Good day, and thank you for standing by. Welcome to the HS Part B Top Line Data Presentation. 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'll need to press star one one on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to speaker today, Tyler Marciniak, Vice President of Investor Relations and Communications for ACELYRIN. Please go ahead. Hello, everyone, and thank you for joining us today. Before we begin, I'd like to remind the audience that today's remarks will contain forward-looking statements, such as those related to the progress of our clinical trials and anticipated data readouts. These forward-looking statements involve risks and uncertainties that could cause our actual results and events to differ materially from those contained in such statements. We urge you to review the Risk Factors section of our Form 10-Q for the quarter ended June 30, filed with the SEC, along with statements contained in today's press release and our slide presentation, which identify certain factors that could cause our actual results, performance, and events to differ materially. Additionally, these statements are based on information available to us today, and we undertake no obligation to update them as circumstances may change. Joining us on today's call are Dr. Shao-Lee Lin, our Founder and Chief Executive Officer, Dr. Paul Peloso, our Chief Medical Officer, and Gil Labrucherie, our Chief Financial Officer. I will now turn the call over to Dr. Lin. Shao-Lee? Thank you, Tyler. Hello, everyone, and thank you for joining us to review the top-line results from our Part B placebo-controlled trial of izokibep in moderate to severe hidradenitis suppurativa. Today, I will discuss the top-line results from this trial and how we intend to apply the learnings from this trial in our continuing efforts to develop izokibep for HS. Turning to the HS Part B top-line results. As we announced in our press release, the primary endpoint of HiSCR75 at week 16 did not meet statistical significance in the primary non-responder imputation analysis. Although the overall study did not meet statistical significance, izokibep appears to be demonstrating consistent, early, and high orders of response without safety or tolerability limitation. Specifically, response rates for izokibep showed early HiSCR100 responses and a clear dose effect supported by both pharmacokinetic exposures and HiSCR responses, favoring 160 milligrams once weekly or Q week dosing. The safety profile was consistent with prior izokibep experience, and safety and tolerability were not dose-limiting. Based on our analyses, we believe statistical significance was impacted by two factors: discontinuation of HiSCR75 to HiSCR100 responders in the Q week arm due to reasons unrelated to adverse events, as well as a marked increase in placebo rates during the course of the study. In a last observation carried forward sensitivity analysis of the data, HiSCR75 did meet statistical significance at week 16. In the course of reviewing the recently unblinded top-line data, we noted that the discontinuations included several responders. The majority of the responder discontinuations were unrelated to safety or tolerability concerns, which is rather unusual, and we performed this analysis to help us understand the impact of those discontinuations. What it showed us, as you'll see shortly, is that the discontinuations mattered and affected the outcome of the study. In addition, a pre-planned, independently conducted week 12 interim analysis demonstrated the potential of izokibep in isolation from the placebo increases observed later in the trial. These data demonstrated HiSCR response rates consistent with the Part A open label results, as well as HiSCR100 responses occurring as early as week 4 and increasing through week 12 to 38% of patients in the Q week arm. The importance of this analysis is twofold. First, it provides a window into izokibep's performance prior to the increase in placebo rates observed later in the study. Second, this was an independent, pre-planned analysis for the Data Monitoring Committee, or DMC, and we were blinded to these results until the time of the primary analysis. Slide 4 is a schematic of the trial design. The trial included both the Part A open label portion, which was designed to inform our internal decision-making, and the Part B dose-ranging placebo-controlled arm. Inclusion/exclusion criteria were consistent with precedent studies for HS. One item to note is that the minimum AN count was changed from 3 to 5 between Part A and Part B based on FDA feedback, which is consistent with other recent and ongoing HS studies. On slide 5, you see the baseline characteristics for Part B, which were balanced across arms and generally consistent with those of Part A and HS trials of other agents. We'll note that the AN count is lower than we anticipated, given the increase in requirement from the inclusion criteria moving from 3 to 5. However, there were more subjects with early stage 3 disease in Part B than in Part A, speaking to the severity of disease captured in this study. On slide 6, you see the subject disposition, which shows balanced randomization across all 3 arms. The study was over-enrolled to account for potential discontinuations, but there were both more discontinuations and importantly, more responder discontinuations, including even HiSCR 75 and HiSCR 100 responders than we would expect. Ordinarily, discontinuations tend to occur due to lack of response or for safety and tolerability issues. We did not see that in this study. It is important to note two things here. First, the majority of these discontinuations occurred for reasons unrelated to safety or tolerability. Second, and as we'll show you soon, these responses were early and deep