Ladies and gentlemen, thank you for standing by. Welcome to Alumis conference call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you would need to press star 11 on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star 11 again. Please be advised that today's conference is being recorded. I would now like to turn the conference over to John Schroer. Sir, please go ahead. Good morning, and thank you for joining us today. Before we begin our formal comments, let me remind you that during today's webcast, we will be making forward-looking statements that represent the company's intentions, expectations, or beliefs concerning future events. These statements represent our views as of this date, are subject to risks and uncertainties, and should not be relied upon as representing our views as of any subsequent date in the future. With me today on the call are Martin Babler, our CEO, and Dr. Jörn Drappa, our CMO. Looking at our agenda today, Martin will begin the call by providing some brief comments on our company, the potential of TYK2 inhibition, and our lead TYK2 candidate, Envudeucitinib. Jörn will then review the ONWARD phase III clinical results, after which Martin will put the data in context of the disease and current treatment paradigm for psoriasis and provide additional comments to wrap up the call. Then we will take questions. I would now like to turn the call over to Martin. Thank you, John, and thank you all for joining us today. We are extremely excited to share these positive phase III results with you today for Envudeucitinib, our next-generation TYK2 inhibitor, and with these data. I could not think of a better way to kick off 2026 for Alumis and our stakeholders. Let me start by briefly summarizing the top-line data, starting with efficacy. Envudeucitinib actually exceeded the results we saw in phase II and delivered a compelling and very competitive clinical profile, demonstrating highly statistically significant efficacy on the primary and all secondary endpoints, and rapid onset in patients with moderate to severe plaque psoriasis. Importantly, skin clearance continued to deepen through week 24, with high 90 and 100 response rates. Envudeucitinib also demonstrated a favorable safety profile and tolerability profile consistent with our phase II program. Additionally, we observed clinically meaningful improvements in patients' reported outcomes related to quality of life and itch. Dr. Jörn Drappa will discuss the data in more detail in a few minutes, but we believe these results are truly remarkable and, compared to previously reported oral plaque psoriasis therapy data, demonstrate leading skin clearance rates. These highly positive phase III data demonstrate that maximal 24-hour inhibition of IL-23 and IL-17 disease-driving pathways can lead to patient benefit, and they begin to highlight just how much of an impact this could have for psoriasis patients, but also potentially in additional immune-mediated diseases as we advance our next-generation TYK2 inhibitors, and today, the Alumis story is really coming into view. For Envudeucitinib, the positive data we shared supports its potential as a new treatment in moderate to severe psoriasis, where there are more than 30 million patients worldwide. Many patients are currently underserved, and the global psoriasis market is expected to be $40 billion by 2030. High-efficacy orals, like Envudeucitinib, if approved, are well-positioned to change the way physicians think about treating psoriasis and are expected to drive this growth. We are also evaluating Envudeucitinib in a potentially pivotal phase IIb trial in SLE, and we plan on sharing top-line data from that program in the Q3 of this year. Additionally, we are applying our next-generation TYK2 approach to our second candidate, A-005, which is a CNS-penetrant TYK2 inhibitor for which we plan to initiate a phase II trial in MS in the first half of this year. With precision-engineered TYK2 inhibitors designed to provide 24-hour maximal inhibition, we believe we are developing differentiated drug candidates that have potential across many immune-mediated disease indications, enabling true pipeline and pill opportunities. We feel that 2026 is indeed a value inflection year for Alumis. It starts today with these phase III results, and we believe will continue as we advance our goal of unlocking the full potential of TYK2 inhibition. As an upstream mediator of pro-inflammatory pathways, including IL-23 and IL-17, TYK2 contributes to the pathogenesis of roughly 20 immune-driven conditions, including psoriasis and lupus. TYK2 as a target has been validated in several immune-mediated diseases in the clinic, and based on our genomic research, we had formulated the hypothesis that maximal inhibition will translate into deeper pathway inhibition, leading to higher clinical efficacy with balanced safety and tolerability. We believe we now have validated this next-generation TYK2 approach with our phase III clinical results. With this backdrop and looking ahead to what's to come in 2026, we believe this year will be a breakout year for Envudeucitinib. The phase III data were the first step in confirming this potential to impact IL-23 and IL-17 