Good morning and welcome to Apogee Therapeutics conference call. At this time, all participants are in listen-only mode. There will be a question- and- answer session after the prepared remarks. Please be advised that this call is being recorded at the company's request. I will now turn the call over to Noel Kurti, Vice President of Investor Relations at Apogee. Noel, you may begin. Thank you, operator, and thank you all for joining us today. During this call, we'll be making forward-looking statements related to our current expectations and plans for the company, as well as our clinical and preclinical programs. These statements represent our views as of this date and should not be relied upon as representing our views as of any subsequent date in the future. Looking at our agenda today, CEO Michael Henderson will begin the call with an introduction to today's Phase II APEX Part A, 16-week data readout, and goals for the program. Chief Medical Officer Carl Dambkowski will then walk us through the Part A results, followed by Kristine Nograles, Senior Vice President, Head of Clinical Development and Medical Affairs, sharing next steps in our development program for APG-777. Before moving on to the Q&A, Michael will summarize our vision for building a leading I&I company. The subsequent Q&A will be led by Michael, Carl, Apogee Therapeutics CFO Jane Pritchett Henderson, and Chief Commercial Officer Jeff Hartness. I'll now turn the call over to Michael. Thanks, Noel, and thank you all for your time today. We are thrilled to be able to share what we believe are truly fantastic results from the Phase IIA APEX study for APG-777 and atopic dermatitis, the next step of our ambitious journey to rapidly bringing APG-777 to patients. This is a landmark moment for the company, as APG-777 met or exceeded all key objectives of the study. With this data, we believe we now have a clear path to a potentially best-in-class therapy across many dimensions, including a quarterly or better dosing interval and potentially improved efficacy results versus approved agents. In a moment, we will dive into the data. First, I want to highlight that the next several quarters are expected to deliver multiple data readouts for Apogee Therapeutics. We expect to have the maintenance data from this study in the first half of next year. Thanks to strong enthusiasm from patients and physicians leading to faster-than-expected enrollment, we are accelerating the readout of Part B of this study, which is testing even higher exposures of 777 with data anticipated in the middle of next year. We expect this acceleration of APEX Part B will enable us to start our Phase III studies next year, potentially accelerating our timeline to a BLA. We have now dosed the first patient in our proof of concept study, testing our combination of IL-13 and OX40 ligand in a head-to-head study against the market leader, Dupixent, one of the largest drugs in the world. As you will see, the results we present today further reinforce our excitement for our combination of the two most active biologics mechanisms, and we are currently on track to deliver these results in the second half of next year, right after the APEX 2B. The APEX study met or exceeded all of the objectives we had previously set out to accomplish, demonstrating deep and rapid results on measures of both lesion severity as well as itch. We demonstrated compelling efficacy results and statistically significant outcomes across the endpoints of interest, along with a favorable safety and tolerability profile, consistent with what has been previously shown with this class of medicines. We developed 777 in order to test two key hypotheses. First, that we can engineer 777 to deliver the same pharmacology as lebrikizumab, but at an every three or every six-month dosing schedule, supported by our 77-day half-life. Second, if we can further increase the exposure, we can improve on and maximize the clinical efficacy observed with this class of medicine. Today, we present our first clinical data that we believe convincingly supports both of our key hypotheses. Whether we look at measures of lesion severity, such as Easi-Change from baseline, EASI-75, or IGA 0/1, or measures of itch, APG-777 demonstrated at least comparable benefits to lebrikizumab and Dupixent, yet with only half as many injection days. To emphasize how exciting these results are, two out of every three patients that received our drug reached an EASI-75, a remarkable readout for the field. As you'll see in a few slides, those patients who saw higher exposures experienced an even greater benefit. More than ever, we are excited for the readout of APEX Part B, where we are testing a higher dose that we believe will allow a greater proportion of patients to achieve the exposures we found to be most efficacious in the results we're presenting today. Our Part B readout testing these higher exposures has now been accelerated, with a readout expected in the middle of next year. We couldn't be more pleased. 777 delivered, and we believe we now have an opportunity for an upside case with a clear path to a potentially best-in-class medicine that reshapes the treatment landscape for patients and physicians. We have a unique opportunity with 777 to potentially transform the future $50 billion atopic dermatitis market. You've seen this map before, showing the white space that exists. Our data today affirms our prior belief that we can deliver a potentially best-in-class drug that improves on standard of care across both dosing and efficacy. The white space between us and our competition here speaks for itself. While we are thrilled with the Part A APEX results, we are always thinking about how we can continue to innovate for patients. If anyone is going to beat us, we want it to be ourselves. We have two ongoing studies with data coming in 2026 that could show even more promise than today's results. First, our Part B trial testing a higher dose range includes an even higher exposure arm of 777. You will see in a moment why we are so excited we included this higher dose. Second, our combination study of 777, our IL-13 inhibitor, and 990, our OX40 ligand inhibitor, is being run head-to-head versus Dupixent, again, one of the largest drugs in the world. This is the first study of its kind combining two of the most promising orthogonal