Good morning, and welcome to Apogee Therapeutics' conference call. At this time, all participants are in a 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. Noelle, you may begin your conference. Thank you, operator, and thank you all for joining us today. This morning, we issued a press release outlining positive pharmacokinetic, pharmacodynamic, and safety data from our ongoing phase 1 healthy volunteer study of APG777 for the treatment of atopic dermatitis and other inflammatory diseases. The press release and the slides that we will be using during our call today are available in the investors section of our website at apogeetherapeutics.com. During this call, we'll be making forward-looking statements related to our current expectations and plans for the company and our clinical programs, including APG777. These statements represent our views as of this call and should not be relied upon as representing our views as of any date in the future. On the call with me today, in order of appearance, is our Chief Executive Officer, Dr. Michael Henderson, Chief Medical Officer, Dr. Carl Dambkowski, and Senior Vice President of Clinical Development, Dr. Kristine Nograles. Following this presentation, we'll have a Q&A session. Let me now turn the call over to Michael. Thanks, Noelle, and thank you all for making the time today. Apogee was founded to create potentially best-in-class medicines for patients living with inflammatory disorders, with an initial focus on atopic dermatitis, asthma, and COPD. Patients with these conditions have limited treatment options, either not responding to therapy or requiring injections every few weeks. We believe these patients deserve improved options and the ability to live more normal lives. We refuse to stop at good enough. Today marks the first major clinical milestone on that journey, and with our new phase 1 data for triple seven, we are well on the way to delivering on that mission. In addition to the phase 1 data release we will walk through today, we are excited to announce a number of updates and accelerations across the pipeline. We plan to initiate the triple seven phase 2 in atopic derm ahead of schedule in the first half of this year and pursue an integrated phase 2 design, which we believe could enable us to shave years off the typical development timeline. In addition, we have a high concentration formulation of 180 milligrams per milliliter, enabling a 44% higher dose than Lebrikizumab in the same volume. Beyond triple seven, we're thrilled to announce we received regulatory clearance to initiate our eight oh eight phase 1 trial in healthy volunteers and plan to begin dosing in the first half of this year, enabling us to bring forward interim data to the end of this year. We see each of these achievements as a sign of the operational excellence we are constantly striving for at Apogee. As a reminder, we designed triple seven to have many characteristics that would minimize the overall risk profile of our program. There are three elements I wanna highlight. First, triple seven and Lebrikizumab have an overlapping epitope, binding IL-13 in a similar manner. This minimizes both target and biology risk, given the robust third-party clinical data from the thousands of patients treated with Lebrikizumab. Second, we confirmed this overlapping biology to the leading drugs in atopic derm preclinically, demonstrating we are as potent as both Lebrikizumab and Dupixent in preclinical studies. These first two points gave us confidence that if we could achieve our intended drug exposures in the clinic, it would be a critical milestone for the program. Finally, as we have shared before, we tested triple seven in non-human primates head-to-head with Lebrikizumab and showed significantly improved half-life. The key question for this program has been whether the improved preclinical profile would translate into humans. Today, we're thrilled to say it has, and in fact, has exceeded all our expectations. We laid out clear goals for the phase 1 for what we needed to achieve in terms of safety, pharmacokinetic, and exposure targets for triple seven. In addition, we saw upside opportunity in looking at key biomarkers. On half-life, we observed a well-behaved PK profile across all cohorts, including initial data from our MAD study. While our target was at least a 33-day half-life, we exceeded that by a wide margin with a 75-day half-life. Consistent with the IL-13 class, we tested doses up to 1,200 milligrams and found the doses to be well-tolerated based on the initial data. In addition, we have initial data from our multiple dose cohort that reinforces our PK profile. Moving to the second goal, we wanted to achieve exposures at least in line with that of Lebrikizumab during the 16-week induction phase. Given the better-than-expected