Welcome to the Aclaris Clinical Program Update Call. At this time our participant are only on listening mode. After the speaker presentation, there will be a question and answer session. To ask a question during the session you need to press star one one on your telephone. You will then hear an automated message, advising your hand is raised. To withdraw your question please press star one one again. Please be advised that todays conference is being recorded. I'd now like to hand the conference over to Will Roberts, Corporate Communications. Please go ahead. Thank you, Liz. Good morning, everyone, and welcome to the Aclaris Therapeutics conference call to discuss this morning's clinical program update, including the positive full top-line results from our ATI-052 phase I-A single and multiple ascending dose clinical trial and our plans to move ATI-2138 into a phase II-B program in lichen planus. The press release on this clinical update was issued earlier this morning and can be found in the press releases subpage of the investor relations section of our corporate website, aclaristx.com. Please note that we've provided slides as part of this discussion. They're now available in the webcast window and as a downloadable PDF document on our website. We'll reference the slide numbers throughout. A Q&A session will follow the prepared remarks. Before we begin, I'd like to remind you that today's webcast contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements represent management's judgment as of today and may involve risk and uncertainties that could cause actual results to differ materially from those expressed in or implied by these statements. For more information on such risks and uncertainties, please refer to our filings with the SEC, which are available from the SEC or on our corporate website. Any forward-looking statement represents our views as of today, April 28, 2026. Joining me on the call today are our CEO, Neal Walker; Hugh Davis, our President and COO; Jesse Hall, our Chief Medical Officer; and Roland Kolbeck, our Chief Scientific Officer. Kevin Balthaser, our Chief Financial Officer, will also be available for questions following the prepared comments. With that, I'll turn the call over to Neal. Neal? Thanks, Will. Good morning, everyone, and thanks for joining us on our call. We are delighted to share a couple of key clinical milestones that we've recently achieved. First, the full SAD MAD results for our lead bispecific antibody, ATI-052, confirm and build upon the remarkable PK, PD, and tolerability interim results announced back in January, providing strong clinical validation of the mechanism of this bispecific across a wide spectrum of single and multiple ascending doses. ATI-052 effectively binds TSLP upstream and immune cells downstream in the TH2 cascade via IL-4R, the shared receptor for both IL-4 and IL-13. As a reminder, the biology is additive, and as such, has the potential to provide strong efficacy in a variety of indications with infrequent dosing, which lowers the injection burden for patients. There are numerous feedback loops and interdependencies in this pathway. Data generated to date strongly suggest the synergistic effect of inhibiting TSLP as initiator of the cascade and IL-4 and IL-13 as the effector cytokines downstream. Second, we've completed a robust indication down selection process for our most advanced oral inhibitor compound, ATI-2138, and have selected lichen planus or LP as the next clinical indication for phase IIb development. As you'll hear from Roland, ATI-2138 is the first and only oral small molecule that inhibits both key JAK-related cytokines and TCR signaling. As such, 2138 has the potential to be an ideal mechanistic fit for LP. Turning to slides three and four. TH2-driven indications represent large and growing market opportunities due to the tremendous unmet need for better treatment options. We believe significant efficacy gaps still remain in many of these indications, including asthma and atopic dermatitis. The opportunity we have with ATI-052, our bispecific that targets both IL-4 and TSLP, is to redefine the standard of care. ATI-052 inhibits three inflammatory cytokines, IL-4, IL-13, and TSLP, to more broadly suppress the TH2 inflammatory pathway that drives many respiratory, dermatologic, and GI diseases, particularly those with heterogeneous subtypes. By inhibiting both upstream and downstream components of the TH2 cascade, ATI-052 has the potential to raise the efficacy ceiling beyond what either target achieves alone, while also addressing the biologic heterogeneity seen across respiratory and dermatologic diseases. This positions us to redefine the standard of care in TH2 disease and pursue first-line therapy status. Further enhancing its profile, ATI-052 has the potential for once every three months dosing, offering meaningful convenience for patients and providers alike. I will now pass the call over to Hugh to provide an overview of the full ATI-052 trial results and the planned next steps. Jesse will discuss our next clinical steps for this bispecific, and Roland will be on to provide more color on our ATI-2138 lichen planus program. I'll be back at the end to conclude the call. Hugh? Thanks, Neal. Good morning to everyone. I'll provide a quick overview of the compound itself before proceeding to the final results of the trial. As Neal mentioned, ATI-052 inhibits TSLP upstream and immune cells downstream in the TH2 cascade, b y simultaneously binding both TSLP and IL-4 receptor effectively and with high