mechanisms for biologics to continue to drive to higher and higher efficacy. All of our programs maintain a quarterly or better dosing profile with the goal of ensuring compliance and persistency and improving quality of life. I'll now hand the call over to Carl to walk us through the data in more detail. Thank you, Michael. I have the great privilege today to share the paradigm-changing results from APG-777 in moderate to severe atopic dermatitis. These results are specifically from APEX Part A, which enrolled 123 patients with moderate to severe atopic dermatitis as defined as having an EASI of 16 or greater, a vIGA of 3 or greater, and a BSA of 10% or greater. Patients were randomized two to one to receive either APG-777 or placebo. Patients assigned to receive APG-777 got an induction regimen of 720 milligrams at weeks zero and two, followed by 360 milligrams at weeks four and 12. As a reminder, this regimen was designed to have approximately 30%- 40% greater exposures compared to lebrikizumab. It is worth noting that 777's induction regimen requires just four dosing days compared to nine for lebrikizumab and Dupixent, representing a more than 50% decrease in injection days. With fewer injections and higher exposures, it offers a simple, convenient start for patients while potentially maintaining or improving clinical outcomes and transforming the treatment paradigm. Baseline characteristics and demographics outlined on this slide were generally well-balanced and in line with expectations for this patient population. Least squares mean percent change from baseline in EASI score was the primary endpoint for the study. We met this primary endpoint at week 16 with a high degree of statistical significance, showing both a substantial absolute percent change from baseline, greater than 70%, as well as a substantial placebo-adjusted effect, surpassing those observed in the registrational programs of Dupixent and lebrikizumab. Moreover, lesion reduction was rapid after APG-777 treatment, showing significance as early as week two. EASI-75, measuring patients who achieve a percent change from baseline in their EASI score of 75% or greater, is the endpoint in atopic dermatitis that physicians cite as the most important for comparing efficacy and communicating with patients. With APG-777, 2/3 of patients, or 66.9%, showed an EASI-75 response by week 16 and a placebo-adjusted rate of 42.5%. No other biologic has demonstrated higher response rates, both on an absolute basis or a placebo-adjusted basis, in a global placebo-controlled 16-week study. To put the magnitude of this result into context, here you can see a non-head-to-head comparison of APG-777 to other agents, including Dupixent and lebrikizumab. APG-777 stands out with absolute data greater than 15 percentage points above current standard of care and improvements in placebo-adjusted EASI-75 as well. We believe this result will be very compelling for patients, physicians, and payers, especially when being delivered by a biologic with the potential to be dosed substantially less frequently. IGA 0/1, which measures changes in IGA score to zero or one with at least a two-point decrease from baseline, is a key secondary endpoint for the study. Here, APG-777 was statistically significant as early as week four and maintained throughout. Our absolute results and the curves over time are highly consistent with leaders in the field. Similarly, EASI-90, measuring patients that achieved a percent change from baseline on their EASI score of 90% or greater, showed statistically significant changes with consistent absolute results to leaders in the field. Itch is a bothersome symptom for patients suffering from atopic dermatitis. Patients want both fast and deep itch relief. APG-777 showed both, with statistically significant decreases in itch as early as week one after starting APG-777 and showing a more than 50% decrease from baseline at week 16, which is comparable or numerically superior to competitors, including lebrikizumab with topical corticosteroids. Notably, this result for APG-777 was without topical corticosteroids. We conducted several additional analyses around EASI-75 to understand the robustness of the result. We used an as-observed analysis, which does not treat rescue medication users as non-responders, like in our primary analysis. Regulators often look and ask for this analysis to ensure the robustness and consistency of the results. Here, the results are even more impressive, with an almost 75% absolute EASI-75 responder rate and an almost 50% placebo-adjusted rate. Fortunately, Dupixent performed the similar sensitivity analysis method, which is provided as a non-head-to-head comparison. For clarity, lebrikizumab data is not publicly available for this analysis method. In this pre-specified analysis, we also looked at efficacy in subpopulations of patients that were either moderate or severe at baseline, as defined by their baseline EASI score. We saw very consistent results regardless of baseline EASI score. It is encouraging to see a robust efficacy result in both subgroups, including those with severe disease. To examine the exposure-response hypothesis, we were testing in APEX Part A and continue to test in APEX Part B. We performed a post-hoc analysis to look at the relationship between exposure and response. Exposure quartiles were constructed based on average APG-777 levels during the induction period. A consistent exposure-dependent relationship was seen across relevant endpoints, with higher exposure quartiles showing the most robust efficacy results. Notably, in the top exposure quartile, 17 out of 19 patients achieved an EASI-75 response, and their exposure approximates the average exposure of the top dose we are testing in APEX Part B, now with an accelerated readout planned for mid-2026. APG-777 had a promising safety profile and was well- tolerated. IL-13 inhibition is a mechanism with a well-established and favorable safety profile, which was seen from APG-777 as well. Overall, the rate of treatment emergent adverse events was lower in APG-777 exposed patients compared to placebo. The most common adverse event is non-infective conjunctivitis, a well-described adverse event for the class. The only other two adverse events occurring in 5% or more of patients are upper respiratory tract infection