PK profile, we are now in a position to test higher exposures of drug and induction to potentially drive improved clinical responses over standard of care, including EASI-75, EASI-90, and IGA 0/1, while still cutting the number of injections patients must take in half. With regards to maintenance, we knew from market research that every two months would be highly differentiated, which is why we set it as the bar. We are thrilled to report that we now have the potential to go beyond that and deliver an every 3- to 6-month maintenance dose. This represents 2-4 injections per year, compared to the current paradigm of 26 injections per year. We achieved a number of highly complementary supporting data as part of this release. These data include positive, prolonged pharmacodynamic effects across the key atopic biomarkers, pSTAT6 and TARC. I'll hand it off to our CMO, Dr. Carl Dambkowski, to walk through the clinical data in more detail. Thanks, Michael, and good morning, everyone. It's my pleasure to be able to share our interim phase I results for APG777. We are really excited about this data, as we believe APG777 has the potential to profoundly impact patients' lives, both patients with atopic dermatitis, as well as other inflammatory conditions. Our interim data demonstrate the potential to test higher exposures in induction, which could lead to improved clinical responses, as well as every 3- to 6-month dosing in the maintenance setting of atopic dermatitis, an up to 13-fold decrease in the injection burden compared to currently available therapies. The data we'll discuss today is from our ongoing phase I healthy volunteer study being conducted in Australia, which has a SAD component and a nested MAD component. In the SAD, we have tested doses up to 1200 milligrams, and in the MAD, we have tested repeat doses of 300 milligrams. The trial is fully enrolled, and today we'll be presenting interim data on safety, PK, and biomarkers from the SAD portion of the study, in addition to preliminary safety and PK data from the MAD portion of the study. Here you can see the baseline characteristics of participants in the study, which are in line with what you'd expect for a phase 1 study. Demographics were well-balanced across cohorts. APG777 has been well-tolerated, with a favorable safety profile across all cohorts, including SAD doses up to 1200 milligrams. The safety profile is in line with expectations for therapies targeting the IL-13 pathway, such as Lebrikizumab and Dupixent, which have well-documented and benign safety profiles. AEs have been mild and generally unrelated to study drug. There have been no SAEs and no dose-dependent trends in AEs. We have seen only 2 injection site reactions in the study, despite giving over 60 injections, and in the 5% of participants that had an injection site reaction, they were mild and resolved quickly. There have been no cases of conjunctivitis. APG777's PK profile has been favorable. The half-life of APG777 is approximately 75 days and is well above the 33-day threshold required to enable every 2-month dosing. Moreover, APG777 demonstrates dose proportionality and low variability, all of which have been consistent with the preliminary MAD data. The PK profile of APG777 will allow us to do 2 important things in the clinic. First, we will be able to test exposures in the induction setting that are designed to exceed those of Lebrikizumab and could lead to improved clinical responses based on recent Lebrikizumab data from the European approval. Second, we will test exposures in the maintenance setting of atopic dermatitis that will equal those of Lebrikizumab, but with much less frequent dosing at an interval of every 3 or 6 months, which will allow patients to inject just 2-4 times a year, compared to 13-26 injections per year with currently available therapies. In this study, APG777 also showed an effect on the two key biomarkers for IL-13 targeting and atopic dermatitis, which are pSTAT6 and TARC. pSTAT6 is the first downstream biomarker after the key pathogenic step in atopic dermatitis, the heterodimerization of IL-13 receptor alpha 1 and IL-4 receptor alpha, with IL-13 as the glue in between. Therefore, this is a critical measure to demonstrate APG777's inhibition of this key inflammatory pathway. TARC is the inflammatory biomarker with the greatest correlation to atopic dermatitis severity and is the most robustly studied biomarker in the field. In our phase I study, APG777 showed deep and sustained inhibition of both of these key biomarkers. Since no clinical comparator exists for p-STAT6, despite it being a central biomarker in the IL-13 pathway, we initially looked at pSTAT6 in non-human primates, comparing an APG777 tool compound to Lebrikizumab. In addition to a significantly prolonged half-life, pSTAT6 