Morning, 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 Kurdi, Vice President of Investor Relations at Apogee. Noel, you may now begin. Thank you, operator, and thank you all for joining us today. During this call, we will 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, CEO Michael Henderson will begin the call with an introduction to today's results and the opportunity in atopic dermatitis. Chief Medical Officer Carl Dambkowski will walk us through the APEX Part B initial results of zumilokibart in patients with moderate to severe atopic dermatitis. Dr. Ruth Ann Vleugels of Brigham and Women's Hospital and Harvard Medical School will then share an update on our current treatment gaps in atopic dermatitis, followed by an overview of our zumilokibart development program by Kristine Nograles, SVP, Head of Clinical Development and Medical Affairs for Dermatology, and Amol Kamboj, SVP, Head of Clinical Development for Respiratory and GI. Michael will summarize our vision for building a leading I&I company and the anticipated future milestones for zumilokibart as we advance its development. The subsequent Q&A will be led by Michael, Carl, Apogee Chief Financial Officer Jane Pritchett Henderson, Chief Commercial Officer Jeff Hartness, and Dr. Vleugels. I will now turn the call over to Michael. Thanks, Noel, and thank you all for your time today. Today is a big day for Apogee. We are thrilled to share positive Part B results that give us a clear path to phase III later this year, with data that we believe will be incredibly exciting for patients and the dermatology community. In addition, today we announced a concurrent strategic financing collaboration with Blackstone Life Sciences, which, when combined with our strong existing balance sheet, will allow us to commercialize Zumi in atopic derm, asthma, and eosinophilic esophagitis without needing to rely on equity capital markets. Taking a step back, Apogee was founded with a goal to transform standard of care for atopic dermatitis and other Type 2 inflammatory conditions. AD is the largest and fastest-growing I&I market, projected to reach over $50 billion, yet treatment options are limited, with significant efficacy benefits left on the table and onerous two-to-four-week dosing required. Today, we will share new data from Part B, the dose -ranging component of our APEX phase II trial, which continues to support Zumi's potentially transformative profile in AD. Zumi demonstrated robust clinical activity across all lesional and itch endpoints at week 16. Importantly, previously disclosed Part A 52-week data showed that Zumi's clinical activity continues to improve beyond week 16, with dosing just two to four days per year in maintenance required. If approved, this could be the first product in any dermatologic indication to offer the option for every three- or six-month dosing. With today's data and the bespoke capital facility provided by Blackstone, we believe Apogee has a path to commercialization and profitability. We are thankful to the patients and physicians that have enabled us to share this with you today. With today's positive data from APEX Part B, we have achieved our objective of identifying a dose regimen that we believe maximizes the potential of IL-13 inhibition in atopic derm. In this trial, evaluating low, mid, and high doses of Zumi versus placebo, we observed similar clinical activity with both the mid and high doses. The low-dose arm achieved relatively lower clinical activity as expected. With this data, we are well-positioned to engage regulators with our plan to take forward mid-dose Zumi to phase III, which is an optimized dose that demonstrated robust clinical activity across all lesional and itch endpoints, a well-tolerated safety profile, and substantially reduced injection burden versus standard of care. Zumi mid-dose was highly statistically significant versus placebo across all endpoints tested. Notably, a meaningful proportion of patients treated with mid-dose Zumi achieved EASI 100 or completely clear skin at 16 weeks. Overall, we believe Zumi's profile has the potential to set a new standard of care in atopic derm. We have a unique opportunity with Zumi to potentially transform the future $50 billion AD market. We previously shared data from APEX Part A showing that two-thirds of patients treated with Zumi achieved an EASI 75 response at week 16, and that these responses were maintained with as few as two to four dosing days per year in maintenance. Today's 16-week data from APEX Part B was remarkably consistent with Part A, providing further evidence that Zumi could be the frontline drug of choice in AD across all lesional and itch endpoints tested in APEX Part B. Zumi demonstrated a highly competitive profile at week 16 on both an absolute and placebo-adjusted basis. Together with data shared earlier this year, showing responses continue to improve after week 16 with maintenance dosing of just two to four days per year, we believe Zumi clearly has the potential to improve upon standard of care. I will now hand the call over to Carl, our Chief Medical Officer, to walk us through today's data in more detail. Thank you, Michael. I'm excited to share the zumilokibart APEX Part B trial results with you all today. In the APEX Part B trial, the modified ITT population consisted of 346 patients that were randomized one to one to one to one in the induction stage to receive either a low, mid, or high-dose regimen of zumilokibart or placebo. The study was designed to determine the dose of zumilokibart that enables the strongest clinical activity while maintaining a safety profile consistent with the IL-13 class and minimizing injection burden. Our goal was to fully explore the dose response of zumilokibart and ensure we did not leave any efficacy on the table, which we feel we have achieved with the study results being presented today. As Michael has noted, with today's results, the mid -dose from the study is the planned phase III dose, pending regulatory interactions. I'll focus today's discussion on the results at week 16, but the study is designed such that all patients are re-randomized into either the three or six-month dosing arms in the maintenance portion of the study, which we'll plan to release next year. As a reminder, zumilokibart's planned phase III induction regimen requires just four dosing days, compared to nine for dupilumab, representing a more than 50% decrease in the injection days during induction. Part A 52-week results shared earlier this year demonstrated zumilokibart's potential to reduce injection burden during maintenance even further, with just two to four dosing days per year compared to 26 for dupilumab, an up to 13-fold decrease in the injection burden for patients with moderate to severe atopic dermatitis. Baseline characteristics and demographics of participants in this trial were generally well-balanced and in line with expectations. The severity of patients enrolled in APEX Part B increased from APEX Part A and is aligned with contemporary trials. Zumilokibart was well-tolerated. Results were consistent with expectations for the IL-13 class. Adverse events that occurred in 5% or more of patients in one or more zumilokibart treatment arms included nasopharyngitis, headache, non-infective conjunctivitis, upper respiratory tract infection, atopic dermatitis, and urinary tract infection. 