responders in the Q week arm. As summarized on slide seven, the safety profile for izokibep in this trial was consistent with prior studies and the anti-IL-17A class. There were no reports of inflammatory bowel disease, no deaths, and seven total serious adverse events, which occurred in five subjects, two in the weekly arm, one in the every other week arm, and two in the placebo group. One SAE, which occurred in the Q week arm, was considered by the investigator to be potentially related to study drug. The subject remains in the study and resumed therapy without recurrence. There were no events of Candida in the high-dose izokibep Q week arm, and five events of Candida in total, all mild and affecting the skin. Two of these events were in the placebo arm, and three occurred in two subjects in the Q2W arm. All observed injection site reactions were mild or moderate, with the vast majority being mild. There were two discontinuations due to moderate ISRs, both in the QW arm. There was a lower rate of discontinuation due to ISRs here in Part B compared to Part A, we believe, due to rollout of site and patient education on ISRs. The primary endpoint for Part B was HiSCR75 at week 16, and our results are detailed on slide 8. Note that there was a dose response in favor of weekly dosing over Q2W. Two factors affecting the outcome of the study. First, again, the discontinuation of responders, the impact of which you will see in the LOCF analysis, and secondly, as you can see here, are placebo response rates that are markedly higher than historical precedent. As a company, we're focused on developing new medicines with the potential to make clinically meaningful differences to patients. As such, we perform multiple sensitivity analyses on these data to see if we could understand the true activity and potential of izokibep outside of the surprising rate of responder discontinuations and rising placebo rates. We asked ourselves two questions. One, is the activity of izokibep what we expected? Yes or no. And two, do we see it enough where we would want to move forward in HS? The answer to both those questions was yes. We'll now discuss these additional analyses. We confirmed multiple points to ensure randomization and drug distribution were properly executed, including analyzing PK samples. Slide 9 is a summary of the exposure curves, which illustrate the clear and early separation in drug exposure between the two dosing arms, consistent with the observed dose response. Of interest, we anticipated the exposure of 160 milligrams weekly izokibep in patients with HS, to be approximately 3 times higher than secukinumab 300 milligrams every two weeks on a micromolar basis, and that's exactly where it landed. There is also a higher affinity of izokibep relative to secukinumab for the IL-17A target. As described on slide 10, to better understand the impact of responder discontinuations on the primary analysis, we conducted a last observation carried forward or LOCF sensitivity analysis. What this analysis does is take the last observed data for subjects who discontinued or did not have a week 16 visit and carries that observation through to the week 16 primary analysis time point. In doing so, LOCF analysis provides a better understanding of the clinical response or lack thereof among subjects who discontinued. This is a well-established approach to handling missing data and a standard sensitivity analysis. The LOCF analysis showed statistical significance for HiSCR75 at week 16, underscoring the effect that responder discontinuations had on the statistical significance of the study. The sensitivity analysis is particularly important for this study, as the majority of responders in the weekly arm discontinued for reasons other than safety or tolerability. In the pre-specified non-responder imputation analysis, which was our agreed-upon primary analysis with the agency, subjects who discontinued or missed the week 16 visit were imputed as non-responders, even if they discontinued due to reasons unrelated to study drug and had clinical response. Discontinuation rates for this study were higher than expected, and we tried to understand the potential drivers. As mentioned earlier, we observed a disproportionate dropout of responders in the weekly arm. Slide 11 shows a Kaplan-Meier curve demonstrating time to end of study. What you can see is that subjects on treatment, particularly in the Q week arm, discontinued earlier than those on placebo. You saw on slide 8 that serum drug concentrations do not peak until after week 8. Even shorter-term exposures for some subjects led to clinical response, including HiSCR 75 and above. The vast majority of responders who dropped out did so for reasons unrelated to adverse events. We have not identified a clear pattern for reasons for dropout. There was no pattern suggestive of safety or tolerability issues leading to discontinuation across all arms. In fact, what we also know is if we look at response rates over time, the treatment arms are also seeing response earlier than placebo, including as early as week 4. Slide 12 shows those responses, particularly higher-order HiSCR100 responses separate from placebo as early as week 4 and continue to separate through the course of the study. We see a similar, though slightly delayed trend for HiSCR75 and HiSCR50 responders. Putting these analyses together, we can see that we're seeing early and deep responses with izokibep, and early discontinuations in the izokibep arms, not due to safety tolerability issues. No other clear patterns have emerged. As I mentioned earlier, an independent pre-planned interim analysis was conducted for the DMC. Slide 13 summarizes these data, which we remained blinded to until the recent top-line primary analysis. This independently