inhibition was also extended and to a greater extent than PK alone would suggest. So prolonged exposures of a therapy targeting IL-13 demonstrated a prolonged duration of pSTAT6 inhibition, which show continued prevention of inflammatory signaling downstream of the key pathogenic step in atopic dermatitis.... and here is our pSTAT6 data from the clinic, where we saw that a single dose of APG777 led to near complete and prolonged inhibition of pSTAT6, up to and including 12 weeks after dosing, the longest available follow-up we currently have on biomarker data. TARC inhibition, shown here, has also been deep and sustained after a single dose of APG777. Here we have a clinical comparator from a non-head-to-head study in healthy volunteers, as Dupixent also looked at TARC changes after a single dose in their phase 1 healthy volunteer study. In comparing light doses, 300 milligrams of APG777 on the left and 300 milligrams of Dupixent on the right, we see that inhibition for TARC is similar to Dupixent, although more prolonged for APG777, up to 12 weeks after dosing, the longest available follow-up we currently have for biomarker data. So both pSTAT6 and TARC, the two key biomarkers for IL-13 targeting in atopic dermatitis, show deep and sustained changes in response to a single dose of APG777. We set out to create an optimized antibody. On the left-hand side, you can see that this included targeting IL-13 with an overlapping epitope to Lebrikizumab and ensuring equivalent or better potency. Today, we have shown the translation of this antibody engineering approach into the clinic. On the right-hand side, you can see the clinical profile of APG777 is favorable. APG777 demonstrated an approximately 75-day half-life, dose proportionality, and low variability. APG777 has been well-tolerated, with a favorable safety profile, as expected for an IL-13 targeted therapy. And finally, on the two key biomarkers for atopic dermatitis, pSTAT6 and TARC, a single dose of APG777 showed deep and sustained inhibition up to 12 weeks after dosing. On every front, these results have exceeded our expectations for APG777. The optimized antibody profile will allow us to test potentially higher induction exposures, which could lead to improved clinical responses and prolonged maintenance dosing of every 3-6 months in our phase 2 study, which is an up to 13-fold decrease in the injection burden for patients with atopic dermatitis. I'll now turn it over to my colleague, Dr. Kristine Nograles. who will discuss how we plan to take APG777's favorable profile into a phase 2 trial in atopic dermatitis, with a planned start first half of this year. Christine is a trained dermatologist with over 15 years' experience across academia and the biopharmaceutical industry. She was part of the core team developing the approved therapeutics Olumiant, KORSUVA, and Otezla. Thanks, Carl. With a planned initiation in the first half of this year, leading to the hallmark 16-week induction readout in the second half of 2025, there are two key elements related to the PK profile we've just shared. First, the optimized PK profile of APG777 has enabled our ability to test exposures in the induction setting of atopic dermatitis that are designed to exceed those of Lebrikizumab by about 30%-40%, which could potentially lead to improved clinical outcomes. And second, APG777 is designed to have prolonged maintenance dosing, with a dose every 3 months that exceeds Lebrikizumab maintenance exposures and a dose every 6 months that equal lebri's maintenance exposures. As a reminder, these maintenance doses could reduce injections to just 2-4 times a year versus 13-26 with currently available therapies. We will walk through the modeling for these doses in subsequent slides. These induction and maintenance dosing options are enabled by APG777's high-concentration formulation at 180 milligrams per mL, which potentially allows for the delivery of 360 milligrams in a 2-mL auto-injector in the commercial setting. Because we believe it is key for APG777 to get to patients as rapidly as possible, we have an integrated phase 2 design that incorporates both phase 2-A and phase 2-B elements, which has the potential to save significant time on the journey to BLA compared to a traditional sequenced approach. Our integrated phase 2 design will begin with a proof-of-concept component, where approximately 110 patients will be randomized 2 to 1 to APG777 or placebo. Patients who complete the induction period will have the opportunity to enter the maintenance period and roll over to an open-label extension. We expect to start this part of the study in the first half of this year, and top-line data is anticipated in the second half of 2025. Since we are combining phase 2-A and phase 2-B elements into a single protocol, we expect to be