or with, or with biomarker control. You remember whenever I showed you these clinical outcomes, and I tried to put it in perspective to what competitors were able to show, we added their long-term data. Why did we do this? Because after the primary endpoint, there is no placebo control. We tried to be as fair as possible and even giving you the often as observed, long-term, non-placebo controlled outcomes from competitors from similar trials. I would say, and again, it's not, it's not a direct apples to apples, but if you look at the baseline characteristics, if you look at the way we try to present these outcomes, if you believe in the validation of the clinical outcomes by MRI, by PET, by biomarkers, you have to walk away from this thinking this is really fantastic data, very exciting data in axSpA. For me, it shows again that the Nanobody story is very alive, and that we obviously can use the Nanobody to move from symptom score, which we want to hit, and we want to hit them on a high level, but really to what we call several times now, preventing structural damage, entering disease modification, because that, for me, is the next step in I&I. This is how I would see the axSpA data. Small but beautiful, Matthias. Perfect. Perfect. I have another question here from Julian Harrison, BTIG: "This is the highest 12-week ASAS40 response rate ever reported in a clinical trial. How much do you expect SLK's small size and albumin binding domain contributed to this? Yeah, I mean, we can only speculate. Allow me to become a little bit passionate. When we all started MoonLake, I think we really started it because we wanted to create an antibody 2.0 scenario. We really hoped that we could use the Nanobody to elevate all the fantastic things that monoclonal antibodies were able to do. Of course, one of these characteristics is because it has a smaller size, because it has the albumin binding, because we know it has the potential to enrich at sites of inflammation, particularly when this inflammation sits at complicated to reach sites. I would think that, A, the rheum studies show that this might really be the case. We showed the MBA data. You reminded us of the ACR70 + PASI 100 data in PsA. I showed you the ASDAS-CRP data. Let me say that you can say: "Yeah, but doesn't the HiSCR data show you that it's not true, and that it was?" I don't think so, because the HiSCR is not the score that really reflects what a molecule can do when it travels deep. Let's look at the Abscess 100, the DT 100, the IHS4 100 data over time. This is what will tell the story about Nanobodies and deep tissue penetration in HS. I think, Jorge, you, you began to share the long-term data. The long-term data looks extremely good, so I'm not giving up on the Nanobody story in HS at all. Perfect. One last question on the, on the S-OLARIS study, and maybe, Jorge, for you, because multiple analysts are asking, for example, Yaron Werber from, from TD Cowen: "Congrats on the data. Can you talk a bit more about next steps in axSpA? Does MLTX expect to conduct a Phase 3 program? When could a Phase 3 program begin and complete? "Other analysts also ask: "Is there a need for a Phase 2? What about the impact of recent FDA guidance on single pivotal studies?" Maybe very briefly, our thoughts on, on the next steps in axSpA. I'm gonna be a little bit more, more guarded than, than Kristian was in his previous answers. To Phil and to all the analysts out there that are asking the questions. Obviously, with this data, very much our intention to continue progressing sonelokimab in axSpA. I think the results are so exciting, and it, it, it could mean so much to, to patients and physicians that I think that answer is obvious. Obviously, we are now finalizing all the data, preparing all the reports, all the books that we will need to put together to engage with the regulators, and we will follow the standard process in terms of finalizing this Phase 2 and start discussing Phase 3 designs, right? Obviously, much road to travel still. We just finished the trial. We are already starting to think about those designs, but obviously, that's gonna be between us and the regulators for the time being, but very much our intention to, to progress it forward. As by the way, I take the opportunity, we always have the intention to continue building this portfolio because we know how many indications could be positively impacted by sonelokimab. Regarding the, you know, the, the discussion that essentially started last summer and now came a bit more to fruition with the, with the recent, The New England Journal of Medicine article, signed by obviously those that run the FDA, obviously very exciting for the industry. I think very timely. I think it's important that we start doing ever more trials that, that really use the resources, the time of the patients, the physicians, for the biggest impact that we can have. Yes, obviously, we will be, we will be considering this. Also considering how much we feel there is such a need in axSpA. We obviously, that will, of course, play into our calculation. What I cannot tell you is exactly when we start, when we end, what is the design, how does it compare to BIMZELX or to any other drugs? Obviously, that we'll keep very close to our chest. Yes, we will take the trends. Yes, we will, as always, listen to what the FDA is guiding us to do. Yes, we of course, we're very interested in axSpA, as we are in many other indications. Perfect. The next question, let's move over to the HS section. We have a question here from Brian Abrahams, RBC. Given that MIRA was a large, well-controlled trial done with a similar approach to the VELA Phase 3s, is your expectation that the clinical efficacy data from MIRA would be incorporated into a future SLK label similar to the VELA-1 data? Has FDA given you any