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. Rates of conjunctivitis across treatment arms were generally in line with standard of care. For the planned phase III zumilokibart dose, the non-infective conjunctivitis rate was 5.9%, and the pooled rate across all conjunctivitis-related preferred terms was 10.6%. There was no effect of ADAs on PK, clinical activity, or safety. APEX Part B met the primary endpoint of the study, which was EASI-75 response at week 16, with significance achieved for all zumilokibart treatment arms starting at week two. Zumilokibart mid- and high-dose arms demonstrated comparable activity with 65.9% and 61.6% of patients achieving EASI-75 at week 16, respectively. As expected, zumilokibart low dose showed relatively lower clinical activity, with 50.5% achieving EASI-75 at week 16. The mid and high doses of zumilokibart replicated the results previously seen in APEX Part A. On both an absolute and placebo-adjusted basis, APEX Part A and Part B mid-dose results were within one percentage point. When we look at the more sensitive, continuous endpoint of percentage change from baseline in EASI score, the trend across treatment arms is consistent with EASI-75, with zumilokibart mid and high doses showing comparable clinical activity and low doses showing relatively lower clinical activity. Importantly, zumilokibart mid -dose showed a rapid effect on lesions, achieving significance as early as week one. As with EASI-75, the mid and high doses of zumilokibart replicated the result previously seen in APEX Part A, here within two percentage points on both an absolute and placebo-adjusted basis. Moving to the more stringent secondary endpoint of IGA 0/1, which will be part of the co-primary endpoint of EASI-75 for the phase III trials of zumilokibart. zumilokibart mid-dose demonstrated robust clinical activity with 46% of patients achieving IGA 0/1 at week 16. zumilokibart high dose generally trended similarly over the 16-week period. As expected, zumilokibart low dose showed relatively lower clinical activity. As expected, EASI-90 showed a similar trend as IGA 0/1, with 47.4% of patients treated with zumilokibart mid-dose achieving EASI-90 at week 16. We also saw deep itch relief. Over half of patients, 50.5% to be exact, treated with the mid-dose of zumilokibart achieved a four-point or greater reduction from baseline on the itch Numerical Rating Scale at week 16, with zumilokibart high dose generally trending similarly over the 16-week period. As expected, and consistent with lesional endpoints, zumilokibart low dose showed relatively lower clinical activity. The APEX Part B results showcase zumilokibart's competitive profile in atopic dermatitis. The zumilokibart planned phase III dose demonstrated an absolute EASI-75 at week 16 of 65.9% and a placebo-adjusted delta of 41.9%. These results compare favorably with standard of care. The non-head-to-head trial comparisons are shown on the right for all approved biologics. zumilokibart mid-dose also demonstrated a competitive profile for the more stringent endpoint of IGA 0/1, with the zumilokibart planned phase III dose demonstrating an absolute IGA 0/1 at week 16 of 46% and a placebo-adjusted delta of 34.8%. Non-head-to-head comparisons for all approved biologics are again shown on the right. Similar to IGA 0/1, zumilokibart mid-dose also compared favorably on the more stringent endpoint of EASI-90, with the zumilokibart planned phase III dose demonstrating an absolute EASI-90 at week 16 of 47.4% and a placebo-adjusted delta of 37.8%. Non-head-to-head comparisons for all approved biologics are again shown on the right. Similar to lesional endpoints, zumilokibart mid-dose demonstrated competitive itch improvement at week 16. The itch improvement seen by zumilokibart compares favorably to standard of care in non-head-to-head trial comparisons shown on the right, including nemolizumab in combination with topical corticosteroids. Specifically, the zumilokibart planned phase III dose demonstrated an itch response of four points or greater in 50.5% of patients and resulted in a placebo-adjusted delta of 36.7%. Prior clinical trials for biologics and atopic dermatitis generally have not reported data for EASI-100 responses, which represent completely clear skin, or composite endpoints, which represent the simultaneous control of lesions and itch for patients with atopic dermatitis. While comparable data is not available for lebrikizumab, nemolizumab, or tralokinumab, these two endpoints are available from a head-to-head trial of the JAK inhibitor upadacitinib versus dupilumab called LEVEL UP. LEVEL UP was the first and only study to use a composite endpoint of EASI-90 and itch NRS of 0 or 1 as a primary endpoint, which is an endpoint classified as showing very low disease activity, or VLDA. In this study, upadacitinib showed EASI-100 and VLDA rates that were two to three times higher than dupilumab. For each of these endpoints, we have added zumilokibart's APEX Part B data as a non-head-to-head comparison to the left of the LEVEL UP data. For EASI-100, the zumilokibart planned phase III dose demonstrated a 16.5% absolute response and a 13% placebo-adjusted delta. Additionally, 20.6% of patients achieved very low disease activity, measured by the composite endpoint of EASI-90 and itch NRS of zero or one. These results demonstrate the depth of response being seen after 16 weeks of treatment with zumilokibart. We couldn't be more thrilled with the study results and the profile of zumilokibart, which provides robust lesion control with reduced injection burden for patients. Before we discuss what is next for zumilokibart, we are pleased to have Dr. Ruth Ann Vleugels of Mass General Brigham Department of Dermatology here on the line with us to discuss treatment gaps in atopic dermatitis. Dr. Vleugels is an expert in inflammatory skin diseases, a Professor of dermatology at Harvard Medical School, and the Director of the Atopic Dermatitis Program at Mass General Brigham Hospital, among her many credentials. Thank you so much for being with us