Thanks for being back with us. Happy to have the Apogee Therapeutics team here live from Paris at EADV. So, you know, we got the whole crew here. So maybe I'll start things off, kicking over to Michael for a brief overview of the company, and then we'll get into a Q&A. So, Michael, over to you. Great. Thanks, Alex. Yeah. And I'm glad to kind of be able to join. Big week for us, obviously, meeting a number of KOLs, but also three different abstracts presentations at EADV, including a late breaker on Friday where we'll have some new data from our phase II, which we're excited to share. So, Apogee, we are creating potentially best-in-class mono or combination therapies for the largest markets in I&I with a large focus on atopic derm. Our lead indication, we have an IL-13 antibody, which read out phase II data earlier this year over the summer. That trial is still ongoing. The Part B of the study we're doing next year. As kind of we see different data coming out at EADV and over the past few months, we believe that we have the next most exciting launch for our frontline drug of choice in atopic derm later this decade. We're following those readouts next year with our combination study as well. We want to be serial innovators in atopic derm and the indications that we pursue so best-in-class monos or combination therapies to really truly own the space. Each of our antibodies are designed de novo so that they can be co-formulated together and administered together as well. Beyond AD, we're also looking at, you know, respiratory indications and the full expansion indications that DUPIXENT has with a full suite of antibodies, including a TSLP and an OX40 ligand as well. Great, so I think that would be helpful to level set right now and talk about, you know, where we're at in atopic derm. What did the commercial landscape look like, especially with the recent launches of lebrikizumab and nemolizumab as well? Yeah. Jeff, you want to take that? Yeah, sure. Yeah. Thanks, Alex. So it's an exciting time, obviously, to be in atopic dermatitis. The biologic space is exploding with growth right now. If you look at the latest IQVIA data, July, so looking this year versus last year, the entire market is up 25% and continues to grow quarter over quarter. Importantly, when you look at the new-to-brand prescriptions, it's up 48%. And that's a lead indicator, as you know, for sort of where that market's going. We don't see really any slowing of the market when you think about the fact that we only have about 10% biologic penetration in the AD space. As far as the new competitors are concerned, so the really strong launches of both EBGLYSS and NEMLUVIO, we are encouraged by both of them, as you can imagine. If you look at how they're performing in their first 10 or 11 months post-launch, their TRx are actually even above that of a couple of the strongest plaque psoriasis launches, looking at SKYRIZI and BIMZELX. In fact, EBGLYSS grew in Q2 versus Q1 about 40%. And if you look at NEMLUVIO, it grew over 100% from Q1 to Q2. So clearly large and growing market and certainly a real need in the market for new entrants like 777. Yeah. And I think, Michael, you alluded to, you know, kind of the recent, you know, data sets that have been coming fast and frequently in the atopic derm space. You know, what are your thoughts on what we've seen, you know, out of the OX40s over the last 12 months and some others? You're on mute. Thanks. I blame the jet lag. It's been a really interesting, you know, set of conferences. When we showed up to EADV last year, right, there was, I think, a lot more excitement about OX40 and OX40 ligands and kind of newer mechanisms. And, you know, the mood this year, conversations we've had so far, it's just this realization that the frontline drug of choice for a while is going to continue to be DUPIXENT. EBGLYSS is getting a little bit of that. For For really itchy patients, there's NEMLUVIO, as Jeff alluded to. But aside from that, while, you know, AD is seen as "crowded," it's really crowded in the second, third, fourth, fifth line where only JAKs exist right now. And that's where amlitelimab and rocatinlimab are going to be situated. But for a frontline drug, and we just did some market research, which we can get into based off of our Part A data, there's really nothing ahead of us that's launching this decade. And when we tell docs about our profile, right, we're talking 60%, 60+% make it their frontline drug of choice versus DUPIXENT and versus EBGLYSS versus NEMLUVIO versus everything else that's out there. So there are just a ton of patients that still need better therapies and a quarterly or better drug, which doesn't sacrifice on efficacy like the OX40 or OX40Ls continues to be, you know, the "SKYRIZI" of AD to a lot of these docs. Yeah. And, you know, obviously, you just had your II-A data a few months ago. You're going to present some more this week. You know, at a high level, what was the goal of this study and maybe some of the key takeaways that we should focus on? Yeah. Carl, do you want to speak to that? Yeah. You know, happy to. And I'll just repeat for everyone, we have a late breaker Friday. And so excited to kind of enhance the data set that we put out, you know, in the summer. The goal of the study is really to show similarity to Dupi and Lebri, you know, and a safety profile in line with those as well, which we think, you know, when you look at the totality of evidence, we're really in line with them. You know, we really focused this proof of concept portion of the study on the endpoints of EASI-75 and percent change from baseline and EASI just because of the size, you know, and the stage that