able to initiate the dose optimization component of the study in a more streamlined approach, which allows for significant timeline acceleration with no delay in site startup between the two parts. In this part of the study, we will further assess additional dosing regimens, the best one of which we will be taking to phase 3. We will continue to look for opportunities like this to speed up our timeline to BLA. We will now step through in detail the regimen selected for the part A portion of the study. Here you can see the modeled exposures for the full 52-week study period for APG777, highlighted in blue, compared to Lebrikizumab, highlighted in gray. First, we want to test APG777 exposures that exceed those of Lebrikizumab in the induction setting, as recent Lebrikizumab data demonstrated an exposure response in that setting. Second, in the maintenance setting where Lebrikizumab has not shown an exposure-response relationship, we will test APG777 exposures that will at least equal Lebrikizumab's exposure, with a focus on maximally prolonging the dosing interval in order to provide the greatest potential to reduce injection burden for patients. The goal of APG777's induction regimen to exceed the exposures of Lebrikizumab stems from recently released data from their EMA approval. Specifically, Lebrikizumab data demonstrated that lower body weight, which was associated with an increase in exposures, showed consistently greater efficacy across all key endpoints, as shown in this graph. This exposure response suggests that greater APG777 exposures could potentially lead to improved outcomes for patients with atopic dermatitis. Compared to the overall phase 3 population for Lebrikizumab, the lightest weight subgroup with the greatest exposures, approximately 30% greater exposures than the overall population, consistently had higher efficacy across key endpoints, such as EASI-75, the primary endpoint, and EASI-90 and IGA 0 and 1 endpoints, reflecting greater depth of response. We have selected an APG777 induction regimen that we believe will have approximately 30%-40% higher exposures when compared to Lebrikizumab, and thus test the hypothesis of how much additional benefit is possible for patients treated with APG777. We will do this with almost 50% fewer injections in the first 16 weeks of treatment. Our induction regimen shown here is anticipated to provide approximately 30%-40% higher exposures than Lebrikizumab, but with approximately 50% fewer injections. After 2 loading doses of 720 milligrams, additional injections of 360 milligrams will be given at weeks 4 and 12, before patients continue on to maintenance treatment. You can see here that APG777's exposures significantly exceed those of Lebrikizumab, with almost half the number of injections. In the maintenance setting, APG777, administered every 3 months, is anticipated to have exposures that will at least equal those of Lebrikizumab. When given to patients long-term, this seasonal dosing regimen is designed to be given 4 times per year, compared to currently available therapies that need to be injected 13-26 times per year. Given the PK results and the 180 mg/mL formulation, we will also be able to test an every 6-month maintenance regimen for APG777 that also matches the exposures of Lebrikizumab in the maintenance setting. This could provide the first twice-yearly biologic for an inflammatory skin disease. We are excited to launch our phase 2 trial this year, where we will be able to test the full potential of APG777, including an induction dose based on APG777's optimized PK profile that will provide exposures exceeding those of Lebrikizumab and could potentially lead to improved clinical outcomes. We will also test maintenance doses of every 3-6 months, which could reduce the injection burden up to 13-fold compared to current standard of care, while equaling Lebrikizumab's exposures. I'll now turn it over to Michael to discuss how APG777 fits into the atopic dermatitis landscape and our corporate vision. Thank you, Christine. As you've heard from the team, we could not be happier with the data we've shared today, along with our plans for future studies. The culmination of today's update de-risk a potentially best-in-class drug for the treatment of atopic derm patients. Treatment options are severely limited for these patients, and we know innovation that can improve efficacy and prolong dosing is what matters to these patients and wins in these markets. The design elements and engineering decisions that have led to triple seven give us the possibility of a highly attractive commercial profile of an every 3- to 6-month dose drug, with the potential for low single-digit COGS and novel IP into the mid-2040s. As many of you know, atopic derm is an enormous opportunity with high unmet need. To contextualize