indications around this, or should we think about the Phase 2 MIRA data as providing support for the overall efficacy of the drug and the legitimacy of the VELA data, but that the specific results would not be described in the label to the same extent as VELA-1? I mean, I, I'm, I'm happy to answer that, and then you, you can add, Kristian. I mean, obviously, I don't know when the question was asked, but I, I, I think I answered it quite emphatically, right? Brian, absolutely, yes, we expect the MIRA data, as other Phase 2s have been included for many other products, to be put there in parallel. As we put on the screen, HS trial 2, that data to be right there, parallel to, to, to VELA-1. VELA-2, whether the data is there or not, as I said, this is a matter for conversation and discussion that will not impact the fact that our label will be extremely advantageous. Yes, we expect MIRA to be there, as, as, as we, as we painted on, on, on the screen. Obviously, yes, we got guidance that this is the path to go forward, as I also reviewed, when I started my section on HS, with, with recapping what the, the guidance that we've gotten. To Brian and others, this is really why, I, I keep saying that the, the path is so narrow. We have been told what we can use where, what, what has more chances versus not so many chances, and what will really require a conversation, which is... The only thing that requires that conversation in terms of uncertainty, big uncertainty, is really whether VELA-2 is part of that table or not, right? Absolutely, MIRA is expected to, to be there. I don't know, Kristian, if you want to add more. Just two quick things. I think we allowed ourselves today to lay out what our view of a potential label is. It's clear to you that label discussions come with the FDA late in the review process of the BLA. As you heard Jorge saying, we think our interpretation of the FDA feedback very clearly is that we have a left border and we have a right border, and what is in between is what you heard today. What I want to emphasize again is nothing of this is new. When I just look in, in, in I&I, if you look at the label of ruxolitinib, topical in AD, or tapinarof, topical in psoriasis, or risankizumab and upadacitinib in, in IBD, the label table, this famous efficacy table that you talked about, includes Phase 2 and Phase 3. That has been seen multiple times before. Number two, if you look at the label table for Cosentyx in HS, Jorge, you briefly mentioned this, one of the two studies didn't meet the primary endpoint, right? You see all these endpoints there, and then you have an asterisk for those that are statistically significant, and then one endpoint does not have this asterisk. What we tried to share with you today, which is our interpretation of the discussions we will have in a year's time, is that we either have VELA-1 or MIRA, or we have all three, both of which I think would be very good for us because we can include fantastic data. I remind you, that the VELA-2 sonelokimab data is on spot and on par with what we saw with sonelokimab in, in VELA-1. Nothing of this is new. I think you summarized it very nicely in saying, do we have a risk? Of course, we have a risk. Everyone has a risk, right? We will submit the BLA, and the BLA will be reviewed. Is our risk fundamentally different from any other company at this stage? We don't think so. Wonderful. One short question that I'm happy to address directly, Yun Zhong from Wedbush: Is your plan still to include data from VELA-2 into the BLA submission for HS in the second half of 2026 to support a broad label? The answer is yes. The study is running in parallel, and we are planning to seek approval for adult and adolescent HS. HS patients 12 years older, which we also believe is a possible strong differentiator. We talk a lot about the efficacy levels, the benefit-risk profile, the convenience, but let's not forget that most of the patients in HS start to develop first symptoms in their teenager years, and that currently we do not have any drug that has been approved based on a dedicated study in adolescents. Humira, yes, they have approval based on data that they've generated and other indications, but we see very, very high levels of hesitation of prescribers, of parents, of patients, to use a TNF inhibitor in the adolescent population. So we believe this will provide a potential additional differentiator of sonidegib in the market. Just allow me to add one shocking number that we recently saw when we analyzed the claims data. It's 1% of patients with moderate to severe HS adolescents that get a biologic. 1%. Knowing that these are probably the only drugs that can prevent the progression to irreversible tissue destruction, we really, really need to do better in adolescent HS, we will try as hard as possible. One more question on HS. It's from Prakhar Agarwal from Cantor: "Can you comment on safety for HS 52-week and whether it is looking similar or differentiated versus bimekizumab? Specifically, were there any signals of SIB? What about liver enzyme elevations, dermatitis cases, et cetera? Yeah, I'm happy to start here. Obviously, this is data that's under evaluation. I think, Jorge, you shared the one-year efficacy data- Mm-hmm. You could see that just above half of the patients have yet made it to this late time point. I will be very careful in reporting on the safety. All I will say is that so far, earlier statements that we made, that we do not see signals for liver, for example. Mm-hmm. We do not see signals for SIB in our data. That holds true. We will work on this closely together with the FDA, how do we present the safety data, how we analyze this. So far, our earlier statements do not change. Perfect. I see some more questions, one here from Kaveri Pohlman from Clear Street: "Can you provide an