we're in overall. And so we're really happy with the data that we walked away from there, which we thought was, you know, again, at least similar to Lebri and Dupi with really some standouts that we were really excited about. One EASI-75 where we saw a 66.9% top line number and a 42.5% placebo-adjusted number. You know, really exciting to see two out of every three patients responding. And the reason that number is so important, right, is because that's what docs are really focused on right now in the AD landscape. You know, we hope that over time we push that bar up. But right now, you know, docs are really looking to get EASI-75 because that really gets a patient from moderate to severe disease to mild disease. And so it's a huge change for patients. You know, and then itch is really important to patients. We showed statistically significant changes in itch as early as one week after treatment. That's the earliest data point we've presented so far, so you know, early itch relief and really deep itch relief over that 16-week period too, so it's really important for patients overall, so excited by the profile, and we're doing all that with four dosing days compared to nine with Lebri and Dupi. So still, you know, really big stepwise change too in terms of number of injections and number of dosing days during that period. So, you know, going into this study, one of the other hypotheses you were testing was whether or not you could push exposure with this mechanism and see, you know, more efficacy based on some of the, you know, data out there for lebrikizumab. I guess based on the data that you presented and you've seen so far, are you more or less confident that there's a thread to pull there? Go ahead, Carl. Go ahead, Michael. You can start it off, and then I'll add. Continue to be glad that we're running the proper experiment. I guess it's just the answer, right? We're a. a. We've always been a data disclosive company, right? We've talked about the data that has been out there for EBGLYSS, right? From phase II-B to the EMA review. Then, right, we showed our own exposure response quartile analysis from our phase II-A. We are. From the very beginning, we wanted to make sure that we were fully exploring the IL-13 exposure response curve and continue to be glad that we are, you know, fully testing that in phase II-B. we kind of leave it up to investors who, you know, are smart and good at this to look at it and come to their own conclusion. In our view, it is only upside. I think this is very important. When we do market research, when we talk to any docs, when we do our profile from Part A, right, full top line placebo-adjusted efficacy on every endpoint, full safety tables compared to the labels of DUPIXENT, EBGLYSS, et cetera, 60% share to us. If we say, "What if we had five to 10 points better efficacy?" The docs kind of laugh and say, "Yeah, sure. Why not?" But it's only upside and not needed. And then maybe on the safety profile, you know, I think the data point that stood out to some folks was conjunctivitis. I guess, you know, given that this is an on-target adverse event, was this higher rate than you were expecting? How should we think about these data in context with what we've seen from DUPIXENT and lebrikizumab? Yeah. I think it's within the range of what has been seen, especially from the more recent studies of DUPIXENT and EBGLYSS, and when we talk to docs, right? When DUPIXENT ran their studies, it wasn't known that it was an on-target adverse event. It's now an adverse event of special interest. People look for it, so it used to be, "Hey, how are you doing?" You know, to get your AEs. Now the site coordinator says, "How are you doing?" And, "Oh, by the way, how have your eyes been? Have you noticed any redness?" so it's just, it's looked for. I think people look for it to, you know, proactively manage it with eye drops, which I think this is important. Nobody knows what conjunctivitis is. Like if we were causing, you know, upper respiratory infection or, you know, like left toe pain, it would be such a, it would not have been such kind of, I think, a data point. But it's just not, it's very known to derms because they deal with this. And they've come to experience it with one in five patients that are on DUPIXENT, which is what we saw in our study. I think importantly, you know, as we think about adverse events, we didn't see any discontinuations. They do happen with DUPIXENT. They're rare. And when we talk to docs and we ask, you know, what do you really care about the most for adverse events? Is it conjunctivitis? Is it, you know, infection risk? Is it fever, chills? Is it injection site pain? It's injection site pain, right? That's why patients most commonly stop these drugs. That's why half of patients drop DUPIXENT within two years. And we were glad to report zero ISRs in our study. That will go up over time. It will not be zero forever. And I imagine our conjunctivitis rate will be, you know, within the range of what's been seen by EBGLYSS and DUPI. I think on the top line, Carl, you made some comments around, you know, your ongoing studies. I guess anything more you can say about the ongoing maintenance study as well as the II-B around safety? Just that, right, these studies are monitored closely and nothing of concern. Yeah. So I guess what should we expect on Friday with your late breaker? What more information are you planning to present beyond the top line? You know, let's kind of run it. I think we're in Vegas, so we won't come to Paris and see Alex. Okay. Sounds good. Looking forward to it. All right. So with the ongoing phase II-B, I guess, you know, what is the kind of, where