today, Dr. Vleugels. Thank you so much for that kind introduction, Carl. I really appreciate it, and I'm actually delighted to be here to speak with you all today about treatment gaps in atopic dermatitis, because this is an area that I'm extremely passionate about. Atopic dermatitis is actually our most common inflammatory skin disease. It affects infants, it affects the elderly, and everyone in between. I'm sure that you can see by looking at this gentleman in the photo that this is profoundly impactful on our patients' quality of life. When I'm teaching medical students at Harvard Medical School, I often try to explain this by saying, Imagine you had a couple of hundred of mosquito bites or poison ivy over your entire body, and then imagine that that goes on for years. This rash and itch is really a severe and systemic problem for our patients that profoundly impacts their quality of life. Let's think about how it does so. Because of this intense itch, patients really lose sleep; adults often miss work; children often miss school. In addition, we have excellent data in children to show that pediatric patients actually have growth restriction. Our kids with atopic dermatitis don't reach their full growth potential because of their atopic dermatitis. Adults have reduced physical activity; we know that we see increased mood disorders in patients with atopic dermatitis, in particular, depression. In addition, patients have many specialist visits. They often have increased hospitalizations, and we actually even see increased skin infections in patients with atopic dermatitis as well. You can ideally see that this is really a multifactorial impact on quality of life from this severe skin disease. Before we think about this, prior to 2017, it's important to level set that we primarily used topical therapies, and dermatologists often would reach for systemic corticosteroids. We know systemic corticosteroids have many side effects that are highly impactful for patients. They cause diabetes, weight gain, high blood pressure, bone damage, et cetera. Our Academy of Dermatology actually recommends against their use in this disease. Since 2017, we have had these therapies: three approved biologics, as well as two orally approved JAK inhibitors. Dupilumab and lebrikizumab are the biologics in the IL-4 and IL-13 family. Both of these medications have improved lesions and also itch. Now, a key thing when we're thinking about these medications is that they are administered by self-injection, and the frequency for these is between every two to four weeks. Patients have to inject up to 26x a year, which is a challenge for many of our patients. Nemolizumab is an anti-IL-31 medication. This is the medication that's known to have rapid itch relief. However, it does have limited improvement in rash, and so that is a limitation of this medication. In addition, it is still dosed by self-injection every four weeks. Our oral JAK inhibitors, upadacitinib and abrocitinib, do have rapid onset of action and can help both lesions and itch. These are oral medications that are dosed daily. In addition, all JAK inhibitors carry a boxed warning for blood clots, major cardiac events, and cancer. This boxed warning is the primary reason why JAK inhibitors have faced practical limitations in their widespread adoption for atopic dermatitis. When I'm seeing patients in my atopic dermatitis program, it's very clear that our patients are looking for improved treatment options. Really what they want is impressive efficacy with a clean safety profile. This is really important because the zumilokibart data not only shows that zumilokibart has numerically improved endpoints than all existing biologics, but in addition, the efficacy is numerically similar to JAK inhibitors at week 16, including on our highest threshold endpoints. These include very low disease activity, as well as EASI 100. It is important to remind ourselves that EASI 100 is completely clear skin. Until now, this is really an endpoint that we are not used to thinking about when we talk about biologic therapies. In addition, we know that after week 16, responses in zumilokibart-treated patients actually improved, and actually, over 40% of patients achieved completely clear skin on every three-month dosing by week 52. Again, this is just a really robust endpoint, and this really is what our patients are looking for. This efficacy is in conjunction with safety data that is comparable to our other IL-4 and 13 medications. This is extremely important because we know that in the dermatology world, both our patients and my colleagues really are making their decision-making about therapies primarily based on safety. We know that the IL-4, IL-13 class is a class that they feel extremely comfortable with. In conjunction with this impressive efficacy data and this clean safety profile, we also need to think about the injection burden because, as I mentioned, this can be a challenge for many of our patients. In the induction period, zumilokibart needs four dosing days, so this is over a 50% reduction from existing biologic therapies. In addition, when we look at the maintenance data, zumilokibart patients would need two-four injections per year. That's actually 22-24 fewer shots than the current standard of care therapy in atopic dermatitis. A highly meaningful difference for our patients in terms of that overall injection burden. From this data, we can really see that zumilokibart could address several unmet needs in atopic dermatitis. Although we do have newer therapies that have greatly improved the lives of our patients, there's still substantial unmet need for a highly efficacious therapy that has a safe profile, but also reduced injection burden. The key takeaways for me are that zumilokibart was not only well-tolerated in patients, but in addition, the safety profile is in line with that of the IL-4 and IL-13 class. Again, this is a class that we know my colleagues feel extremely comfortable with because of this clean safety profile. In addition, the data we saw today demonstrates that zumilokibart has efficacy that's numerically similar to JAK inhibitors, which is really a bar that we've been reaching for, and that previously we have not seen from a biologic medication. This is highly meaningful. In addition, the itch data is numerically similar to nemolizumab, which is the biologic that we consider to have the highest efficacy for itch. Again, this will be extremely meaningful, not only to patients but also to my dermatology colleagues. From previously presented data, we also know that zumilokibart shows improved responses over time, and that even with dosing as infrequent as every three to six months, we have high efficacy, which will allow our patients