conducted interim was pre-specified to be an as-observed week 12 analysis. I want to reiterate the relevance of this in that it provides a window into understanding the activity of izokibep at an earlier juncture in the study before placebo rates rose over time. Due to these earlier results relative to the overall study, what you might note first is placebo response rates are much more aligned with historical placebo rates at this juncture in the study. You also can observe the activity of izokibep. You can see in this as-observed analysis, which again, we remained blinded to until the time of the primary analysis, that statistical significance was seen with weekly izokibep in HiSCR 75, 90, and 100. This analysis contributes to our encouraging view of the potential of izokibep. Slide 14 shows the interim analysis compared to our open label Part A. Both were pre-specified to be as-observed week 12 analyses. As you can see, izokibep performed very similarly in these two analyses and in line with our Part B expectations. Slide 15 gives us an opportunity to compare our week 12 interim analysis as-observed data to as-observed week 16 phase 3 data for bimekizumab. Recognizing that this was not a head-to-head study, you can appreciate that absolute and placebo-adjusted rates for izokibep are greater, and izokibep is achieving HiSCR100 levels of response that were not reported for bimekizumab. Slide 16 gives another look at the preplanned interim analysis, this time with responses over time. Of note, the response rates continue to improve and occur as early as week 4 for HiSCR100, increasing to 38% by week 12. Here in slide 17, we show an NRI analysis, which was the analysis performed for our primary endpoint for the overall study, now applied to the preplanned interim week 12 data set. What you see is that even with this relatively small data set, at this early juncture in the study, HiSCR75 response rates approach statistical significance. This is despite imputing the responder discontinuations as non-responders. This tells us that the overall study was well-powered relative to historical placebo rates and highlights the effect of having the placebo rates rise to unprecedented levels during the course of the study and the impact on overall study significance. Slide 18 represents a modified NRI analysis of the preplanned interim analysis. The modified NRI is a component of an approach that is becoming more commonly used called the estimand approach. Described simply, the modified NRI treats discontinuations largely according to the reason for discontinuation. If a subject discontinues due to a safety or tolerability issue, or due to lack of response, or for prohibited antibiotic use, they are imputed as non-responders even if a clinical response is seen. On the other hand, if a responder discontinues or has missing data for other reasons, such as loss to follow-up or missing visit, they are imputed as a responder. This is a more stringent way of handling discontinuations than LOCF, as responder discontinuations due to safety or tolerability or other drug-related reasons are still handled as non-responders. You can see the performance of izokibep within the context of this modified NRI at this juncture in the study, when placebo rates were still at the levels we generally see in HS studies. Again, despite small numbers, the magnitude of response and separation from placebo achieves a high level of statistical significance. It also clearly highlights again the impact of responder discontinuations due to reasons unrelated to safety or tolerability. In summary, the primary endpoint of HiSCR75 at week 16 did not meet statistical significance with the primary NRI analysis. Statistical significance was impacted by the number of discontinuations in the Q week arm, the majority of which were first treatment responders and second, unrelated to adverse events. Statistical significance was further impacted by the unexplained and marked increase in placebo rates during the course of the study to unprecedented levels. The magnitude of impact of responder discontinuations on the primary analysis is well characterized by a last observation carried forward sensitivity analysis... which demonstrated statistical significance of HiSCR75 at week 16. An independently conducted, pre-planned interim analysis allowed us the opportunity to understand the performance of izokibep at a juncture in the study in isolation, relative to the rise in placebo response observed later in the trial. This was not a post-hoc analysis, but rather the full data set at a point in time earlier in the study. This opportunity was critical for demonstrating that izokibep responses appear to be both consistent and have the potential to be clinically meaningfully differentiated. HiSCR response rates of izokibep on an as observed week 12 basis in the pre-planned interim analysis, compared favorably to secukinumab, where dose ordered, consistent with Part A results, and showed HiSCR100 responses as early as week 4, which increased over time to 38% at week 12. Application of a modified NRI approach to the pre-planned interim data set showed high statistical significance, with a placebo-adjusted HiSCR75 of 30% and HiSCR100 of 25% at week 12. Safety was consistent with prior izokibep experience and was not dose-limiting. The early and continued achievement of higher orders of HiSCR, including HiSCR100, demonstrate the potential for resolution of disease with izokibep, especially in difficult to treat tissues such as abscesses and nodules. We continue to learn about the disease, the HS patient population, and the activity and potential of izokibep. Because of the consistent and high orders of response without safety or tolerability limitation, we believe the potential for a