do the doses fit in relative to what you were testing in the phase II-A? Yeah. Please, Carl. Yeah. So, you phase II-B ongoing with a mid-2026 readout. So really excited about how enrollment's going overall. I think a lot of excitement from our sites and docs overall testing three doses here versus placebo. The mid dose of it, I'll start in the middle just because that's the Part A dose. So 30%-40% greater exposures than lebrikizumab, same dose as was tested in Part A. And then from there, we're testing one dose higher and one dose lower. So the dose higher is about 90%-100% greater than lebrikizumab's exposure. So essentially double the exposure of lebrikizumab, which aligns with kind of quartile four of the quartile breakdown that we showed with the Part A data. You know, I think to your earlier point, Alex, like I think if we had the data in hand and we weren't testing that dose, you know, a lot of people would be looking at it and say, like, "Why aren't you testing a different dose? Why aren't you testing a higher dose too?" You know, docs and KOLs, you know, whether it's in blinded market research or one-on-one with us, repeatedly tell us they don't need better efficacy with the every three to six-month dosing paradigm that we're testing and only four injections or, sorry, four dosing days in induction. But, you know, as Michael said, right, you know, additional benefit, icing on the cake, whatever you want to call it, we want to make sure we're running this right scientific experiment. And then we're testing one dose lower. It's about half the exposure of lebrikizumab. That's really to make sure we have the right package for regulatory filings moving forward too. So we don't necessarily expect that to be as efficacious as the mid or high dose, but also want to make sure that we, you know, show a full dose response curve to regulators so we're not tripped up with anything there having to repeat, you know, multiple doses in phase III. Makes sense. And then you obviously mentioned your ongoing maintenance study for the II-A that reads out the first half of next year. What does good look like when we think about the top line data for that study? Yeah. Please, Carl. You're on a roll. Yeah. Sounds good. Yeah. You know, excited to see, you know, maintenance of response. So generally, how people have looked at this is taking those that responded in the induction period and looking at how long and what percent of them maintain response during the next 36 weeks. So out to 52 weeks. You know, for DUPI, somewhere in the 60-ish% range for EASI-75. That's kind of what they've shown as maintenance of response and around half of patients maintaining IGA 0/1. So looking for something, you know, at least in line with those drugs, obviously testing the paradigm of whether we can do that with every three-month dosing or even every six-month dosing there. So excited for that first half of next year. I guess do you need six-month dosing? It's a similar story as with the efficacy and induction. You know, I think that, yeah, I'll let Jeff. I'll start and maybe hand it over to Jeff what he's heard on the more commercial side of things. But what I say is, you know, we're one of the first companies, not the first company to actually look at maintenance dosing in a phase II-A trial, right? That has not been done before. So what we get out of that obviously is safety data. We get patients on long-term treatment. All those are really important for us. But what we also get is the ability to then understand how those two doses worked and then adapt in the phase III, right? Most people are just picking out of thin air in the phase III, hoping they have something that maintains responses. So we will have the ability to have an every three and six-month dosing. It's kind of how many milligrams of drug do we need to maintain responses since we'll be able to adapt to the data. But Jeff, you know, what you've been hearing on the KOL side of things? Sure. Yeah. Commercially, a quarterly dose is transformative, right? That's really the game changer in AD. The Q6 month dose is going to be a really nice one to have just because when you talk to physicians, what you get is you get about 10% more market share from physicians if there's that option for their patients. But I think really it's both from patients and physicians. The Q3 month dose is really what's going to change the market just as it has in plaque psoriasis. Yep. Makes sense. So maybe you wanted to pivot a bit to the combo study and the combo approach generally. I guess, you know, maybe to start off, you know, I'd love to hear your philosophy on why combos versus bispecifics. I don't know who wants to start, Michael. Yeah. Happy to. You know, when we think about, when we were kind of thinking, should we, because we could have pursued either, right? There's nothing magical to bispecifics versus kind of, you know, monos. They take a few more months preclinically in CMC, but, you know, they're very achievable. Our approach was, right, these are large markets where ultimately the best commercial presentation and fully kind of optimized target product profile is going to win, right? If you come in second or third, that's a lot of, those are billions that you're leaving on the table. So what is that? And how can we achieve it? Well, if you can co-formulate by engineering your antibodies preclinically to monospecifics, then you can get to a much better half-life and you can avoid the ADA risk that comes with bispecifics. You know, that's kind of step one. Step two is when you look at where bispecifics traditionally have been great, they're really great in areas where you want to bring two