affinity. Antagonism of the shared receptor IL-4R blocks signaling of both IL-4 and IL-13 activity. We believe that ATI-052 has the potential to raise the efficacy ceiling in a variety of immunoinflammatory diseases. As a reminder of the construct itself, slide five shows a diagrammatic representation of ATI-052. It has the same anti-TSLP ligand binding regions as our anti-TSLP monoclonal antibody, bosakitug, allowing it to retain the potential class-leading attributes and potency advantages over tezepelumab and comparator clinical stage assets. You'll also see that it has 2 single-chain variable fragments that have high affinity to the IL-4 receptor. This antibody contains a YTE mutation to bind FcRn more tightly, designed to extend the half-life, and an AQQ mutation designed to reduce off-target binding and potential toxicity. As you will see in the results, we believe these mutations contribute to the strong behavior of the molecule. The next set of slides describe the key attributes of ATI-052, most of which were covered in detail on the January interim results call. First, on slide six, both ATI-052 and bosakitug show a very low dissociation rate from TSLP. The inverse of dissociation rate is residence time. As you can see on the right panel, both bosakitug and the bispecific have over 400 hours of residence time on TSLP, which is considerably longer than comparator antibodies and about 25-30 times long higher than tezepelumab. We recently characterized the crystal structure of bosakitug bound to TSLP, which is the same anti-TSLP Fab binding region as in ATI-052. As shown on slide seven, bosakitug has a much more extensive TSLP binding interface than tezepelumab, including all six light chain and heavy chain complementarity determining regions, or CDRs, whereas tezepelumab only has three heavy chain CDRs in contact with TSLP. Bosakitug and ATI-052 bispecific anti-TSLP Fab interfaces with the entire TSLP molecule, spanning from the N-terminal tyrosine at 29 to the C-terminal proline at 154. It virtually envelops the TSLP molecule, while tezi only engages the C-terminal portion. This explains the long residence time on TSLP by both bosakitug and ATI-052. This is important because TSLP is a very potent alarmin that drives a number of inflammatory diseases when produced at high chronic levels, as such, it's necessary to have a very potent therapeutic that can bind and neutralize its pathological effects. On slides eight and nine, you'll see that ATI-052 can also effectively bind two molecules of TSLP and two molecules of IL-4R simultaneously with high affinity, meaning that all four binding sites are acting independently. Importantly, binding to one target first does not affect its ability to bind to the other, and all four binding sites act independently and maintain the same high affinity to their target at the same time. Functionally, the bispecific inhibits the activity of all three targets, TSLP, IL-4, and IL-13, leading to a significant potency advantage over the combination of dupilumab and tezepelumab, which we show on slide 10. This isn't surprising. Pfizer's data with their trispecific antibody, tilrekimig, show this synergistic potential when addressing these same three important biologically distinct targets. Moving to the results of the phase I-A SAD and MAD trial itself. As you see on slide 11, this was a randomized, blinded, placebo-controlled phase I trial, first in human, designed to evaluate the safety, tolerability, PK, and PD of subcutaneously administered ATI-052 in healthy adults receiving both single-ascending doses and multiple-ascending doses. In the SAD portion, all 4 cohorts of 8 healthy volunteers were randomized 3-to-1 to receive a single dose of ATI-052 of 30 mg, 120 mg, 360 mg, or 720 mg or placebo. In the MAD portion, 2 cohorts of eight healthy volunteers each were randomized 3-to-1 to receive 5 doses of either 240 mg or 480 mg of ATI-052 or a placebo administered every seven days. As a reminder, the baseline characteristics were generally balanced across cohorts and were typical of a healthy population. Let's start with the pharmacokinetic results. On slide 12, the concentration time profile of the 4 SAD cohorts and the 240 mg and 400 mg MAD cohorts are shown. This continues to be a very well-behaved molecule pharmacokinetically. Dose proportional increases in PK for both Cmax and AUC were observed across all SAD and MAD dose levels. Focusing now on the 2 MAD cohorts, we see at least 12 weeks duration above the target-mediated drug disposition or TMDD for both cohorts. We note that we did not measure PK at week 14. The accumulation ratio, calculated using the AUC after the fifth dose divided by that of the first dose, measures how much a drug accumulates in the body after repeated dosing compared to the single dose. This analysis provides an estimated half-life of approximately 45 days. Considering this dose proportional PK profile, along with the remarkable PD effect I'll describe momentarily, these results help confirm our expectation that ATI-052 can be dosed as infrequently as every three months. Let's move now to the compelling pharmacodynamic results. The CCL17 inhibition assay is widely considered the gold standard in our industry to quantify the inhibitory activity of certain antibodies and serves as an early surrogate for clinical effect. The stronger and more sustained the inhibition, the better the molecule. Both TSLP and IL-4 stimulate the release of CCL17, also known as TARC. Given that this trial was conducted in healthy volunteers and there's