clinically meaningful, differentiated therapeutic persists and supports continued evaluation in the ongoing phase 3 trial in HS. There are modifications we are considering to address discontinuations and placebo rates, such as sample size, baseline characteristics, time point, and subject to further discussion with health authorities, endpoint and statistical approaches in our continued efforts to bring izokibep to patients with HS. Before we open it up for questions, I'd like to take a moment to touch on our program, psoriatic arthritis, for which we expect top-line data for our ongoing phase 2b/3 trial in the first quarter of 2024. The primary endpoint in PsA is ACR50. We previously completed a placebo-controlled phase 2 trial, which tested 40 milligrams and 80 milligrams every other week dosing, with a primary endpoint at week 16, assessing ACR50. Our phase 2 trial in PsA was positive and showed statistically significant, clinically meaningful placebo-adjusted results and deepening responses out to 46 weeks, comparing favorably within the PsA treatment landscape. Beyond ACR50, izokibep demonstrated clinically meaningful, differentiated responses for skin improvement as measured by the PASI75 endpoint and enthesitis resolution as measured by the Leeds Enthesitis Index. These clinical responses grew in magnitude by week 46 for ACR50, and also for higher measures of response, including ACR70 and PASI100, both of which are considered to approximate clinical remission or resolution of disease. Our internal PK/PD modeling, summarized on slide 24, suggested that increasing duration of treatment, as well as higher doses, could result in improvement of clinical outcomes. This was shown for duration of treatment by improvements in responses out to 40-46 weeks in the completed phase 2 study. For higher dosing, our ongoing phase 2b trial in PsA evaluates izokibep at both 160 milligrams weekly and 160 milligrams every other week dosing. Enrollment of this trial is complete, and we expect top-line data in the first quarter of 2024. While we remain blinded, we do know that overall discontinuation rates for this study are less than 5% currently. We are also fortunate to be in a strong financial position to fund operations through multiple key clinical milestones, including both the upcoming PsA Phase 2b/3 top-line for izokibep, as well as the proof of concept in thyroid eye disease for lonigutamab, each by end of first quarter 2024. And so in closing, we remain excited to advance our portfolio of programs targeting numerous diseases for which significant unmet needs exist, including the potential for resolution of disease manifestations with izokibep in HS as well as PsA, which is the largest indication we are currently pursuing. And now we are ready to open it up for questions. Operator? Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. One moment for our first question. Our first question comes from the line of Tyler Van Buren from TD Cowen. Your line is open. Hey, guys. Thanks for the presentation and all the detail. I have a couple for you. First one is just, on the regulatory front, what are the next steps with the FDA, and what do you think is the likelihood that the agency accepts the pre-planned interim modified NRI approach for this trial for filing, assuming that the second phase 3 hits its primary endpoint? And then the second question is related. So how do you ensure that early response discontinuations don't occur and the placebo rate is kept in line in the second phase 3 that is- ... already ongoing. You mentioned modifications, so perhaps you could elaborate on those and how quickly they could be implemented? Yeah, so thanks so much for that, Tyler. And, I think your first question was about conversations with the health authorities in terms of statistical approaches. And there, there are a couple of interesting points to make. Our currently agreed upon, NRI approach was actually a bit modified already in itself, in that it took into account different kinds of antibiotics use and how we would handle that. So we, we know that the agency is open to talking about modifications, relative to the NRI approach. You know, separately, one of the reasons that the LOCF analysis was so interesting, is that it has been, an acceptable approach in the past for how we might handle missing data. So I think both of these were therefore important analyses to do, both so we could understand our data set in terms of the impact of those discontinuations, as well as the exploratory modified NRI with regards to, given the knowledge that those discontinuations included in the two-week arm, even a majority of responders, and the majority of those not having been related to adverse events, the importance of exploring a modified NRI. So I think that's the backdrop in which we'll have those conversations with the agency. And you know, obviously more to come, as we talk about that. But with regards to the phase 3 study, and I really appreciate that question and line of conversation, we do think that there are modifications that we can do to address both discontinuations as well as placebo response. An obvious one is that one can talk about sample size adjustments. So currently, our ongoing phase 3 has 125 subjects per arm. If we were simply to power relative to the, you know, sort of new, if you will, unprecedented placebo response rates as well as discontinuations, that comes to about 200 subjects per arm. So that's one thing that one can do. It's not the most elegant, and there are additional approaches. You know, we do know that we had more severe patients within the context of this study from an early stage three perspective, about 40% early stage three. One can talk about adjusting percentages in terms of what we require within the context of