targets together, right? Here, you actually want the opposite. You don't want to mix antagonism with agonism. So you don't want to bring these targets together. There's nothing to be gained there. There's a theoretical risk that there's something to be lost. So the knock against, right, our approach versus the bispecifics is, well, you have to prove it. You have to prove that two monos are better. Well, if you want payers eventually to cover something frontline, you're going to have to prove it there too. So, you know, there's no free lunch in market access. If you want payers to eventually cover a bispecific or a co-form, a combination of any sort, then you're going to need to run a head-to-head study at some point. I think we're seeing J&J do that right now with their IL-4 receptor alpha, IL-31, and guess what? That drug has like a four- to seven-day half-life and it's dosed every two weeks in that study. Our approach is IL-13, where you need to push exposure combined with a very safe OX40L, whereas Amgen just showed us there's not really a dose response, so you need minimal drug co-formulated in every three-month injection so that we can get the right dose, and we will run the head-to-head study and we're doing that right now, so we're excited about it and are excited to read that out second half of next year. Yeah. I guess, you know, in the context of the trial design specifically, you know, I think the question is, is this a big enough and a robust enough study to answer that question that you have, you know, a better drug with this combination approach? Maybe Michael, if you want to start or Carl. Yeah. I'll start and then Carl can take time to sound smarter than what I say. So I think if you were to run a JAK versus DUPI in 50 to 100 patients, you would expect that it looks better, right? You would expect that it'd be noisy. Maybe it's not stat-sig, but you would expect to see better data on certain endpoints. Our view is that we should be able to run the study and identify where is the strongest signal that we're seeing to then power the larger studies, right? JAKs, when they went up against DUPI, those were three, four hundred patient head-to-head studies against a composite endpoint of speed to resolution and itch. JAKs ran those once they knew where they performed best. So, our view is, let's run this study. Let's see where we start to see the better data and the biggest delta versus DUPIXENT, which will inform later development. It is not powered for significance. Makes sense. Sorry to add too much to that, but I would just say I think biomarkers are important here too, right? So, you know, what we're really trying to do just from a scientific rationale piece is really deep type two inhibition. So, right, we're going to get that with 777, but also breadth of inhibition too across type one and type three. And so we'll be able to see that from biomarker responses as well. As Michael said, I think we've designed it in a way where we should see trends, right? But, you know, so phase I-B safety is important here. First combo that we know of in atopic dermatitis or inflammatory skin diseases in general too. So, you know, we're taking a, I think the right approach here that we'll be able to, you know, if the hypothesis plays out, we'll be able to show the trends we need to really power us for the next step, meaning, you know, convince people that it's the right thing to do and understand, you know, where our key standouts are, but not necessarily right off the bat doing, you know, like Michael said, a 500, 600, 700 patient study for like 95% power for some endpoint, right? But we'll do those over time, and you know, I think we're taking the right approach here. I think, you know, obviously a lot more to talk about, but in the last few minutes, I think the one thing I also wanted to cover was this question around, you know, your cash runway and how you think about, you know, pursuing all these different indications and while being focused on atopic dermatitis and getting across the finish line, how can you do that in a way that's both efficient and also maximizes the potential of 777? Please, Jane. Yeah. So first of all, we're in a very strong balance sheet position, $620 million of cash, which provides runway into Q1 of 2028. That supports the execution of a data-rich 2026, which we think could be transformative to us. As Michael started off the conversation earlier, our priority is to be a serial innovator in atopic dermatitis. From capital allocation, that is where we're prioritizing those dollars. For 777 readouts, the first half of 2026 with the maintenance data really enhances that best-in-class transformative every three-month dosing. The mid-2026 Part B induction data then enables us to select a phase III dose, and we will initiate that phase III by the end of 2026. Balance sheet supports all of those activities. In the near term here, we're going to be a late-stage development company. The serial innovator, of course, is the 279 data in the second half of 2026, and then as we think about capital allocation, that data-rich year will support the expansion indications. First, we've selected asthma. It is because of that overlap between AD and asthma patients. The 1-B data for 777 reads out in the first half, and then with that, we'll announce additional plans on both the expansions as well as the combos in these expansion indications, remembering what the priority is, which is to launch 777 as a monotherapy in AD in 2029. Great. Well, Michael, Jeff, Jane, and Carl, always a pleasure. Thanks for joining us and enjoy EADV. Thanks. Thanks for having us, Alex. Thanks for the time. Take care. Bye. Bye.