this, here you can see the number of moderate to severe patients with atopic derm compared to the other large I and I markets. Atopic derm is both the largest and least mature, with more projected growth than any other. Penetration is currently in the single digits for atopic derm, versus 25%-60% for the more mature markets, with each point of market penetration representing $1 billion top line. Given the high unmet need and transformational potential of triple seven, we feel we have a potentially best-in-class agent that, if approved, could become the leader in an over $50 billion market. Psoriasis remains an instructive analog of how these markets develop and what wins over time. Here, you can see efficacy on the Y-axis and dosing interval on the X-axis. A few points to take away. First, each of the drugs you see on this slide happily coexist and are blockbusters in their own right. These are not winner-take-all markets. Second, the major driver of commercial success in the more mature years of psoriasis has been driving towards more convenient dosing intervals. Skyrizi, with its every 3-month seasonal dosing, has taken the number one spot despite being launched last. We believe this is how the atopic derm market will mature and how Apogee can win. Atopic derm, by contrast, is the veritable definition of white space, with nothing beyond every 2- to 4-week dosing available. With the data today, we feel confident in our potential to transform this treatment paradigm out to every 3- to 6-month dosing, and with higher exposures and induction, we have the potential to achieve greater efficacy as well. Market research shows triple seven with every 3- and 6-month dosing is highly differentiated, which could take 90+% of new starts and the majority to two-thirds of patients switching over to triple seven from standard of care. Based on these numbers, we estimate a drug well north of $10 billion in peak sales potential if approved. I'd like to close with a summary of what we have accomplished and where we are going. With triple seven, we have consistently beat timelines, starting our phase one study early, reporting PK results that beat in every sense well ahead of schedule, and now starting a phase two sooner than anticipated. Looking forward, we're guiding the phase two A 16-week proof of concept data in the second half of next year and plan to launch additional expansion indications next year as well. With APG808, we are excited to announce today we've also significantly accelerated our timelines. We received a regulatory clearance last month and look forward to initiating the phase 1 in the first half of this year. We now expect PK data similar to today's release in the second half of this year, with early proof of concept in asthma patients in the first half of next year. We aim to rinse and repeat the success of APG777 with this program and the full pipeline. This type of operational excellence is what we strive for at Apogee. We continue to make progress with our earlier pipeline and expect OX40L to enter the clinic next year. We plan to disclose additional details around our combination strategy, as well as a new target to support that effort at our R&D day later this year. With a strong balance sheet that funds us a full 12 months past all the catalysts you see here and an exceptional team, we are excited to keep advancing this pipeline as expeditiously as possible. Thank you for your time and attention today. We can now switch to the Q&A portion of the call. Thank you. At this time, I would like to remind our teleconference participants, in order to ask a question, please press the star followed by the number 1 on your telephone keypad. We'll pause for just a moment to compile the Q&A roster. Our first question comes from the line of Akash Tewari of Jefferies. Please go ahead. Hey, thanks so much. So we've seen with both APG777, and I think the Viridian YTE mutation, that the half-life jump from non-human primate to human seems to be meaningfully better than your base case expectations. You know, what's really leading to that? Is that primarily from moving away from the Lebrikizumab scaffold, or are there improvements your team's making on volume of distribution and binding kinetics that apply to your pipeline more broadly? And kinda given that better-than-expected half-life, would it be possible for your APG808 to potentially look at biannual dosing beyond just the natural recycling of the IL-4 receptor, which occurs, every 1 or 2 months? Thank you. Hi, Akash. Thanks for the question and for joining, nice and early. So we were very excited to see the outcome, as you suggested, which, you know, was above the expectations that we had. You know, I think it's important just when we think about making an antibody towards the targets that we go after, be