who we enroll in the study. And we know that more severe patients, like the early stage three patients, actually have a lower response, placebo response rate, just like when we look for HiSCR 100s, we have a lower placebo response rate. You know, we also can have conversations about definitions of endpoints. So for instance, we know that our drug effect is happening early in terms of our Kaplan-Meiers and time to response. And so one can have conversations about whether or not, for instance, a time to response to achieve a HiSCR 100 would be an approach that would make sense in this instance. All right. Thank you. One moment for our next question. Our next question will come from the line of Akash Tewari from Jefferies. Your line is open. Hi, this is Amy on for Akash. Thanks so much for taking our questions. So we just have a couple. We're trying to wrap our head around the data here. Can you go over the reasons for the discontinuation, specifically, for the patients who are not discontinuing due to treatment or a side effect? And then in terms of the placebo rate, this one seems a little higher than what you've previously reported. So what were the major reasons for discontinuations in the placebo, and how do we think about the high, you know, the discontinuations in the placebo along with that high placebo response that you're seeing? Thanks so much. Yeah. Thanks for that, Amy. So in terms of the reasons for discontinuations, you know, other than the pattern that we are getting, you know, this with the majority of people who are discontinuing in the high-dose arm, as responders, we're actually not seeing a pattern. So we've drilled down to the subject level across arms, and looked at things like baseline characteristics, at sites and geographies, et cetera. And we're really not seeing a pattern at all that we can speak to. Typically, what you would expect is that people are discontinuing because of lack of response. And that's not actually the pattern necessarily that we're seeing here. Really what we can say that we're seeing is this, in the treatment arm, the only pattern that's emerging is this early discontinuations in addition to our early responses. And that's where we are currently in this. With regards to the placebo response rates, you know, we, as we shared with regards to the interim analysis that was conducted for the DMC, there was no increase relative to historical precedents at that time in the trial. By the end of the trial, as you can see in the primary analysis, that placebo rate had doubled relative to historical precedents. And, you know, that's. That's what we understand at this juncture. We really don't have a good explanation for why that should be happening. To be honest, this is the first time in my career that I've seen responders discontinuing without adverse events like this, and also placebo responses sort of increasing in rates during the course of a study to these unprecedented high levels. I think that there is something that we will learn through this about the population, et cetera. From our perspective, what we feel extraordinarily, you know, sort of fortunate about, I suppose, in this context, is that we did have that interim cut early in the study that allowed us to understand the performance of the drug, at least in isolation, relative to the increase in placebo rates, and then also allowed us to apply some ways that would take into account the discontinuations, and hence the modified NRI, you know, sort of analysis that we shared. Got it. That's super helpful. And then just a quick one on the placebo response. I guess, do you think this is kind of a temporal aspect where people may be seeing a kink between week 12 and week 16, or more of a, as you enroll more patients past the interim, maybe... Was there a difference in, you know, the baseline characteristics? Yeah. Any sort of trends you're seeing there would be helpful. That's a terrific question, Amy, and thanks for that, because there is a distinction. I think if you look at, you know, historical trials of others, even, you do see a bit of increase in placebo response between week 12 and 16, for others. But that's not actually what we're talking about here. I mean, you know, that may be a component as well, but really, the increase in placebo response over the course of the study is actually sort of as, month by month, as we're marching through, enrolling patients in the study. Obviously, again, up to the time of the interim cut, we were spot on with regards to historical precedents in those placebo responses, but by end of study, that had doubled. That's what we're talking about as unprecedented from our perspective, and not really understanding at this juncture what was driving that. Great. Thanks so much. One moment for our next question. Our next question comes from the line of Emily Bodnar from H.C. Wainwright. Your line is open. Hi, thank you for taking the questions, and sorry if there's any loud background noise. Are you still evaluating patients out to week 45? And if you are, what are you kind of looking to see in that longer period of time now that you've seen the results from week 16? And are there any changes in the same timeline for the phase 3 study if, if you have to make adjustments, such as enrolling more patients? Yeah, thanks for that, Emily. I think I caught those questions, but if I get them wrong, please interrupt again. So with regards to this particular study and sort of forward moving, you know, we do anticipate to continue this obviously in conjunction with conversation with the health authorities. But that is our plan at this juncture. We think that that will provide us continued important safety information for the drug and the population overall. And in addition, I think it will provide us