to have excellent outcomes, but also not to have frequent injections, which is something our patients are really asking for in the clinic on a regular basis. Together, this strong efficacy and safety data, coupled with an extremely meaningful reduction in injection burden, highlights that zumilokibart is poised to become the biologic of choice for patients with atopic dermatitis. Thank you so much for your interest in our patients with atopic dermatitis. Thanks, Dr. Vleugels, for highlighting the treatment gaps in atopic dermatitis and the potential for zumilokibart to address these unmet needs. The exciting results from Part B have now enabled us to select the dosing regimen for our phase III program, which we plan to initiate in the second half of this year, pending regulatory alignment. The ADventure phase III program for zumilokibart will include three clinical trials, beginning with the ADventure 1 and 2 monotherapy studies, each of which is expected to enroll approximately 400 patients with moderate to severe AD. During the induction phase, patients will be randomized to receive either mid-dose Zumi or a placebo. Patients will then transition into the maintenance phase, where we will continue to evaluate both three and six-month maintenance regimens. The trial design will be very similar to Part B with respect to the patient population and geographic footprint, and the studies will evaluate EASI-75 and IGA 0/1 as co-primary endpoints, both of which were robustly assessed in our phase II study. The third trial in our phase III program is the ADventure TCS trial, which will evaluate zumilokibart in combination with topical corticosteroids. ADventure TCS is also expected to enroll approximately 400 patients who will be randomized to receive either mid-dose Zumi or placebo, both in combination with topical corticosteroids. During the maintenance phase, we will evaluate every three-month maintenance dosing of Zumi and TCS. As with the monotherapy studies, ADventure TCS will be very similar to Part B in terms of the patient population and geographic footprint. EASI-75 and IGA 0/1 will also serve as the co-primary endpoints in this study. We are very excited to initiate the phase III program for zumilokibart planned in the second half of this year, incredibly grateful to the patients, investigators, and site staff who have participated in our AD trials to date. Their partnership and commitment have been instrumental in advancing our clinical development program in atopic dermatitis. With that, I'll now turn the call over to Amol, who will discuss our development plans for zumilokibart beyond AD. Thank you, Kristine. Good morning, everybody. I'm pleased to join today's call to provide a closer look into our plans for zumilokibart beyond atopic dermatitis. We are excited to evaluate its pipeline and product potential across multiple I&I indications, starting with phase II programs for asthma and eosinophilic esophagitis, or EoE, both of which we expect to initiate over the coming quarters. We know that patients very often suffer with multiple Type 2 inflammatory conditions. For example, an estimated 25% of patients with atopic dermatitis and 40% of patients with EoE have comorbid asthma. As an allergist, I've seen how debilitating these conditions can be, and especially so for patients suffering with more than one. The potential for Zumi to treat a broad spectrum of T ype 2 inflammatory disorders could transform standard of care for these patients. We've now twice seen what zumilokibart may offer for patients with atopic dermatitis. We're incredibly excited about Zumi's potential in asthma and EoE as well. Beyond these conditions, Zumi has potential in other dermatologic, respiratory, and GI indications with the potential for a straight to phase III approach using optimized phase IIb dosing regimens in each of these therapeutic areas. Following this year's positive phase I-B asthma readout, where a single dose of zumilokibart drove deep, sustained FeNO suppression for up to 32 weeks, we plan to initiate the ASPIRE phase II-B trial enrolling patients with moderate to severe asthma. This randomized placebo-controlled study will include patients with elevated Type 2 biomarkers and a history of exacerbation in the prior year and is designed to be registrational. Participants will be randomized to one of three zumilokibart arms in every 3, 6, or 12-month dosing regimen or placebo. The primary endpoint will be annualized exacerbation rate at week 52. We plan to initiate the ASPIRE trial in the first quarter of next year. ELEVATE is our phase II-A proof of concept study in eosinophilic esophagitis, which we also plan to initiate in the coming quarters. This study will enroll 30 - 50 patients who will receive a zumilokibart induction regimen, followed by a maintenance treatment period, testing both every three- and six-month dosing as we've done in atopic dermatitis. The primary endpoint of the trial is histologic improvement as assessed by eosinophil counts. We will also be assessing endoscopic change and patient symptoms. Our plans to launch the ASPIRE and ELEVATE trials over the coming quarters underscore zumilokibart's potential to redefine the treatment paradigm across Type 2 inflammatory disorders. Zumilokibart could become the first long-acting biologic approved for both atopic dermatitis and asthma. Currently, only Dupixent, dosed every two weeks, is approved for both indications. It is also the most commonly prescribed biologic in both AD and asthma. We recognize that Dupixent being approved in both indications is an important driver of this, given the opportunity to treat patients suffering with both conditions. In EoE, zumilokibart has the potential to be dosed just 2x-4x per year. As a reminder, Dupixent is the only biologic approved in EoE and is dosed weekly in this indication. That's 52 injections per year. Imagine how transformative two-four annual injections would be for patients and families living with EoE. On the heels of the exciting atopic dermatitis data that Carl presented earlier, the initiation of these two important studies is the next step in exploring Zumi's potential to deliver a best-in-class profile across Type 2 inflammatory diseases, and we're excited for these next steps. I will now pass the call back over to Michael for closing remarks. Thank you, Amol. Atopic derm is the largest and fastest-growing I&I market, with Dupixent's launch outpacing the entire $25 billion plaque psoriasis market. New entrants with limited differentiation are quickly becoming blockbusters in their own right. While Dupixent continues to grow rapidly, it speaks to the unmet need and significant under-penetration of this market. Zumi's anticipated launch in 