pathways and to articulate the resulting clinical benefit, and we'll continue to share more data while we also prepare to file an NDA in the second half of the year. With the SLE trial, we hope to demonstrate Envudeucitinib's potential with the type I interferon pathway, opening up opportunities in several additional indications. Combined, we believe these data sets will set the stage for strategic optionality with our oral TYK2 franchise. With that introduction, I would like to turn the call over to Dr. Jörn Drappa, Alumis' Chief Medical Officer, to take us through more detail of the phase III data. Thank you, Martin. As Martin said, we are very happy to share with you these positive phase III results. Let me first review the ONWARD study design. ONWARD is a global phase III randomized double-blind placebo-controlled clinical program that was designed to evaluate the efficacy and safety of Envudeucitinib in adult participants with moderate to severe plaque psoriasis. In ONWARD 1 and ONWARD 2, more than 1,700 participants were randomized and received in a 2:1:1 allocation, either 40 milligrams b.i.d. of Envudeucitinib, placebo, or apremilast over a treatment period of 24 weeks. Patients in the placebo arm were switched to active treatment with Envudeucitinib at week 16, while patients on Envudeucitinib and apremilast arms continued the treatment assigned at randomization. Following the end of treatment at week 24, eligible study patients had the option to participate in a long-term extension or LTE study called ONWARD 3. The vast majority of patients opted to participate in this LTE study. The LTE also includes a randomized withdrawal period that will help assess durability and maintenance of response. In ONWARD 1 and 2, the co-primary endpoints were the proportion of patients achieving the greater than or equal to 75% reduction in the PASI, the psoriasis area and severity index, and the proportion of patients achieving a static physician global assessment, or sPGA 0/1, which indicates clear or almost clear skin at week 16 compared to placebo. Additional endpoints assess measures of skin clearance, patient-reported outcomes, and safety at weeks 16 and 24 compared to either placebo or the active comparator apremilast. I will discuss those additional endpoints in a subsequent slide. I'm excited to report that both of the phase III trials met all primary and secondary endpoints with high statistical significance. With respect to the co-primary endpoints, superior skin clearance compared with placebo was achieved with a p-value of less than 0.0001, as measured by both PASI 75 and sPGA 0/1 at week 16. Averaged across the two studies, Envudeucitinib-treated patients achieved 74% PASI 75 and 59% sPGA 0/1 at week 16. The placebo-adjusted response rates for the co-primary endpoints were consistent between the two trials. Both of the phase III trials demonstrated rapid responses, with separation from placebo and PASI 90 responses emerging as early as week 4. Envudeucitinib delivered leading skin clearance rates at high threshold measures, and these continued to deepen through week 24, with approximately 65% of patients achieving PASI 90 and more than 40% achieving PASI 100 on average across both trials at week 24. Additionally, treatment with Envudeucitinib led to clinically meaningful improvements in patient-reported outcomes related to quality of life and itch. Importantly, in both ONWARD studies, clear or almost clear skin endpoints, PASI 90, PASI 100, sPGA 0, reached efficacy in the range of biologics at week 24, and the response curves we observed suggest the potential to reach even higher rates beyond 24 weeks. With respect to safety, we were pleased to see that Envudeucitinib treatment was generally well tolerated through week 24, with a profile consistent with our previous phase II program, including our OLE data. Treatment-emergent adverse events. Frequency and severity were similar across studies, with the majority of events being mild to moderate, transient, and responding to standard therapy if required. The most commonly reported adverse events included headaches, nasopharyngitis, upper respiratory tract infections, and acne. No new safety signals were observed. With these exciting top-line data in mind, I want to take a few minutes to review some additional information on the population enrolled into the ONWARD trials, on the study conduct, and on additional endpoints to be presented at a medical conference in the near future. This comprehensive phase III development program enrolled 1,771 patients at 271 study sites in the United States, Europe, and Asia in only 10 months, which I think is a remarkable achievement for a company of our size. When we look at the key inclusion and exclusion criteria, we see this reflects a fairly typical adult population with moderate to severe plaque psoriasis, consistent with many other phase III trials in this population. Patients had to be 18 years or older, with a diagnosis of plaque psoriasis for at least six months prior to screening, a minimum affected body surface area of 10%, a minimum PASI of 12, and a minimum sPGA of 3, both at screening and on day one. Patients with potentially confounding or unstable medical