interesting information with regards to those individuals who are on placebo currently, who or sorry, those individuals who were on placebo, who rolled over at week 16 onto treatment. I think that we would anticipate that those subjects should get a bump with regards to their effect at that time, and that will be interesting to see for that study continuation. I think did you have a second question about timing of the ongoing phase 3 trial. We are, you know, sort of a green go there. We are considering the modifications that we talked about a bit earlier in terms of you know sample size, baseline characteristics, time point, and then again with discussion with the health authorities on endpoint as well as statistical approaches. Those are all things that we think are important potential learnings that we can apply as we're moving forward. We haven't provided sort of overarching guidance with regards to timing. But you know, our intention is to move forward as rapidly as we can because, as we've shared, we believe we have a very interesting window into the performance of this drug, despite the performance of the study. That gives us confidence that what we are looking at is potentially meaningfully differentiated opportunity for us to help HS patients. Great. Thank you so much. One moment for our next question. Our next question will come from the line of Yasmin Rahimi from Piper Sandler. Your line is open. Thank you, team, and I'm really sorry about this, shocking data set. I guess, Shao-Lee, would you kindly comment on the, maybe the integrity or the quality of the sites that were selected in Part B? How much site overlap exists between Part B and the second HS study? That could be really helpful, whether this is just a function of site selection or this is maybe the best sites conducted the study, and it just was puzzling on patient dropping out. Then in regards to the PsA study, I think you noted that currently the discontinuation rates are less than 5%. Could you maybe quantify on how many of the patients have completed, you know, sort of more 12 weeks just because, you know, could it be that discontinuation could happen later during the course of treatment? Just to kind of give us confidence that, you know, the discontinuation was just an anomaly for the HS study and should not occur in the PsA study. Appreciate any color on those topics. Well, really, really appreciate that, Yas. And thank you for the sentiments. You know, we understand that sentiment, certainly. I have to say that we're at a point at this juncture where we've looked at the data, and we feel that everything we've learned about the drug and its performance within the context of this disease state actually has been positive for this study. So we have responses that are exactly in line with what we expected, given our Part A experience. We have a safety profile that I think has answered a lot of the questions relative to what we've been in terms of ISRs not being an issue, in terms of Candida not being an issue. And so we actually feel that we've learned a great deal that is incredibly positive in terms of what this molecule is kind of might do for HS patients. You know, that having been said, your question was about quality of sites and overlap of the sites. You know, and Paul, correct me, but I believe the majority of our Part A sites were actually participants in Part B as well. Is that right? That is correct. Terrific. And then in terms of quality of sites, we think our sites are terrific. So fundamentally, we have some of the, you know, world's leaders within the context of HS across geographies. We can tell you that we've done a deep dive with regards, even site by site, with regards to experience level, with regards to prior participation in HS studies, et cetera, across geographies, and see absolutely no pattern relative to what we're seeing in these placebo rates. I know it's incredibly unsatisfying, but this is some anomaly that happened within the context of, of, you know, post our DMC look. The other question was about potential impact to PsA, and I really appreciate that question because I don't think that there is any read-through to our PsA program, which is our largest indication. I think based on the results that we've seen, have maybe special implications for axial spondyloarthritis, which we intend to move forward with as well. We have, you know, one of the biggest differences between where we were with HS and where we are with PsA, is that we already have a positive, statistically significant, clinically meaningfully different result in our phase 2 trial for PsA at the 80-milligram every other week dose level. And this phase 2b/3 trial that's reading out in the first quarter was really about continuing to optimize that dose, considering our modeling that suggested that dosing higher could continue to give us greater efficacy in these patients, and that seemed like the right thing to do. So that study has completed enrollment. We do expect those results in first quarter, and, you know, that's probably the most granular I can get at this juncture in terms of how far along we are. Thank you so much. Let's jump back into the queue. Thank you, Yas. Thank you. With no further questions in the queue, I'd like to turn the conference back to Dr. Lin for closing remarks. Thank you so much. There was just one thing I wanted to make sure to add, which is that we would really like to thank the patients and clinicians who participated in this trial and helped us to continue to advance our understanding of HS and the potential for izokibep. We really look forward to continuing our efforts to serve those patients. Thank you, all. This concludes today's conference call. Thank you for participating. You may now disconnect. Everyone, have a great day.