and nasopharyngitis, both numerically lower for APG-777 exposed patients compared to placebo. Conjunctivitis is a known benign adverse event that has been seen with all agents in atopic dermatitis that target either IL-13 or IL-4 receptor alpha. For APG-777 patients experiencing conjunctivitis, none discontinued, adjusted dose, or interrupted dosing. The vast majority of cases resolved while patients remained on drug, with just 3.7% of APG-777 exposed patients having ongoing conjunctivitis at week 16. Cases were also short in duration, with a median time of 29 days. Similar to lebrikizumab and Dupixent, we did not observe any evidence of a relationship between exposure and conjunctivitis. Importantly, for APG-777, there were zero injection site reactions in the study. Injection pain, swelling, and redness can be a reason patients decide to discontinue taking their medication, and for Dupixent, it was the leading cause of discontinuation in some studies. The fact that we saw zero injection site reactions for APG-777 in this study further enhances the potential decrease in injection burden for APG-777, having just four dosing days over the induction period and potentially only two to four doses per year in maintenance. In conclusion, APG-777 demonstrated a promising safety profile and was well- tolerated, as expected, based on mechanism. Now I'll turn it over to Kristine Nograles, who will discuss the APG-777 development program, starting with the maintenance portion of APEX Part A, where we are testing every three and six-month dosing of APG-777. Thanks, Carl. I am really excited about these results and look forward to our next clinical readouts. First, for APEX Part A, where we are testing every three and six-month maintenance dosing, and second, for APEX Part B, where we are testing even higher exposures compared to Part A. Our next major readout for APEX Part A will be for the week 52 time point, where we are testing maintenance dosing of every three and six months. Patients on APG-777 who complete the induction period are randomized one to one to receive either 360 milligrams of APG-777 every 12 weeks or every 24 weeks. Patients who received placebo during the induction period will receive APG-777 in the maintenance period. The week 52 data for Part A are expected in the first half of 2026 and could confirm the potential for best-in-class dosing of every three months or better in the maintenance setting. Before we move on to discuss APEX Part B that is currently ongoing, I would like to reiterate the highly differentiated characteristics of APG-777. Not only do we believe that we have a well-tolerated agent with a very promising safety and efficacy profile, we can potentially reduce the injection burden to as few as two to four injections per year in the maintenance setting. This represents approximately 70%- 90% fewer injections compared to current standard-of-care maintenance dosing. This alone would represent a huge improvement over current standard of care. We know from conversations with patients, caregivers, and physicians that they want fewer injections, and now we have the potential to deliver that without compromising on efficacy or safety. As a reminder, the APEX study was designed to be an operationally efficient two-part study that integrates both proof of concept and dose optimization components. Part B, which has been enrolling since earlier this year, is the placebo-controlled dose optimization component with a planned enrollment of approximately 280 patients randomized evenly to high, mid, or low-dose APG-777 versus placebo. As you can see here, our Part B high dose is testing higher induction exposures compared to Part A and is modeled to have 90%- 100% greater exposures than lebrikizumab. It is also similar to Part A quartile four that showed the best clinical responses in the exposure-response graphs that Carl described earlier in the presentation. We think this gives us the best chance to ensure we are not leaving any efficacy on the table prior to going into Phase III. The primary endpoint of Part B is EASI-75 at week 16, and the secondary endpoints include EASI-90 and IGA 0/1 at week 16. We initiated enrollment for APEX Part B shortly after we completed enrollment in Part A, and due to strong enrollment and enthusiastic support from sites, we are pleased to share that APEX Part B is currently ahead of schedule. This enables us to accelerate the planned APEX Part B induction readout to mid-2026. I'll now turn the call back over to Michael to discuss our plans for building a leading I&I company. Thank you, Kristine. I want to use this slide to remind everyone just how important and de-risking we believe this data is for our long-term success. On the left, you can see the correlation between Phase II and Phase III efficacy in third-party atopic dermatitis trials. There is a very strong relationship, and historically, 100% of programs with positive Phase II data have had successful Phase III trials. Interestingly, the historical data tells us that key efficacy endpoints actually improve on average from Phase II to Phase III for other agents, giving us high conviction and reproducibility. As a reminder, many of the comparisons we've walked through today are for our Phase II data versus competitor Phase III studies. We look forward to kicking off our Phase III studies next year. We are thrilled with the results from APEX and are excited to continue executing and build on these results as we push to advance the field and patient care even further. It has been a great start to the year for Apogee, and we think next year could be even more impactful. We are encouraged by the strong momentum in Part B of the study and are looking forward to confirming the profile seen today while also testing a higher dose that matches the highest exposure from Part A. With those results in hand, we plan to initiate our Phase III program next year, subject to regulatory alignment. We also are looking forward to reading out our combination study, which is currently dosing patients and being run head-to-head versus Dupixent, another opportunity to deliver even further differentiation for atopic dermatitis patients. Lastly, we have additional respiratory products progressing through early studies that we are also planning to advance and look forward to Phase I data for our T-slip