conditions were excluded. This slide describes the demographics and baseline characteristics of patients enrolled into ONWARD 1 and ONWARD 2. Without going through all the numbers, I would like to highlight that approximately 25% of patients had previous treatment with biologics, approximately 75% had an sPGA of 3, indicating moderate psoriasis, and approximately 25% had an sPGA of 4, indicating severe disease. The mean PASI was 20 at baseline, and patients had an average disease duration of approximately 19 years. We look forward to presenting additional phase III results at future medical meetings, including many additional secondary endpoints that we believe will further support differentiation of Envudeucitinib as a next-generation oral treatment in psoriasis. These include additional measures of skin clearance at weeks 16 and 24, patient-reported outcomes relating to quality of life and itch, and exploratory data on special areas such as the scalp, palmoplantar disease, and nail psoriasis. We also plan to conduct a comprehensive analysis of pharmacodynamic markers and biomarkers to see whether any of these are associated with a clinical response. Now, I'd like to put the Envudeucitinib data in the context of the current landscape of approved or investigational treatments for psoriasis. This comparison is for illustrative purposes only, since head-to-head studies with Envudeucitinib have not been performed, and studies can vary across agents. With these caveats, as we look across reported outcomes for approved or investigational oral agents, it is clear that Envudeucitinib has delivered highly competitive and potentially leading skin clearance rates in these phase III trials. This is in addition to consistent and meaningful improvements across patient-reported outcomes and itch, with no fasting requirements in these studies. The three graphs on this slide list PASI 75 responses at week 16, as well as PASI 90 and PASI 100 responses at week 24, which are increasingly recognized as very clinically important outcomes. The blue bars represent the average response rates in the ONWARD program. The light and dark red bars are the rates reported for Icotrokinra in the pivotal advanced one and two trials, and the purple bars represent Deucravacitinib. In summary, the Envudeucitinib phase III results are very impressive and suggest an efficacy and safety profile that corroborates and extends the findings from our long-term phase II study. With rapid responses and broad therapeutic impact across skin clearance and quality of life symptoms that matter most to patients, together with favorable safety and oral convenience, we believe that this represents a true advance in treatment for patients living with moderate to severe psoriasis. With that, I would now like to turn the call back to Martin. Thank you very much, Jörn. Based on the profile that Jörn outlined, we believe that Envudeucitinib presents a very attractive opportunity for patients and healthcare providers, especially given the potentially broad role that next-generation TYK2 inhibition may play across many immune-mediated diseases. The phase III results and strong clinical profile support the positioning of Envudeucitinib as a potential innovative leader in the psoriasis oral therapy space. I'd now like to put these data in context of the broader psoriasis landscape. First, let me provide a brief overview of the disease burden associated with moderate to severe psoriasis. As you all know, this is a chronic systemic disease characterized by red, scaly skin plaques that can itch, crack, and cause discomfort. Despite current therapies, significant disease burden remains for many patients, as symptoms such as itch, pain, and visible lesions persist. There's a real negative impact on quality of life of these patients. They live with physical discomfort and emotional distress, which interrupts daily functioning, social interactions, and emotional well-being. Next, it's important to understand the current treatment paradigm since most patients remain untreated or undertreated. You'll see from the graphic on the right that despite this being a systemic disease, fewer than 20% of patients receive systemic treatment. In fact, only 8% of the diagnosed patients are currently treated with high-efficacy drugs, including biologics. Most patients are receiving suboptimal treatments that provide limited benefit, either with topical therapies that aim to address symptoms or low-efficacy orals. This dynamic leads to high discontinuation of treatment due to lack of efficacy or poor tolerability. 