2029 could be the next meaningful frontline launch for this population. Taking a step back, when we consider the profile of an atopic derm treatment that will truly be transformative to patients, we look at lesion control, itch relief, and dosing. These are the three areas that patients and physicians tell us are in most need of innovation, where current biologics come up short. Zumi delivered against all three, and we are confident in its potential to be the next clearly differentiated first-line product to launch in atopic derm. In today's APEX Part B readout, Zumi demonstrated robust clinical activity at week 16, and we know from maintenance data shared earlier this year that patients continued to improve after week 16, with 41% of patients achieving EASI-100 at week 52, representing completely clear skin. It's clear that Zumi could be a transformative therapy for atopic derm patients with just two to four dosing days per year in maintenance, compared to 26 injections per year for standard of care, which has not demonstrated improved responses after week 16. Today, we also announced a major strategic financing collaboration with Blackstone, a trusted partner to our industry who shares our conviction in Zumi's potential to transform standard of care for patients living with Type 2 inflammatory conditions. Our partnership with Blackstone provides up to $1.3 billion in additional capital, significantly bolstering the financial resources we can deploy to develop and deliver Zumi for as many patients as we can as quickly as possible, including today's announced phase III development program in atopic derm. The customized structure matches cash flow to Apogee's future funding needs at a competitive cost of capital and without equity dilution to our shareholders. We are pleased to have found the right partner in Blackstone to help realize our expansive vision for Zumi. With an exciting 2026 for Apogee well underway, we wanted to wrap up today's call with a look ahead to the coming years, which includes multiple expected value-creating catalysts for Zumi through 2028, including additional data in atopic derm and eosinophilic esophagitis next year. In addition to our lead program, we are advancing multiple innovative combination programs, which have the potential to raise the bar over monotherapy. We are looking forward to sharing more detail on these programs later this year. I will now hand the call back over to the operator to begin Q&A. Thank you. Thank you so much. We are now opening the floor for question and answer session. If you'd like to ask a question, please press star one followed by one on your telephone keypad. Kindly limit your question to one question only. We will take our first question from the line of Tyler Van Buren from TD Cowen. Your line is now open. Please go ahead. Hey, guys. Congratulations on the data, and thanks for the presentation. Considering that the mid-dose induction data improved in Part B compared to Part A on the higher -order endpoints, can you and perhaps Dr. Vleugels elaborate on the importance of EASI-90, EASI-100, and IGA 0/1 in the treatment of atopic dermatitis today and the focus on these endpoints among KOLs and patients? Just as a follow-up or a second question, forgive me, but can you also just elaborate on why you felt the need to do the Blackstone deal now? Thanks. Thanks, Tyler. I appreciate the questions. I'll hand it off to Carl and then Dr. Vleugels for the first, and then we'll circle back on the second. Yeah. Thanks so much for the question. Obviously, we were really excited to see the improvements, especially on deeper endpoints here. I think part of the key trial design here in doing a Part A and Part B is that we designed Part B to most clearly represent what we would go forward with in terms of our phase III program. It's a bigger study, a more global footprint, and we think that's really important in terms of the replicability of our Part B data to our phase III program overall. That also, just the size of the study, also gave us more power on these deeper endpoints, like EASI-90, IGA 0/1, and EASI-100, as well as itch NRS of four, among other pieces. That's why I think we're seeing really the true effect of zumilokibart in the mid-dose Part B data. Really to contextualize that, obviously, Dr. Vleugels is much better in terms of that piece, so I'll turn it over to her to discuss the meaningfulness of these endpoints and what she's seeing with zumilokibart. Yeah. Thank you for this important question. I really appreciate it. Maybe just to level set, in clinic, when we're prescribing medications for patients with atopic dermatitis, even the substantial number of decreased injections would be a dramatic shift in the atopic derm market. The enhanced efficacy based on these higher order endpoints that you mentioned is actually what is even more impressive. To kind of describe that, essentially, when we look at EASI-90 or IGA 0/1, the fact that these are essentially 10%-15% numerically higher than the other biologics in the market is highly meaningful to us, because these are the endpoints that our patients would really like to dramatically improve their quality of life. As I mentioned in my brief comments, we've really been looking for years for essentially a biologic that would approach or equal JAK-like efficacy but have the safety profile of a biologic. Because dermatologists, more than pretty much any other field I work for, are driven by the safety field. The fact that we have this JAK-like efficacy from a biologic is highly impactful. To comment on that, the EASI-100 actually hasn't been reported in any biologic phase III study. This isn't something that we would even expect to track. The fact that in the 52-week data, we have nearly half of patients meeting EASI-100, that is sort of more than I could have even dreamt of when these trials started. I think in speaking with my colleagues about these higher -order endpoints, these are really exciting to my colleagues. When we think of this ability, these are the types of therapies we actually start talking to patients about in clinic, even prior to their approval. Like, This is coming. Keep this in mind. The reason for that is because patients are really sick of doing their frequent injections, and they're also looking for therapies that can have improved efficacy. Here we're sort of able to see that on both sides. This is something my colleagues will really be looking forward to. Thank you, Dr. Vleugels. On the second question, Tyler, about why the transaction with Blackstone now, I think it was important to us in our discussions with them. We felt that they were a great partner that provided us a bespoke capital structure and an attractive cost of capital