it for IL-13 with 777, or IL-4 receptor alpha for 808, or OX40 ligand with 990, we make sure that we are always trying every permutation of different backbones, of different half-life extension mutations, both YTE, LS, others. and every permutation that we can around the antibody to get to the very best antibody against these targets. We do this by testing them head-to-head pre-clinically in non-human primates, to get to all the characteristics that you want to see: lower clearance, improved volume of distribution, as good or better kinetics than parent compounds. And with triple seven and with eight oh eight, we've been really happy with the profiles that we've shared. And this translation, we think, today, shows that it does kind of hit on our our best-case scenario and enables us to test the higher induction exposures, but also move to 3-6-month in maintenance. So with eight oh eight, we're excited now to have accelerated that, and we'll have data at the end of this year. We'll see where that lands. We think that an every 6-to-8-week regimen, in the context of COPD, where there's yet to be an approved biologic, do be likely to be approved within every 2-week maintenance dose could be a game changer for patients. Thank you. Our next question comes on the line of Tyler Van Buren of TD Cowen. Please go ahead. Hey, guys. Congratulations on the tremendous data and exceeding all expectations. Have a couple. On the first one, on efficacy, so just to be clear, the 30%-40% higher exposure that's planned in induction versus Lebrikizumab should lead to clinical responses and outcomes in line with patients weighing below 60 kilograms that have the highest clinical response to lebri, right? And as we think about the EASI IGA endpoints, do you believe one endpoint is more sensitive to increased exposure versus the other, as we think about it improving patients' daily lives? Thanks, Tyler. I'll hand it off to Carl to walk through this. Yeah, thanks, Tyler, for the question. You know, I think this is a really important part of what we're targeting in terms of our exposures in the induction setting. You know, so on the efficacy standpoint, we've specifically designed the exposures in the induction setting to hit a target of 30%-40% greater than the modeled exposures for Lebrikizumab, to really try to harness the potential for improved clinical responses there. You know, as we showed, and you can see from the EMA approval, in that lower body weight group, the less than 60-kg group, you know, they did have numerically higher responses across the EASI-75, EASI-90, and IGA 0/1. You know, and according to the data, they're about 30% higher exposures as well. So that was the design specifically related to the new data from Lebrikizumab and really looking at those exposures. In terms of the endpoints, we think the trend was seen in that low body weight group for all the endpoints, EASI-75, EASI-90, and IGA 0/1. But if you look at it, right, it's probably the strongest for the more stringent endpoints, being EASI-90 and IGA 0/1. W e're really excited to move APG777 forward this year into a phase 2 trial, where we'll target that higher exposure of 30%-40% greater than the exposures of Lebrikizumab in the induction setting, and present that data second half of 2025. Okay, and just one more. So the human half-life is obviously way up there, and the threshold for maintaining clinical response appears quite low based on the Lebrikizumab data. So what's the probability that you guys might even be able to maintain some patients by dosing APG777 annually? Yeah, good question, and it is something that we've talked about. I think when we look at all the data that exists, right, we don't know, to the point of your question, where the floor concentration is. So in our phase two, we'll be testing, of course, a 6-month arm, and that will teach us a lot about, right, the characteristics of patients that do respond and are maintained on that 6-month arm. And, you know, we'll be thinking through what could a yearly option look like, be it either, right, that dose or a higher dose, and I think more to come there, but it's definitely something that, in line with kind of the mantra of the company, refuse to stop at good enough. We would love to be the first to keep pushing the bar and get there if it's possible. Thank you. Our next question comes on the line of Alexander Thompson of Stifel. Please go ahead. Hey, guys, congrats again on the data. Charles here for Alex. I just wanted to ask a quick question, if you expect to share OLE data at the time of the 16-week top line. Thank you. Yeah, great. Thanks for the question. T he planned second half of 2025 data will be for just the top-line 16-week induction data, right? That has really become the hallmark readout for atopic dermatitis. As you