program later this year. This is a landmark day for Apogee. With the Part A APEX data in hand, we have now demonstrated a high degree of differentiation from our competition. This gives us the opportunity to transform the standard of care and the future of a $50 billion atopic derm market. There is a lot more that we are excited to do with 777, as well as with our broad immunology pipeline. We're looking forward to many additional readouts over the coming quarters to continue to deliver potentially best-in-class medicines across a wide range of I&I disorders. I will now hand the call back over to the operator to begin Q&A. Thank you. Thank you. We will now begin the question and answer session. At this time, I would like to remind everyone, in order to ask a question, press star, then the number one on your telephone keypad. We will pause for just a moment to compile the Q&A roster. Your first question comes from the line of Seamus Fernerndez with Guggenheim. Your line is open. Thanks very much for the questions. First, let me just extend my congratulations to the entire team for really a phenomenally executed clinical program and very comprehensive data analysis here. In terms of just a couple of questions that we're getting from investors this morning, can you just help us understand a little bit of the dynamics with the placebo between weeks 12 and 16? It looked like there was a bit of a rise there for the IgA 0/1. I'm just interested to know what impact that may have had and how that can be managed in the full Phase III clinical program. It looks, though, that the EASI-90 really kind of may disabuse folks of a concern there just because of the strength of the EASI-90 data that obviously looks extremely strong there. As it relates to the exposure-response relationship, can you just remind us what the magnitude of exposure was predicted to be in Part A versus lebrikizumab? In this study, it sounds like you're clearly pursuing a much higher potential exposure to really pursue that exposure-response relationship in the Part B section. I just wanted to clarify what that relative exposure was in the Part A induction versus what we're likely to see in Part B. With those questions, I'll jump back in the queue. Great. Thank you, Seamus. Really appreciate the questions and the congrats. On the placebo kind of week 12- 16 and IgA, I'll hand it to Carl, and then we'll jump to the second question on exposure response. Yeah, sounds great. Again, thanks for the question. I think obviously we're really excited about the data across the board, with really standout results in EASI-75, but also across other time points. As this is a smaller proof of concept study, we see a couple interesting small data points: IgA placebo rate, not necessarily absolute, but placebo rate at week 16 being one of them, where we saw a big jump between week 12 and week 16 in the placebo rate. I think that's probably really attributable to the small n of the placebo arm in this study and random fluctuations there. If you look over the whole time course of IgA, you can see at week 12, really stellar results there, above 35% on IgA on an absolute basis and approaching 30% on a placebo-adjusted basis. Over the whole course of the 16-week period, we're tracking with lebrikizumab at some time points slightly better than them, and at some time points just minor numerically different than them. I think that's really due to the small size of the study. As we move not only from Part A to Part B, but eventually to Phase III trials, I think there's two components in Part B of this study that will really help with that, which are one is the placebo arm, which is almost twice the size in Part B. I think that's an important factor. Secondly, the distribution of countries and sites that we're using in Part B has a much more European focus. For Part B, we're adding over 40 more sites in six additional countries in Europe, which has historically had the lowest placebo rate. We think both of those will be important factors moving forward. Yep. On your second question around kind of the exposure response, this is a key hypothesis that we wanted to test from the beginning. Our kind of view is that differentiation on dosing would be transformational for the field. With this Part A, we tested 30%- 40% higher exposures than what lebrikizumab is labeled for. I think that we're seeing, especially on the more sensitive endpoints, change from baseline EASI and EASI-75, which is what 70% of physicians look for on an absolute basis to guide their decision-making. We're seeing really exciting results that get us excited that we have dosing and efficacy on the table. It was important for us throughout to make sure that we're running the proper experiment and fully testing what is the full range of exposure response for IL-13 inhibition. In the Part B, the mid-dose is the Part A dose, that 30%- 40% higher exposure, and the top dose is 90%- 100% higher exposure. Importantly, that is roughly equivalent on a C average basis to what that quartile four showed in the exposure response data that we put up. We know from FDA, we know from EMA that there is an exposure response for IL-13 from the review documents. This is our first chance to have the richness of the data from our own study. We find it just very, very provocative. We're very excited now to be testing that higher quartile four exposure in both the Part B of the ongoing study top dose, and that's also the APG-777 dose that we're testing along with OX40 ligand in our combination head-to-head versus Dupixent. Thanks again. Your next question comes from the line of Akash Tawari with Jefferies. Your line is open. Hey, thanks so much and great results here. A few questions on my end. On the exposure response you saw in your trial, roughly what were the weight cutoffs for the quartiles, and how surprised were you to see that kind of jump in IgA for quartile four? Was there something unique about its baseline characteristics, perhaps severity that could have driven that benefit? Maybe stepping back also, can you comment on baseline severity and geographic variability for the trial overall? It did look like placebo came out a bit higher than I think what we had internally expected. Finally, when we're thinking about that Phase II head-to-head against Dupixent for next year, do you think OX40 