2/3 of patients discontinue current oral therapies within 12 months. Importantly, undertreatment or untreated disease can lead to long-term risk of comorbidities such as arthritis, cardiovascular disease, and other systemic complications. It's clear that psoriasis is undertreated because there haven't been simple, effective treatment options, and that's what we've set out to deliver as a company, as we believe patients deserve more. As we take this a step further and look at the dynamics of the psoriasis market, including prescription patterns, we see a highly fragmented market. Among systemic treatments, physicians routinely use multiple treatment options across brands and mechanisms as patients cycle through treatments that don't work for them, and biologic uptake is limited by high cost, payer restrictions, and administrative hurdles. In light of this, we believe it is clear to see why this is a market with significant opportunity and multiple entry points for differentiated oral therapies. High-efficacy orals are well-positioned to change the way physicians think about treating psoriasis and accelerate growth in what is projected to be a $40 billion market by 2030. I want to briefly share some patient and provider insights that support this belief. Our qualitative and quantitative market research provided some interesting insights about the criteria that matter to healthcare providers and patients. Treatment goals are actually similar among doctors and patients. Skin clearance is the top priority, and safety and symptom control, including itch, also being important. When we drill down into treatment preferences, physicians would like to treat harder and earlier to reduce long-term disease and quality of life impact. They also want simplicity, easy regimens with minimal monitoring and reduced administrative steps. Patients prefer oral therapies that are convenient. 75% would choose an oral over a biologic and desire flexible dosing without food restriction. We believe a next-generation oral treatment that delivers high efficacy in the range of biologic levels, with favorable safety and simple oral convenience, will fill a critical unmet need, and that is what Envudeucitinib has demonstrated across all of these key areas that are important to physicians and patients: leading skin clearance with rapid onset of action, improvements across symptom-related measures, convenient oral dosing with no fasting requirement, and a well-tolerated profile. We believe this is a highly compelling profile that we're excited to take forward with the goal of providing a new treatment option for patients and physicians. We've reviewed the potential significant opportunity in psoriasis. Now, I'd like to provide perspective on the broader opportunity we have in front of us. As I mentioned earlier, through its comprehensive mechanism, TYK2 inhibition regulates several disease-driving pathways. Maximal TYK2 inhibition offers the opportunity to treat a wide range of immune-mediated diseases. Built on significant genetic and clinical validation, we and other companies are demonstrating the value of TYK2 in many of these areas, which support pipeline-in-a-pill opportunities for our TYK2 franchise, Envudeucitinib, and A-005. With maximal TYK2 inhibition for our differentiated molecules, we believe we are well-positioned to play a key role in disease areas that are estimated to be worth more than $180 billion worldwide. Before we end our prepared remarks, I want to point out that we focused on Envudeucitinib primarily today, with good reason. But I'd like to highlight additional value we are creating with advancement of our early-stage pipeline programs. This includes A-005, our CNS-penetrant TYK2 inhibitor that has demonstrated positive phase I clinical data, and is anticipated to enter a phase II trial in multiple sclerosis in the first half of this year. We also have lonigutamab that came to us from our merger with ACELYRIN, and the fourth program that we're planning to put into the clinic this year in our portfolio. We will apply the same rigor and precision approach to these pipeline programs that we applied to Envudeucitinib. Last but not least, I want to reiterate our anticipated Envudeucitinib milestones. For psoriasis, we'll share additional phase III data at an upcoming medical meeting. We will provide long-term data from our program, and we plan to file an NDA in the second half of 2026. Additionally, we are continuing to work on a once-daily formulation for Envudeucitinib. We did successfully identify a once-daily formulation, and while it did solidly achieve a once-a-day PK profile, it did not meet all parameters of our target product profile, so we're continuing this effort. We will provide an update on this as we move forward. We are confident in our current product profile, as fortunately, our market research suggests that 2/3 of patients prefer a twice-daily oral treatment over a once-daily option with a fasting requirement. For SLE, we anticipate phase two top-line data in the Q3 of 2026, and this trial has the potential to be a pivotal trial. As we conclude, on behalf of the entire team here at Alumis. I would like to thank the patients who participated in ONWARD, along with our clinical trial investigators and site staff who collaborated with us on this program. I'd like to acknowledge our entire team at Alumis that has worked tirelessly to advance our pipeline and support all areas of the company. With that, we'll take your questions. Operator. Mr. Babler, and as a reminder to ask a question, please press star 11 on your telephone and wait for your name to be announced, and to withdraw your question, please press star 11 again, and our first question will come from Eric Schmidt with Cantor. Your line is now open. Thanks, and congrats to Alumis team on some game-changing data. Martin, you