saw from the trial design, we will allow all patients to roll over to a maintenance arm and then an OLE after that, if they continue to benefit from treatment, and those data will be presented at a later date. Thank you. Our next question comes on the line of David Nierengarten of Wedbush Securities. Please go ahead. Hey, thanks for taking the question. I had one. If you had plans for, like an exploratory switching study, maybe from patients, switching off of Lebri, maybe in heavier patients, switching off of Lebrikizumab, obviously after a potential approval for, Lebri. That was my question, and the quick one on if you detected any, anti-drug antibodies. Thanks. Yep, thanks, David. So, I think we're excited for the phase 2 as we've designed it, because, right, the integrated design will get us to our optimized dose as well. I think with that optimized dose in, you know, a number of studies that we'll look to, look to consider. Switching studies are definitely 1. I think that, right, we see from our market research and from all of our interactions with physicians and patients, you know, switching from Lebrikizumab to be one potential option, also switching from Dupixent, which is where our market research has been focused, and where, right, and every two-week option leaves a lot on the table, potentially for patients, to be something that we'll definitely look to consider, along with additional expansion indications to prove out the full pipeline and the product potential of this drug. And then your second question, on, you know, did we see any ADAs in the trial? I'll hand to Carl. Yeah. There was no apparent ADAs that were noticed on the PK profile in the trial at this date. Great, thanks. Thank you. Our final question comes from the line of Julian Harrison of BTIG. Please go ahead. Hi, good morning. Congrats on this update, and thank you for taking my question. Considering the exposure response curve for Lebrikizumab in atopic derm that became more apparent in the EMA review documents late last year, and also your pSTAT6 and TARC comparisons shared today, I'm curious if this collectively suggests a wider therapeutic window than prior expectations for APG777 in asthma and maybe other indications as well? Yeah, I'm happy to touch on that. So I think it, I think it suggests that there could be. Right, we When we look at kind of the, the indication where, right, we have the most data from atopic derm, there's clearly something there, and we are very excited to explore that. And we also, right, we, we know what the higher exposure group for Lebri look like, but we don't know if that did peak out either. Right? We, we just are responding to the data that we have. I think when we look at asthma, right, in January of this year, for instance, there was a post hoc analysis of the Lebrikizumab phase 3 asthma studies that showed that even at a, you know, roughly 5x lower dose than what we'll end up taking into asthma, there was in the high eosinophil at least one exacerbation group. A post hoc analysis showed that they did respond as you would expect to treatment. So I think higher doses there, data could suggest would lead to improved responses. So I think that we'll look to do that kind of and explore those dose ranges across any indication that we take triple 7 into. Excellent. Thank you. Thank you. We have an additional question from Seamus Fernandez of Guggenheim Securities. Please go ahead. Hi, this is Colleen on for Seamus. Thanks for taking our question. Congrats on the data. So we just had a question about some of the language of the AEs in the PR, vascular access, pain and bruising and vessel puncture site bruises were listed as common to AEs. Could you expand on these observations? Is there anything unusual, or are these typical events seen with other subQ? Thanks. Yeah, thanks for the question. And, you know, those are actually related to actually blood draws. So not actually related to the injection of APG777. So vascular access, pain, vascular access, bruising, et cetera, are actually when they're getting their blood drawn for labs and PK, et cetera. So actually, you know, unrelated to study drug or study injection from that standpoint. You know, fairly common. We draw a lot of blood to create these PK and PD curves, and so, you know, not every one of those goes perfectly. In terms of the injection site reactions, as we said, 2 injection site reactions across over 60 injections that were given during the study. And in those participants, 1 was injection site pain and 1 was injection site erythema. They were both grade 1, and both resolved very quickly after the injection. Thank you, ladies and gentlemen. As we have no further questions at this time, we will conclude today's conference call. We thank you for participating, and you may now disconnect.