update on your commercialization and manufacturing efforts for HS? What initiatives have you undertaken? Is there anything further needed before advancing? Do you want me to start? Sure. I mean, the manufacturing's part I can quickly take out. We've shared a bit about this. I'll share today where we produce our drug substance, which is an FDA-approved manufacturer that also serves other pharmas and other folk doing nanobodies. We have commercial capacity up to year four or five of commercialization, so we're well into the volume that we will require over the next years. I think important, Kaveri, also on the drug product side and then all the distribution, this is already all also at commercial level into year four or five. That's something that we wanted to make sure we tested during all these trials. I mean, we've been providing this drug for thousands and thousands of patients by now. All of that is there. All of that is very mature, FDA-approved partners, but obviously, we'll continue exploring opportunities to second source and manage the U.S. and other regions differently, but all, all in good time. I would say that that's a, a clear checkbox there. Commercial is obviously not yet, not yet a checkbox. We've been working very hard on this, and of course, we've done a lot of pricing, payer, work, organizational structure work, sales structures, commercial strategy, et cetera. Obviously, now it's all of this is starting to come to fruition. I would say, Kaveri, that you should look at Q3, Q4 as the time of the year that we are really starting doing those bigger appointments in terms of those that that will lead the U.S. structure, and then help us establish that commercial structure that will then start towards the end of 2027, hopefully, with the commercialization of the asset. In our experience, we're well in time. We know exactly the folk that we want to hire. Obviously, now in the summer starts the big push, which was always the plan already last year. And I would say that we have... The way I think about it, simply, maybe my CFO will tell me that that's not the right way, but the simple way is we, as you saw, as you heard, we have $400 million in cash. That allows us to run the company, make all these appointments, drive our clinical trials, et cetera. We then also have this pool of $400 million that is available to us to spend and activate as we get closer to market, therefore, lower risk and also already with the contribution of revenues. I think with these funds, we're more than equipped to, to, to set up the machine that, as I, as I said, Kaveri, we want to, to really start with people on the ground as of, as of this summer. Perfect. One last question I have here, again from Brian Abrahams, RBC: "What are your latest thoughts on how you would position SLK commercially? How might you price versus BIMI? Where are you with the development of the commercial subQ injector?" Happy, happy to take this one. I mean, starting maybe with the, with the subQ injector, this one we have run all the necessary studies in terms of human factors studies, PK study to demonstrate bioequivalence. In fact, the auto-injector is being used in our open label extension study on the HS program. Patients right now are using the auto-injector. Feedback is very good, very positive, we expect to go to market with the auto-injector as an approved device for the administration of sonidegib.... pricing versus BIMI and commercial positioning, I mean, this goes a little bit hand in hand because what we see, how the market is evolving and what all our payer research shows is indeed that we will probably look with a more maturing market at a first line that's more leaning towards biosimilars. You see some payers that start to insist on an adalimumab biosimilar being used in the first line setting. With Cosentyx, at some point also going biosimilar, we would expect similar things to happen, so that you have some payers that in the first line will insist on first a biosimilar adalimumab or secukinumab being prescribed. Thereafter, from everything we see and hear, it's pretty much open playing field. We expect to be on par when it comes to pricing and when it comes to formulary access with bimekizumab. We do not believe that there is any real incentive for any of the companies that develop innovative medicines to compete with biosimilar prices. We believe we will be in a very good position. We also think it's actually a very good thing that the biosimilars are there and further help grow the market. I mean, one question that I also saw here, coming in is like, "What will you be doing to support the HS market expansion?" We think that the biosimilar entrance is actually a very important ingredient, that patients get access to treatment, get a first biologic, obviously with the treatments that we anticipate to being used in the first line, TNF inhibitors have not shown any durable efficacy, even in their own clinical studies, also certainly in the real world data, we do see very, very high dropout rates, discontinuation. The KOL supports this as well, that you do not have durable efficacy with adalimumab. With Cosentyx, secukinumab, yes, you do have durable, but you do have efficacy that's more on the lower end, so leaving ample room for patients and, and clinicians to step up to a more efficacious and certainly more efficacious, efficacious IL-17A/F inhibitor, especially when it comes with a favorable benefit-risk profile. I think we are at the end of time. Apologies for not having been able to answer all the questions, we hope that we covered a large variety of this. Thank you very much for joining us here. We hope that you share our excitement for this data update and the future, the catalyst that will come this year. Thank you so much. Have a good day. Thank you. Have a nice day.