might be limited in what you can say here, but Takeda did provide us with PASI 90 and 100 data at week 16 on Zazo. Can you give us a sense of how you stack up versus their results? Yeah, I'll let Jörn answer that question. Yeah, hi, Eric. So let me start by saying that it's very important for us to preserve our ability to really present the entirety of the data at a medical conference, and so that's why we didn't release all of the data points today. But what I can say is that our profile in the PASI 75 and PASI 90 and 100 at week 16 was strong. It was on par, and in some endpoints, better than Icotrokinra. And for Takeda, we obviously don't have the precise numbers. They didn't give the exact numbers, but we also believe we are very competitive there. Thank you. And then a lot of emphasis today on itch and quality of life measurements. I guess that's probably the NRS scale that was used in the trial. Can you just confirm that the data were statistically significantly positive on itch as measured by NRS, and whether you think that can make it into the label as well? Thank you. Yes, the data was statistically significant and of a magnitude that has traditionally been used by the FDA to include itch reduction in the label. Great. Thanks, Jörn. Thank you. And our next question will come from Terence Flynn with Morgan Stanley. Your line is open. Hi, good morning. Thanks for taking the questions. Just wondering if you can elaborate in terms of the NDA filing, what's specifically gating there, and then in terms of any interactions you've had with the FDA personnel, if those personnel have generally been consistent post the end of phase two meeting through now, and then also wondering if you can provide us with the discontinuation rate due to adverse events. Thanks so much. Let me start with the last part. So the discontinuation rate for adverse events was very low, in the low single digits, actually lower than in many other comparable trials. With respect to NDA filing, we expect that to happen towards the end of this year. And what's gating in part is that we need to see the randomized withdrawal portion from our ONWARD phase III trial. That is going to help generate the information on durability and maintenance. So we're waiting for that data, and then once that data is available, we will expeditiously file. And your third question, there was really no further discussions with FDA since the end of phase two meeting, but we have obviously had interactions on the statistical analysis plan and submitted that, etc. So the folks on the, excuse me, FDA side that we interact with directly so far have been consistent. We just don't know on the leadership side how high up something like this would go, and there were definitely changes on the leadership side in the division. Thank you. And our next question will come from Thomas Smith with Leerink. Your line is open. Hey, guys. Good morning. Thanks for taking the questions, and congrats on the really stellar data here. Maybe first on efficacy. I know you're saving a lot of the details here for presentation at an upcoming medical meeting, but I was wondering if you could expand a bit on some of the comments with respect to the kinetics of response and the shape of the response curves. Are you seeing any plateauing at week 24, or can you speculate about where you think these PASI 90, 100 response rates could go with longer treatment? Speculate I will not, but what I can tell you is that different endpoints behave differently, right? So typically, you see the PASI 75 plateau earlier than the high-hurdle responses such as PASI 90 and PASI 100. And that is what we've seen in our study as well. So we've seen a plateauing of the PASI 75, but at week 24, the PASI 90 and the 100 are still pointing upwards, and where they will eventually end up, we will see when we have the 48-week data. Understood. And I just asked about lupus, and just wondering how these data impact your confidence on the SLE opportunity and your expectations for the phase IIb data that we're going to see here in Q3? Thanks so much. Sure. Yeah, so I think there's two aspects to highlight here. Number one, obviously, it's very reassuring that we've seen a really nice risk-benefit ratio, and that is encouraging for the SLE program as well. And secondly, I think we have now, beyond any doubt, proven that a higher degree of TYK2 inhibition can result in a meaningful increment in efficacy, and I believe that is likely to be true in SLE as well as in psoriasis. Helpful. Thanks so much, guys. Congrats again on the data. Thank you. Thank you, and our next question comes from Yatin Suneja with Guggenheim. Your line is open. Hey, guys. Congrats on the data. Just a couple of questions for me. I think you did touch a little bit on how placebo performed, but if you can articulate a little bit more, what exactly did you see from placebo on the responder rate? What about Otezla? How was Otezla? How was the performance of Otezla? So that's number one. And also, it seems like you are trying to benchmark data to Icotrokinra, not necessarily the Takeda molecule. So the question is on the mechanism. Can you maybe touch a little bit about what contribution from the interferon