will be additive on the more stringent endpoints like EASI-90 and the IgA 0/1 when combined with IL-13? Thanks so much. Thanks, Akash. Appreciate the questions. In terms of the exposure response to the weight cutoffs, do you want to take that one first, Carl? Yeah, happy to, right? The exposure quartiles that we showed were constructed purely based on the APG-777 average exposure levels over the first 16-week period. Not necessarily any weight cutoff. However, I think Akash, as you're pointing to, there is an inverse relationship between exposure and weight, meaning as weight decreases, exposure increases for us, but just monoclonal antibodies in general. We do see quartile four has a lower weight on average than the overall study, but that's really just related to the exposures we're seeing in those patients. As you expand from quartile four to quartile three as well, which also showed really strong results, especially in% change from baseline in EASI and EASI-75, you see quite a distribution of weight across there. On your second question related to that, which was baseline severity across the quartiles in terms of exposure quartiles, we see a really nice distribution or similarity in our severity across those quartiles. If anything, quartile three and quartile four had slightly more severe disease on a baseline EASI basis, so a couple points higher than maybe the lower quartiles. Nothing significant, but maybe slightly higher baseline severity in those top two cohorts. Yep. I think what was important to us was to see the kind of the sensitivity analysis that we ran show for EASI-75 that we're seeing really robust responses both in the kind of moderate and the severe population, right? In fact, an improved placebo-adjusted response in that severe population. On your third point, where will OX40 ligand help with regard to the endpoints, I think we're still digesting this data, and we're excited that our combo is headed. We have a lot to kind of just digest when we think about what that quartile four looks like on the deeper endpoints as well. We're seeing the quartile four monotherapy of APG-777 get to JAK-like numbers even ahead of JAKs in some of these endpoints. I think as we think about, are we thinking about more rapid responses, deeper responses, kind of across IgA, 90, but also 75 itch, I think that we're just excited to be running the study so that we can find out. The nice thing is that next year, we'll get both the Part B high dose results and those combo results in a pretty short amount of time. As we said during the call, we're already excited about the monotherapy results that we had today for the Part A. If anybody can improve upon these results, we want it to be us. Your next question comes from the line of Tyler Van Buren with TD Cowen. Your line is open. Great, thanks. Good morning, guys. Congratulations on the tremendous data package. I have a couple for you. Given the data, is there a hypothesis as to why APG-777 might be significantly better on itch than Dupixent and lebrikizumab? The similar rate of conjunctivitis to Dupixent at week 16 is encouraging, but how would you expect the incidence of that adverse event in particular to evolve with much higher exposures in Part B? Great. Thanks, Tyler. I appreciate the questions. In terms of triple seven on itch, I think that when you look at our exposures, and if you were to overlay the curves and encourage folks to overlay our curves versus others kind of across the endpoints, I think it tells a very compelling picture beyond just kind of the week 16 numbers as well. On itch in particular, we see when our exposures are highest with the Part A regimen, right in that first four weeks when we're really 50% - 60% higher versus a 30%- 40% higher on average, we're seeing a really nice and rapid decrease in itch. I think that we're getting patients as early as week one to have a statistically significant impact on weak itch, and I think that it is a function of the higher exposures that we're seeing. Of course, tampering down itch quickly helps with lesion reduction to follow. In terms of the conjunctivitis rates and kind of what we're seeing there overall in the exposure, I'll hand it to Carl. Yeah, great question. We looked at this too in terms of the exposure-conjunctivitis relationship for APG-777 and saw no exposure-conjunctivitis relationship. In fact, quartile four seems to have the lowest rates of conjunctivitis among all the quartiles too. This is really similar to what we've seen previously with lebrikizumab and Dupixent (dupilumab) data, where there doesn't seem to be any relationship between exposures and conjunctivitis. That's been called out in multiple places. As we move forward, testing this higher dose with really, I think, strong data from the exposure response analysis we did, as well as other supporting data, we don't necessarily expect to see any difference in conjunctivitis or other AEs in Part B. Your next question comes from the line of Alex Thompson with Stifel. Your line is open. Good morning. Let me add my congratulations on the data. I guess now that the next major update here will be your maintenance data at 52 weeks for the Phase IIA. I wonder if you could kind of give us a little sense of putting that data into context and how we should think about what good looks like for that update. More broadly, as you digest these data, how are you thinking about this in the context of other indications like asthma or EOE? What's the read-through there? Thanks. Yeah, thanks, Alex. Appreciate the congrats and the questions. In terms of maintenance and what good looks like, I think we think that lebrikizumab has very strong maintenance data, both maintenance response on EASI-75 and IGA 0/1. If we can see something in the ballpark of what they see with our ongoing maintenance study, we would be very happy. We're talking 80%- 90% maintenance on different endpoints in some cases. I think, importantly, when you compare their maintenance data to Dupixent, I think people are seeing this in the real world. It is stronger. If we can approach what they're doing, we would be very happy. In terms of other indications and how we're thinking about developing the full pipeline and the product potential for 777, we've been pretty clear that we really like how Dupixent pursued their development. They established a