that gives us a path to commercialization and even profitability without needing to rely on the equity markets anymore. I think that was something we had heard from investors in the past. How will you fund this through launch and even profitability? We have that now. What was also quite essential was that we maximize, coming out of this data set, our strategic optionality and flexibility. They met us where we were on that, and I encourage folks to read the 8-K, where you can see that there are specific provisions around change of control, et cetera, including within the first 180 days that give us an ability to buy down that royalty to quite an attractive low single-digit rate as well. It was kind of a no-brainer for us because it gives us a clear path forward while keeping all optionality clearly on the table. Thanks so much. The next question comes from Seamus Fernandez from Guggenheim. Please go ahead. Great. Thanks so much for the question. Two questions. Can you guys talk a little bit about the strength of the EASI-90 data and the IGA 0/1? That seems quite a bit more consistent with the data in this data set than perhaps what was perceived in Part A. Just hoping you could maybe put a finer point on the importance of those endpoints. Then with regard to the conjunctivitis, maybe just help us understand, also from the physician's perspective, the non-infective conjunctivitis frequency versus the overall conjunctivitis and the potential impact of ascertainment bias as people seek to compare across data sets. Thanks so much. Great. Thanks, Seamus. Yeah, I'll hand it to Carl, and then, of course, welcome Dr. Vleugels' input as well on these two questions. Yeah. Thanks so much, Seamus. I think that you're really pointing out something important in this data set, too. One is, as we mentioned in the presentation, really good replicability of the EASI-75 endpoint and% change from baseline in EASI. That was really what Part A was designed around, those two endpoints based on the size as well as the geographic footprint. We really replicated those with high fidelity here. In Part A, I saw a very competitive EASI-90 and IGA 0/1, but maybe I didn't see that we were getting something more with the additional exposures that the mid-dose has. Right? As a reminder, even the mid-dose has 30%-40% greater exposures compared to lebrikizumab. Really, in the first four-six weeks, it's actually more like 50%-60% greater exposures compared to lebrikizumab. We really felt like in Part A, we tapped into that in terms of the greater than 40% placebo-adjusted delta on EASI-75, but maybe didn't see what we expected in terms of the deeper endpoints. Here, with a bigger study and a more global footprint, I think we've tapped into that greater exposure driving these deeper endpoints of EASI-90 and IGA 0/1, both well above 30% on a placebo-adjusted basis, which I think, as Dr. Vleugels said, is very competitive and numerically higher by approximately 10 percentage points or more compared to the non-head-to-head comparators of Dupixent and Lebry. We're really excited about that. I think conjunctivitis, we continue to see most importantly, that it's in line with the class, and it doesn't change treatment for the patients that get conjunctivitis. We saw at the mid-dose 10.6%, which is very in line with the class overall. Short-lived cases, again, median duration here, very similar to Part A, which was 30 days, both here and a couple of days less than that in Part A. That compares to our one comparison of Dupixent, which had a mean duration in a study of 172 days, and more than 80% of cases resolved within 90 days compared to lebrikizumab, which showed about 41%. We're obviously not causing longer cases, and patients are doing well on this. Really, again, to contextualize this and what conjunctivitis means in the clinic, I'll turn to Dr. Vleugels to talk through that. Thank you, Carl. I really appreciate it. Perhaps just one comment on your first question. I think what's meaningful to me as an expert is that these higher -order endpoints actually are much less susceptible to placebo responses. In fact, the data that's presented here is actually sort of more impressive even than perhaps we would have expected. The fact that we see these high responses compared to other agents numerically is meaningful to us, and we would expect these to be replicated in the phase III. Again, just sort of point to that increased efficacy that I mentioned that we think is truly mechanistically driven by what Carl just mentioned, including the higher exposures. I think those higher -order endpoint data are really what's going to help drive clinical decision-making in addition to the reduction of injection burden. Those two things coupled together is really what my colleagues will be extremely excited about. In terms of the conjunctivitis, I know it was mentioned that I'm an inflammatory skin disease expert; I see lots of inflammatory skin diseases other than atopic dermatitis. I feel really fortunate when I get to speak about a therapy whose main side effect is conjunctivitis because this is essentially something that my colleagues do not worry about. I can explain that by the fact that you can see that dupilumab and lebrikizumab are prescribed all the time by my colleagues, right? These are the biologics that we use and we have extreme comfort with because of their safety profile. When we think about conjunctivitis, first it's important to level set that atopic dermatitis patients have a higher rate of conjunctivitis at baseline. That is just a common thing we see in these patients. The kind that we're talking about with these IL-4 and IL-13 medications is non-infective conjunctivitis. When you're counseling patients, you can say, You may get a little red eye, and if that's the case, it's not from an infection. If you get that, let me know. When patients get that, essentially, we almost always just give them eyedrops, so literally over-the-counter eyedrops, and that is it. Oftentimes, we don't have to do anything because it's very short-lived. I've prescribed these medicines several thousand times since 2017 at this point, and I can count on one hand where I've actually had to discontinue one of these therapies due to the conjunctivitis. Again, this is not a side effect profile that is concerning to the prescribers of biologic therapies for atopic dermatitis. I think that's just important to level set on. When we think about the data presented today, I think the zumilokibart data for the dose that's going to move forward into the phase III is completely on par with other agents in this class. This is a class effect, and I think there is nothing to suggest that we would have a higher concern with zumilokibart