arm or the interferon mechanism you are sort of expecting versus the IL-23? Thank you. Okay, so to start with placebo response rates, placebo response rates for most endpoints, especially the higher-hurdle ones, were in line with what has been shown in many other phase III trials in moderate to severe plaque psoriasis. The placebo response rate for the PASI 75 in one of the trials at week 16 was slightly higher than has previously been seen, but for all of the other endpoints, including PASI 90, PASI 100, and other time points, this was well in line with previous responses, as was the response to apremilast for most endpoints. With respect to the mechanistic question, then you were asking about Takeda. So the reason we are comparing mostly to Icotrokinra is that we really just don't have a lot of information on Takeda. They've basically just given quite scant information in their press release, so there's really not much we can say by way of comparison. And then with respect to the mechanistic contribution of Type I interferon, that's a really interesting question. I think that's an area of ongoing research. It is certainly possible that for subsets of patients or particular aspects of psoriasis such as itch, that the Type I interferon pathway may play a role. I think most people believe that IL-23 and IL-17 are the dominant drivers of disease in psoriasis, but I think that's a really important and interesting question to further pursue. And we certainly have plans to have a pretty extensive biomarker analysis to see whether we can make any correlation, for example, between the degree of the Type I axis inhibition and certain responses. Yeah, let me just add a few things. So in terms of the comparison with Takeda, I think Eric also asked the question of we didn't disclose PASI 90 and 100 at week 16. Based on our data and based on what they've released, and as Jörn said, it's really hard to articulate what exactly those numbers are, but we believe that we are as good or better on those endpoints than Takeda based on what they released, if we interpret this right. With regards to interferon and other mechanisms that might apply to TYK2, we do believe that even if you look at the head-to-head trials of an IL-23 and the TYK2 inhibitor that was performed before, there were some endpoints where the IL-23 molecule actually did not statistically significantly beat the TYK2 inhibitor. So we do believe there are certain symptoms and certain efficacy results in our study that show that TYK2 can actually potentially outperform the IL-23-only mechanism. So there seem to be additional benefits that TYK2 can impart on for psoriasis patients. And amongst them, certainly, itch is one of them that has been shown, but we believe that there are others as well. So I think we will understand a lot more about that, and as Jörn alluded, but overall, we do believe the profile is not just a very strong inhibition of the IL-23 pathway, but there are additional benefits that TYK2 could provide for patients, and we'll certainly be happy to share that data in the near future. Thank you. And our next question comes from Derek Archila with Wells Fargo. Your line is open. Hey, good morning, and congrats on the positive data. Obviously, a nice way to start the year. Just a couple of questions for us. I guess first, do you think that NVU's onset of action could be a key differentiator here relative to the other worlds? And I guess the data that you plan to present at a future medical meeting, will you flesh that out? And then I guess the second question is just given the results today, what's your plan to maximize NVU's value? Obviously, you have SLE, you have psoriasis, but does this require partnering? And if so, when would you do that? Thanks. So let me start with the latter question and give a comment on the first one. So in terms of how we're moving forward, we're planning on filing, as we said, in the second half, and we certainly do a lot of market preparation. We currently have a small but mighty commercial team, and we have a group of MSLs already out there. But the best way I can describe it to you, as I just alluded earlier, we believe that we have now the entire IL-23 set of indications open, and we believe that the strong interferon inhibition could lead to opening many indications on the interferon pathway. So the likelihood that we're going to launch as a company on a global level in multiple indications is very small, but we do want to make sure that we are doing the right thing at the right time here. We will prepare or continue to market, prepare the market for this molecule, and then see when and how it is strategically most beneficial to partner this asset. We also believe, based on the data we have, there certainly should be interest for this asset from potential strategic partners. With respect to onset of action, we were actually very pleased to see the rapidity with which clinical responses occurred. TYK2 in the past had a bit of a rap as a slow mechanism. We did not see that in our trials. We had a pretty quick onset of action, and as I said in the presentation, even at week four, we saw a substantial proportion of patients already reaching PASI 90, which is