dose in derm and then used that to go straight to Phase III expansions in other derm indications. Similarly, they established a Phase II dose in respiratory via asthma, which they then used to go straight to Phase III in other indications like COPD. The other therapeutic area where they play is GI. We're excited to see what we can do in EOE as well, where the injection burden is quite high at weekly currently, and patients are hoping for something more. Phase II in asthma later this year and a Phase II in EOE next year, we're maintaining kind of our guidance to kick off those indications. Your next question comes from the line of Julian Harrison with BTIG. Your line is open. Good morning. Congratulations on these results, and thank you for taking my questions. First, I'm wondering if you could talk about how much market share in atopic dermatitis you expect APG-777 to command if these initial results from the APEX study are replicated in Phase III. Beyond efficacy, what do you expect physicians to be most receptive to in APG-777's therapeutic profile? Finally, can you talk more about the rescue criteria in the APEX study and the differences across key trials that are worth highlighting there? Yeah, thanks, Julian. Sorry, you just cut out for me on the second question. Was it around what payers are looking for, just to confirm? Correct. Okay, great. Thank you for the clarification. Yeah, so you know around market share, I think when we've done market testing, I think the results have been very positive. Jeff, I don't know if you want to comment briefly. We haven't actually tested this profile yet. Yeah, sure. Julian, I would say first and foremost, we see APG-777 as having the opportunity to be the market leader in atopic dermatitis. 94% of patients say that they would prefer APG-777 over the available options in the market, and they would take action to be placed on this product. That was looking at equal efficacy and a quarterly dose in maintenance. Physicians, more than 80%, said that they would start their new patients on APG-777 versus the competitors. To Michael's point, we have not done market research to look at a product that is 17 points better than the standard of care in EASI-75. As noted earlier, market research is clear that physicians look first and foremost at EASI-75 scores in order to make decisions for their AD patients. We have 2/3 of patients that are going to reach EASI-75 with APG-777. This has not been seen before. To answer your first question, I would say we expect to be the market leader in the biologic AD space. In terms of payers and kind of what they're looking for, can you comment on that? Yeah. From a payer perspective, we've said from the beginning, even with equal efficacy, so think about an EASI-75 score of 50, equal efficacy with this transformational dosing, we know that patients and physicians prefer this. We've said that that in and of itself would be a first-line biologic. That in and of itself would be a leader and be looked at positively from payers. I would point, Julian, to the two launches that have recently taken place in the biologic space, one being Lilly's lebrikizumab and the other being Galderma's Nemolizumab, both of which are off to really strong launches. If you look at lebrikizumab, they have quickly captured over 80% access in the commercial space. That's with limited differentiation versus what we're bringing to the market. We expect to have early first-line access and a strong out-of-the-gate launch with both volume and share. Thanks, Jeff. Your third question, rescue criteria. Carl, do you want to speak to how we treated patients using steroids? Yeah, yeah, of course. It's a really important piece as we look at comparing trials and how they treated rescue medication use. It's similar to what lebrikizumab did in their Phase III trials, but not necessarily their Phase II trial, but their Phase III trials, as well as what Dupixent did in their Phase III trials. We treat all rescue med use, any kind of topicals or systemic treatment, as non-responders. From the time they use topicals, moving forward, they're treated as non-responders in the analysis. This is kind of, I'd say, the most fair way to assess how well your drug is working. An important aspect of the analysis that we're showing here. Excellent, very helpful. Thank you and congrats again. Your next question comes from the line of David Nierengarten with Wedbush Securities. Your line is open. Hey, thanks for taking the question. Maybe it's too early, maybe it's not too early to think about commercial slotting of both APG-777 and the combo. I was just curious, do you see that evolving over time if you plan on maybe having a higher dose format, lower dose format, plus a combo to treat maybe bio-experienced non-responders? How do you see that matrix evolving and what to look for in the clinical trials to help you decide on those potential commercial products? Thanks. Yeah, no, thanks, David. I'm glad that we've had the coffee to think through it. I think that we're digesting this data and kind of the profound improvement that we're seeing in EASI-75 and just the overall profile. We're thrilled because we think it is going to become the frontline drug of choice. I think when we think about the combination, I think it could fill a number of different areas within the market. It could be, as you point out, into this bio-experienced, refractory population. It could also, over time, depending on the profile, given that it's still going to be in that quarterly maintenance dosing or better with a single injection, it could also become the frontline drug of choice. What we're really excited about is that we think that this is the potential to become the drug of choice with APG-777 mono. We'll see if Part B can drive even higher efficacy improvements to further differentiate ourselves from any current standard of care or future competition in the combo. We know that JAKs, despite having the safety profile that they do, are doing quite well in that refractory population. It could fit there, or it could also play in frontline as well, given that it's still such an advantage dosing profile. Maybe just to cut to the chase, is the commercial goal here to own every single spot, frontline, high dose, non-responders, bio-experienced, or is it to really push forward just the best