relative to the other IL-4 and IL-13 therapies that my colleagues are extremely comfortable with. Thank you. The next question comes from the line of Akash Tewari from Jefferies. Your line is now open. Please go ahead. Hi, this is Phoebe on for Akash. Thank you for taking our question. On the respiratory pipeline, we were just wondering what external validation would you like to see before potentially moving Zumi or the combo into COPD? Thank you. Yeah. Thank you, Phoebe. I appreciate the question. There, I think we're excited about moving Zumi into asthma. Both Zumi and our combo, we'll plan to think about COPD likely after asthma for the mono. For the combo, that's something that we'll think about, and we'll share plans later this year, potentially around combo plans in respiratory for our IL-13 TSLP, which could be inclusive of COPD. Thank you. The next question comes from the line of Alex Thompson from Stifel. Please go ahead. Great. Thanks for taking our question, and congrats on the data. I guess a quick clarification and then a question. Could you comment on overall discontinuations beyond those due to adverse events at week 16 across arms? Then maybe, in part A, you showed some NRS changes quite early in the study. I wonder if you could comment on what you're seeing in part B and if that's a trend that you're seeing pull through at this point. Thank you. Yep. Thanks, Alex. I'll hand it to Carl for the two questions. Yeah, thanks for the questions, Alex. I think on the first one, our overall discontinuation rate, we actually had a very low discontinuation rate here. It was about 6% across the whole study. Really low, especially compared to other phase II-B trials, and really lower than most phase III trials. Really speaks to patients' ability to stay on the drug and treatment, as well as what we expect to be really consistent results regardless of analysis method or study moving forward. Great question regarding the early itch changes. Here, this is our top -line data. Showing as much as we can here. We're seeing early itch and lesion changes on a weekly basis. This is what we reviewed here. We're seeing a lot of those in this data set already with lesion changes as early as one week and itch changes as early as the first two weeks. As we move forward and dig in more to this data over the coming weeks and months, we'll present more of that at upcoming medical conferences as well. Really excited for the profile we're seeing here and excited to continue to release more on the Zumi profile throughout the year. Thank you. Our next question comes from the line of Michael Yee from UBS. Your line is now open. Please go ahead. Hey, guys. Thanks for taking our questions. This is Kyle Yang for Michael Yee. Congrats on the data. On the higher -order endpoints, could you please help us understand, is there any particular reason that you saw better results for EASI-90-IGA 0/1 in your Part B, given that you're using the same mg dose as the part A study? The second question for Dr. Vleugels. Could you please help us understand how you would use this drug, assuming that the phase III study replicates the results? Would you prefer to use this in biologics-naive patients or experienced patients? Thank you. Yeah. Thanks, Kyle. I'll hand it to Carl and then, of course, Dr. Vleugels. Yeah. Great question. I think that really on the higher order endpoints, I think the key here was the size of the trial and geographic distribution in terms of the updates to Part B. I think that was really important for the study and really important for what we expect to do in the phase III. We designed Part B to be as close as possible to our phase III design. I think that replicability from phase II-B, our Part B, to phase III is really important too. The bigger trial size, both on a treatment arm basis and especially on a placebo arm basis, I think is also an important aspect of that. Gave us a lot more power to detect the changes that we expected in EASI-90, IGA 0/1, and here, as talked about earlier, EASI-100 and even VLDA or very low disease activity. I think the size of the trial and the global footprint are expected to be part of the phase III trial. I'll turn it to Dr. Vleugels for the second part of that question regarding how she would use the drug in the clinic. Thanks. This is a great question. If this drug were available today for both me and my dermatology colleagues who actually prescribe these medications, I would use this in over 95% of new starts. The reason for that is that differentiated in terms of efficacy and injection burden. It's really the first time we can say that in this field. I think this is really very important because other than a handful of patients where they have a concomitant disease that may need a different mechanistic pathway or, for example, someone who has full body erythroderma or full body disease that might need to be hospitalized, this is really the agent that is differentiated enough that it would take over the vast majority of new start patients. I think we know for existing patients, we do have some percentage of patients that just like to stay on what they're on, and we know this from our psoriasis patients that we've followed for a couple of decades. It's typically about 4/5 or 80% of patients, that are willing to change as long as there's a reduced injection burden even. What's interesting here is not only do we have a reduced injection burden, but we have what we seem to think would be higher efficacy as well. That would take me probably to my last comment on this, which is what's really interesting is what we know in dermatology is that we see dermatologists prefer to cycle between biologics before they move on to JAK inhibitors. The reason for that is because they are aligned with wanting to use biologics for safety, even though these medicines don't have a substantially different efficacy profile. What's really unique here is that not only would we see a very high percentage of this for new starts as well as existing patients with efficacy, but patients who've been on a biologic and have so-so efficacy, this would be, of course, the treatment of choice to change because we also would expect a bump in efficacy. I think that's another really impactful category because we just haven't had anything that would move the needle in that category previously. Thank you. The next question comes from the line of Julian Harrison from BTIG. Your line is now open. Please go ahead. Hi. Good morning. Congrats on the progress, and thank you for taking the questions. First, I'm wondering if you have any thoughts on what is driving Zumi's itch benefit relative to other IL-13 and IL-4 receptor alpha inhibitors as well as nemolizumab. Is there maybe a prevailing