really a pretty quick onset of treatment effect. Yeah. And in terms of mechanism of action, I would just, and speed of onset, I would just make one additional comment, which is for patients, really, there are multiple aspects. One is skin clearance. The other one really is how they feel. And we do believe that one of the aspects that is important to patients, and it's actually the number one symptom they want to resolve, is itch. And given that we have such a strong effect on itch, patients probably feel better faster when you reduce the itching very fast. And so the overall perception of speed of onset is probably not just driven by PASI, but it's driven by additional factors and will present more patient-reported outcome data. But we do believe that actually plays into the perception, at least, of onset of action as well. Excellent. Thank you so much. Thank you, Derek. Thank you. And our next question comes from Brian Skorney with Baird. Your line is open. Hey, good morning, everyone. Let me just offer congrats on really stellar data as well. So there's a mix of clinical data from both TYK2 inhibition as well as IL-23 and IL-17 inhibition out there with various degrees of validation. Sort of having proven out the thesis of potent 24/7 inhibition being able to at least match oral IL-23 and clearly substantially improve upon first-gen TYK2 inhibition, I would assume this would build a lot more confidence on additional indications. So how do you think about prioritization of programs beyond psoriasis and lupus given this data? Where do you think the dollar value is best placed going forward? Yeah. Good question, Brian. I think we're not going to disclose yet exactly what our priorities are, but I think you basically ask a good question in terms of where do we have higher PTS now? And we do believe for the IL23 indications, the PTS just went up significantly. We hope the same will happen in the summer with lupus, where we see that good inhibition for interferon is also possible with this molecule. Certainly, we've already shown that in phase one. We've shown it actually in phase two in psoriasis patients. We now just need to show it in actually an interferon-related indication. And if you look at an analog, if you so want, and you look at SAPHNELO, there's quite a few indications that they're now pursuing on the IL23, sorry, on the interferon axis. But in our minds, the most important step now for the overall TYK2 program is to make sure that we're pursuing high value, but also high PTS indications. At the same time, we have a portfolio behind this that we want to make sure we diversify a little bit, but it is very clear that the majority of our resources will go to probably two key areas. One is to strengthen the psoriasis profile of the molecule with additional work. The other one is into high value, but also high PTS indications that are related to what we already know at this point in time. Great. Thanks, and congrats again. Thank you. Thank you, and the next question will come from Jeff Jones with Oppenheimer. Your line is open. Good morning, guys, and congrats again on the outstanding data here. I think a lot of key questions have been asked. Maybe to touch on SLE, and as you just mentioned, SAPHNELO and other indications, can you provide some thoughts on how this sets you up in SLE, given we don't have Takeda or Ico in that space right now, and how that impacts your confidence? And maybe one follow-up. Yeah. So I think confidence definitely increases for two reasons. Number one, really good safety. That's always reassuring. And hopefully, it will also apply to the SLE study. And number two, really prove that a higher degree of TYK2 inhibition can result in higher efficacy. And so I don't really see any reason why that would not also apply to SLE. So these are basically the thoughts. These are obviously very different diseases that are driven by different pathways. And so there's not a direct read-through from psoriasis to SLE, but I do think that confidence in the molecule, in its potency and its safety, is overall substantially increased after this set of results. Yeah. Let me just add to the answer from the commercial side and the business side. We do believe that SLE really could use an oral therapy that is safe, well-tolerated, and efficacious. We do see the same result in market research that SLE patients actually prefer simplicity and having a molecule that has a safety profile like we've seen so far in our psoriasis studies for SLE, but that also is efficacious, we believe, is extremely attractive. As you pointed out, there's not a lot of competition so far in SLE. There are some other orals that are in clinical studies right now, but we do believe that is a very significant opportunity with less competition, but also with a lot of unmet need. I think the fact that Safnello, as the interferon inhibitor, is growing by leaps and bounds right now, and eventually probably will reach at least $1 billion in sales, is a good indicator of what a molecule, an oral molecule, simple to administer could be in those indications. And then the other piece for us really is that the lupus results will open up or could open up a lot more diseases on the interferon