product possible? Over time, maybe other companies or other candidates come into play on experienced or refractory patients. Do you see what I'm saying? Are you going for breadth in terms of multiple products approved here or depth in getting the best absolute number out in a single product? Jeff. Yeah, David, thank you for the question. I would say the simple answer is we want to own the biologic AD market, period. I would say first and foremost, and we are excited about both products, but first and foremost, 777 mono has the potential to be a mega blockbuster on its own, and we expect that to be the case. We think in time, as we do the studies and get the results of the combination, in order to really raise the ceiling of efficacy and continue to help more patients, we think that the I&I market as a whole is heading toward combinations. In time, we believe that, in fact, revenues can shift from the monotherapy to the combo therapy, and that is a strategic evolution, David. We are looking at both products as first-line biologics in this space. Got it. Okay, thank you. Your next question comes from the line of Salveen Richter with Goldman Sachs. Your line is open. Hi, team. This is Srinath Rowan for Salveen. Thank you for taking my question and congratulations on the data. Just two quick ones from us. Given you're evaluating much higher exposures in Part B, do you see any risks to the safety profile as you get to the highest dose in Part B? The second, it might be a little too early, but any initial thoughts on the Phase III trial design? Thank you so much for the questions. In terms of exposures in Part B and safety profile, do you want to speak to the evidence that exists? Yeah, happy to, right? Great question. As we move forward with a dose in Part B that now has 90%- 100% greater exposures compared to lebrikizumab, similar to quartile four, where we're really seeing standout efficacy data across endpoints in our exposure response analysis, I think one of the exciting things is we do not expect any difference in the safety profile for that. As we've examined both our own data for exposure safety relationships, and also the totality of evidence we have from lebrikizumab and Dupixent, APG-777, nor those drugs have any relationship between exposure and safety profile or exposure and adverse event. We don't expect to see anything different in the safety profile as we go from 30%- 40% greater exposures in Part A, where we saw two out of every three patients having an EASI-75 response, to even higher exposures in Part B. We expect no change in the safety profile. Yeah, there's actually been a lot of interesting data published for Dupixent and lebrikizumab both. If anything, there's an inverse exposure relationship with the AEs, especially on conjunctivitis. As you get higher exposures, you see lower rates, and we actually see this in our own data with our quartile four having the lowest rate of conjunctivitis. I think it's just because you're getting more anti-inflammatory drug on board. I encourage you to kind of look at the data. I think it's very interesting. On the Phase III design, our assumption right now is that similar to others, we'll do two Phase IIIs, placebo-controlled and then one with topical corticosteroids, really during my kind of safety database requirements historically for atopic derm drugs. Of course, like every other biotech, I'm looking at how to best engage with the current administration and the agency to see if for a validated target that's obviously safe and well tolerated and potential to drive better outcomes, if there's a more expeditious path. I think that's all going to be a negotiation. Thank you. Your next question comes from the line of Tim Anderson with BofA Securities. Your line is open. Thanks so much for the questions. Can you talk about baseline characteristics for patients in the trial? There's obviously different ways of reporting this. Just looking for something that would help us compare this data to competitor data sets. If you can't disclose it now, will that be published at some point or not until we have the 52-week data? Another question, I think you may have made a comment on this. Is there any potential for a narrowing of clinical effect when going from Phase II to Phase III? I think you said it might have actually been the opposite when you look at competitor data sets where strength is in Phase III. If you could just confirm. Last question is, you'll be starting Phase III in 2026. Presumably that's back half 2026. Does that imply a potential regulatory filing in something like early 2029? Thank you. Questions. In terms of baseline characteristics, I think you shared a pretty extensive kind of baseline demographics, but Carl? Yeah, happy to comment on this too. Probably went quickly in the presentation. Overall, baseline characteristics for this study, I think in line with our expectations and what others have shown for moderate to severe atopic dermatitis, well balanced across the two arms, APG-777 and placebo, and in a severity that is as expected too in terms of baseline EASI as well as IgA 3 versus 4 for the patient population. Yeah. On narrowing from Phase II to Phase III, I think here it's actually a kind of counterintuitive data set. When you go from Phase II to Phase III, and we provided just all the data that's publicly available for different antibodies and systemics alike, Phase II to Phase III data points for week 16 endpoints with similar doses, you actually see an improvement on EASI-75 and a greater improvement for EASI-90 and IgA, which I think when we think about the data that we're disclosing today, it's our initial Phase II data, and we're comparing against competitor Phase III data sets after they've seen that bump from Phase II to Phase III. I think it's due to a number of things. These trials become much more global as you move into more European sites. It's more of a typical kind of type 2-driven purine disease, and you also just get lower placebo rates. I think you get benefits from both of those, which we would expect. You also just learn more about which sites to focus on and which territories to focus on. We'll be implementing a lot of our own lessons for that. With your last question, kind of Phase III in 2026, and does that mean filing in 2029? I think with our acceleration today, we're confident