explanation there? Second, given the strong data you've generated so far with Zumi on a monotherapy basis, both in atopic derm and asthma, can you remind us how you're thinking about the combination opportunities going forward in both of those indications? Are they segmented to some extent? Thank you. Thanks, Julian. I'll hand it to Carl for the first question, and then I'm happy to take the second. Yeah. Great question. Obviously, we're really excited today with what we're seeing in terms of itch benefit, with the itch NRS of four, which would be the itch data that would eventually end up on the label. That's a really important aspect of that data. With over 50% of patients having that benefit by week 16. Very clear itch benefit with zumilokibart. I really think two aspects of Zumi are really driving this. One is we know that IL-13 has a direct impact on sensory neurons too, so that early exposure and those higher exposures we think are really important for having that sensory neuron benefit during the course of zumilokibart treatment. I think that's one piece of it. The second piece of it is the profound lesion control that we're seeing too, as you decrease lesions. You get an itch benefit from that because the lesions are decreasing as well, too. The more lesion control we get right here, with almost two-thirds of patients getting to an EASI-75 and approaching half of patients getting to an EASI-90 and IGA 0/1, we're having a real huge decrease in lesions, which is also helping the itch too. Direct impact on sensory neurons and lesion control are both important to that itch benefit. For the second question, I think that we've always said that the better Zumi monotherapy does, obviously the higher the bar for combinations. I think in atopic derm, when we think about our APG279 program, we want to see 10 points of better efficacy, not just versus Dupi. But also on a cross-trial comparison basis versus Zumi. I think the bar will be high there, appropriately so. We'll allocate capital if it does meet that bar, because it could still be the second-line drug of choice in atopic derm prior to JAKs, given JAKs have myriad black box warnings, as has kind of been talked about. For IL-13, TSLP, and asthma, I think IL-13 is a Type 2, so a high eosinophil -targeted drug, and that's how we've designed the trial to go after that same population as Dupi. The addition of TSLP could expand the population to all eosinophils. We think that There's potential efficacy benefit, but also just a broader population play that we'll consider as well. Thank you. The next question comes from the line of Yigal Nochomovitz from Citigroup. Your line is now open. Please go ahead. Hey, guys. Good morning. Thanks for the question. This is Jay Ahn for Jeff. First of all, congrats on the EASI-75. I think we can all appreciate that the mid-dose and high -dose were pretty much on top of each other. When looking at the higher -order endpoints, were there any PK or PD data that might explain why we didn't see similar levels of efficacy at week 16 for those endpoints? I'm just trying to better understand maybe why we didn't see some incremental benefits there. Maybe for Dr. Vleugels, building on an earlier question about use, given that Zumi does have a higher efficacy, could you envision a scenario where you would pull patients off a JAK inhibitor and turn them back to Zumi? As a follow-up, we did notice that there were some UTIs in the dose arm. Do you find that clinically meaningful? How does that relate to conjunctivitis as a treatment burden? Thanks. Thanks. Yeah. Appreciate the question. I think with the high dose, what we're seeing at that single data point, we did see over on the EASI-90 and IGA, it's just noise. I think when we put out maintenance data next year, it'll look very similar to the mid -dose. We did recapitulate the exposure response that we know exists with Allergen, and we're just capturing all that with the mid -dose, which is a huge win because we're getting there with four dosing days. I think further data in the future that we'll release will show that they are just quite similar. Happy to hand it to Dr. Vleugels for her thoughts as well. Thank you. I'm going to try to answer both questions. The first is whether a dermatologist would pull patients off a JAK inhibitor. I think that this is highly likely, and this is coming from someone who is considered a world expert in JAK inhibitor use in inflammatory diseases. The challenge with JAK inhibitors is not that they don't have efficacy; it's that, by and large, the dermatology profession, both physicians and APPs, have some hesitancy, some substantial hesitancy, with their use given their box warning. The vast majority of prescriptions for JAK inhibitors are for the lower dose when there's two doses available. We often have, as I mentioned, our clinicians cycling through many biologics, even when they don't have substantial improvements in efficacy, rather than putting patients on JAK inhibitors. Once a patient actually gets on a JAK inhibitor, what we often see is use of the lower dose, trying to taper them off as quickly as possible, trying to stop them as quickly as possible. As I mentioned in my brief remarks, atopic dermatitis is a chronic illness, right? You could see from the patient demographics, the vast majority of patients had had their disease for over 20 years, right? What we need is a highly efficacious therapy with a clean safety profile. The average dermatology provider will 100% take a patient off a medicine that has a box warning if they have a therapy that has similar clinical efficacy. I think that is a fairly simple and straightforward question. The second is about urinary tract infection. I think that this is just essentially somewhat random. There's no mechanistic reason to have an increased risk of urinary tract infection on this type of medicine based on this mechanism. One thing I will align on, just to kind of put this into clinical context, is that urinary tract infections are common enough that in major medical centers, we actually have visit pathways where our patients can send in a message and get their UTI treated without a traditional visit, because they are so common. One of the challenges of doing clinical trials is when there are common things that happen to large pools of patients, and there are ends in our study that are on the smaller side when we're comparing dose ranges, we can have an increased number of something as common as a UTI seen. I have no concerns about this being a mechanistic concern of this class and don't expect to see any concerns in the phase III. Thank you so much. Ladies and gentlemen, that concludes today's call. Thank you all for joining. You may now disconnect