side that are very attractive. If you just think about Sjogren's as one of them, that's a huge market, a huge unmet need, and we do believe that there's a really good rationale, both genomically and scientifically from a biology standpoint, that a molecule like this could benefit those patients as well. Great. Appreciate it. And then, just the last question on the BID to QD dosing, obviously still in progress. Any feel for when you might have an update there and how that fits into the regulatory strategy? Yeah. So let me start by just citing our market research again. So we did actually ask more than 400 patients whether if they had the choice between a once-a-day drug that has a fasting requirement or a twice-a-day drug that has no food restrictions, 2/3 of patients actually prefer a twice-a-day with no food restriction. And so that actually was part of what drove ultimately our decision. We have a formulation. It has the PK profile that we desired, but there are other parameters that we set to make this successful in a competitive market, and we didn't hit one of them. And so we decided to continue to do that. Our plan originally was to have this formulation within the first year of launch. We certainly are still working towards that, but this will be very, very tough to do. Our goal is to have that formulation as fast as possible. Once we have more information, we will update on that. We do believe with the data we have currently, we have a competitive molecule. Our market research also suggests that there's other aspects that certainly play into this, and BID is viable. We continue to work on this and will update as soon as we have more information and have a clear timeline. Great. Thank you very much, guys. Thank you. Thank you. As a reminder, to ask a question, please press star 11 on your telephone. The next question comes from Mitchell Kapoor with H.C. Wainwright. Your line is open. Hey, team. Again, big congrats on this data. This is really big for patients. A few questions. I wanted to ask firstly, it seems broadly on both ONWARD trials, the results were similar across both trials. Could you just comment on any differences that have shown up between trials and specifically were PASI 100 results similar between trials? And then with those patients who had reached PASI 75 by week 16, would you characterize the majority as eventually converting to PASI 90 or PASI 100 with continued dosing? So start with the first question. Yes, the results were broadly similar between the two studies. So as I alluded to, one of the differences, that in one study, the PASI 75 placebo response was a little bit higher. But so if you basically eliminate that by doing a placebo-adjusted response, they were exactly the same between the two trials. And those differences between the trials diminished the more you look at high-hurdle endpoints such as PASI 90 and PASI 100. Those were actually highly consistent in between the two studies. And I'm sorry, what was the second part of your question? Yeah. The second question there was the patients who had reached PASI 75 at week 16, would you kind of characterize the majority of those who reached that PASI 75 at that week 16 time point as eventually converting to PASI 90 or PASI 100? We haven't done the analysis in exactly that way that you asked, but what we can say is that by week 24, the majority of patients actually reach PASI 90 at the very least, and so yes, many of the patients who will have a PASI 75 at week 16 will go on to have deepening responses and eventually reach PASI 90 and PASI 100, but we haven't done the breakdown exactly in the way you suggest by looking only at the proportion of patients who reached PASI 75 at week 16 and then breaking it down. Okay. Great. And then just one final one, if I can. If you look across the competitive landscape with kind of the limited data that we have, could you comment on any particular ways that you're looking at the data versus how other competitors might in terms of modified non-responder analysis or anything particular that we may should pay attention to as conferences come about like AAD? So I think the statistical methods we're using are pretty much industry standard. So there are subtle differences in ways that you impute missing data, and it's always important to look at the details on how exactly this is done. But in general, the way the endpoints are analyzed with non-responder imputation, modified non-responder imputation are quite similar in between different phase III trials. But in this trial, we used very conservative non-responder imputation methods. Great. Thanks again, and congrats again. Thank you. Thank you. I show no further questions at this time. I would now like to turn the call back to Mr. Babler for closing remarks. Thanks, everybody, for your questions and for joining us today. We truly believe that 2026 will be a value-inflecting year for Alumis, and we look forward to sharing additional progress across our pipeline with you this year and share these data in an upcoming medical meeting. And so thank you for joining us, and have a good rest of your day. This concludes today's conference call. 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