that we have the chance to get an approval this decade, kind of in line with what you're suggesting. Thank you. Your next question comes from the line of Geoff Meacham with Jefferies. Your line is open. Hey, guys. Thanks for the question and congrats on the great data. On the higher exposure, what do you think the upper end of the EASI-75 can be on induction? Is that something that you guys are focused on? Michael, I know you talked about the risk of conjunctivitis, RTIs, being sort of lower and with higher doses, but is there any special consideration as you look to future trials to have to mitigate any or monitor the risk of any of these AEs? Thank you very much. Yeah, no, thanks, Geoff. Carl, do you want to kind of talk about upper end? Yeah, happy to. Right? We look at kind of the higher exposure quartile and what might be the upper end of endpoints, including kind of EASI-75. I think to date, what we've seen is high dose lebrikizumab has really set the bar for what's possible in AD, and they're tracking around 75% EASI-75 on an absolute basis. As you see, even the top two quartiles from APG-777 were above that number. I think that what we're seeing there is potentially reaching kind of the limits of what you could do in terms of EASI-75 results. Really excited to be testing those higher exposures in the Part B of the study now with that accelerated readout mid-2026. Yeah, with regard to safety, anything to add? Yeah, you know, I think that as we move forward, again, the lack of exposure AE relationship, especially with conjunctivitis, I think is a really important piece as we decided what doses and exposures to test moving forward. Like Michael said, if anything, an inverse relationship between exposures and conjunctivitis. We don't expect to see anything new on the AE profile as we move forward. From this mechanism, IL-13 and IL-4 receptor alpha, they've just been incredibly well tolerated to date, and we're seeing that in our data. Conjunctivitis has been the only thing across the entire class that has stood out, and it's not a reason for discontinuation generally. In the APG-777 data, we saw that it was generally benign and short-lived, no discontinuations, no dose adjustments, no missing doses for it. You don't expect anything new in Part B or beyond. Yeah, the last thing I would add is Part B has been ongoing since February as well. We've been dosing Part B for quite some time now and obviously have an independent safety monitoring committee. We have been testing those higher exposures in that study and are now testing them also in the combo with no findings that are worrisome to date. I think just a continued validation of the lack of exposure safety relationship. Great. Thank you. Your next question comes from the line of Seamus Fernandez with Guggenheim. Your line is open. Oh, thanks, guys. I just wanted to ask a couple of quick follow-ups. First off, the path to Phase III obviously suggests that you are good on clinical supply or have very strong plans from a clinical supply perspective to be able to advance to Phase III even with the higher dose. Can you just clarify for us how far along you are with regard to manufacturing capacity and capabilities and what you would see the cost of goods of 777 being as you kind of advance through Phase III? It clearly is something that's very important to potential strategics. There is some interest in oral STAT6 agents. Just interested to know what data you guys have in terms of STAT6 knockdown and if we're likely to see additional biomarker data from not just this data set, but data sets going forward in terms of the robust biomarker data that you've used to inform your results so far. Thanks so much. Great. Thanks, Jane. I'll hand it to Jane to kind of talk through our supply and COGS. Thank you for the question. We're in a really strong balance sheet position and very fortunate that that cash takes us as a runway into Q1 of 2028. Not only does that support all the milestones that we've spoken about today, including accelerating the Part B to mid-2026, as well as the startup of the Phase III, that balance sheet also includes the startup activities as it relates to manufacturing and the material that we will need for those Phase III trials. In terms of COGS, you've heard us talk about how we have optimized the antibody across many parameters, including backbone, including formulation. We're in the position that we see COGS from a commercial point of view being in the low single digits, which we think is going to be very important here in terms of flexibility on a launch and a commercialization. I'll turn to Michael to talk about the orals and STAT6. Yeah, briefly the question, we're really excited at the data we have today. This is just the initial data set, top-line release. Much more to come, including on biomarkers, patient-reported outcomes, additional endpoints in the future as we think about continuing to build the momentum that we have in this space. We're hopeful that more agents can enter this space. More agents, as we're seeing with lebrikizumab and nemolizumab entering this space, lead to more rapid growth in TRx and NRx in this space as a share of voice just gets higher and awareness drives more patients to systemic therapy. Eventually, we think to a quarterly or better drug with potentially best-in-class efficacy. On STAT6 in particular, there we show 99+% inhibition, full suppression throughout. We've shown that in our Phase I data, and we're seeing that. We expect to see that here, and we'll release more data on that in the future. Thanks so much. Thank you. I'm not showing any further questions in the queue. I would now like to turn it over to Apogee Therapeutics CEO Michael Henderson for closing remarks. Great. Thank you so much, everyone, for joining the call, especially those on the West Coast with us on an early Monday after the holiday. We're really excited at this data. It is a landmark day for Apogee Therapeutics as we go from a. Kind of an early clinical company now to a later stage development company, with a path towards commercializing what we feel is potentially one of the largest drugs in biotech. Really appreciate the questions and look forward to further engagement and future data releases. Ladies and gentlemen, that concludes today's call. Thank you all for joining. You may now disconnect.