no disease, as such, endogenous levels of TSLP and IL-4, and consequently CCL17, are very low and variable. To overcome this limitation, as we show on slide 13, we developed a rigorous whole blood assay to assess the inhibitory activity of ATI-052. We stimulated whole blood samples from participants in the trial with optimal quantities of TSLP and IL-4, which was up to 500-fold above endogenous levels seen in healthy volunteers in order to induce maximal CCL17 release, then directly measure the inhibition of CCL17 by the act of ATI-052 onboard in the blood at the various time points. Using the supra biological levels of TSLP and IL-4 for maximum stimulation even exceeded those that would be seen in disease provides a very high hurdle to demonstrate the inhibitory activity of ATI-052. On slide 14, you see the full PD results. Overall, we observed a sustained dose proportional PD profile across all SAD and MAD cohorts. Looking at the top panel, when we assess inhibition of TSLP-stimulated CCL17 in the 480 mg MAD cohort shown in dark blue, we observed 100% inhibition through the 20-week final sampling time point, four months beyond the last dose. We observed a similar result with the 240 mg MAD cohort shown in green, with nearly 100% inhibition out to the same 20-week time point. On the bottom panel describing inhibition of IL-4 stimulated CCL17, the 480 mg cohort of ATI-052 showed 100% inhibition of CCL17 for at least three months, two months beyond the last dose. It is expected, based on the concentration of ATI-052 at week 14, that near complete inhibition would be achieved through the week 14 time point as well. It's worth noting that these results represent data from isolated systems. They don't take into account the expected synergy from the mechanism in vivo. We have summarized the results of these potential best-in-class PD results on slide 15. Overall, these PD results support the potential to raise the efficacy ceiling with ATI-052 with an extended dosing schedule. Slide 16 serves as a reminder of the strong tolerability and safety profile of ATI-052 in this trial. These results confirm the strong profile we described at the interim look in January. No safety signals were observed, and more importantly, no conjunctivitis was seen. Regarding immunogenicity, in general, the impact of ADA is observed as either rapid clearance observed in a PK analysis or rapid loss of activity in a PD analysis. No impact of ADA on PK or PD has been observed in this trial. These trial results not only corroborate, but also dramatically improve on the compelling interim results we presented in January and clinically validate the potential best-in-class binding and potency attributes. They also provide important clinical evidence supporting ATI-052 as a molecule with a particularly strong safety and tolerability profile and a robust PK and PD package, all of which support the potential for synergistically driven efficacy with an extended dosing schedule of up to every three months. I'll now turn the call over to Jesse to provide an update to our ongoing clinical program for ATI-052. Jesse? Thanks, Hugh. Good morning, everyone. First, I wanna echo Hugh's sentiments regarding the strength and importance of these results. They reinforce that this molecule has best-in-class potential and potential therapeutic utility in a wide variety of indications. In parallel, we've been focused on execution. We have initiated two randomized double-blind placebo-controlled phase Ib proof-of-concept trials. These trials are designed to build the foundation that we need to move into our phase IIb programs with confidence. At this stage, while we will be looking for initial efficacy signals, the objective is more about translational clarity. Specifically, we're looking to define PK, target engagement, and biomarker response in disease populations, and to use those data to inform next steps. Turning to slide 17, in January, we initiated a phase Ib study in approximately 12 patients with AD, with EASI scores of greater than 21, evaluating 480 mg of ATI-052 using a regimen consistent with our phase I-A MAD cohorts, five weekly doses over 4 weeks, identical to what we did in healthy volunteers. The trial will assess clinical endpoints at week eight, including EASI, IGA, and PP-NRS, followed by an additional 12 weeks of follow-up. We'll have 16 weeks of evaluation following the last dose. Importantly, we're also collecting PK and PD data, including lesional and non-lesional tape strips, which provide a direct bridge to established data sets, including dupilumab, and should help contextualize biological activity. Next, on slide 18, in February, we initiated a second proof-of-concept study in asthma, a 3-to-1 placebo-controlled single-dose trial in approximately 16 patients on GINA step 2 through 4 therapy. We expect top-line readout at day 29 with approximately six weeks of follow-up. Endpoints include safety, PK, and PD biomarkers with a focus on FeNO, eosinophils, and FEV1 to assess biological effect and consistency with mechanism. Both studies are actively enrolling with top-line data expected in the second half of 2026. In parallel, and shown on slide 19, we are advancing phase IIb planning in both asthma and AD, with the goal of initiating the asthma study in the 4th quarter of this year. We believe that ATI-052 has the potential to be differentiated and competitive across multiple important indications. With this, we'll now transition the call to ATI-2138. I'll turn the call over to Roland. Thanks, Jesse, and good morning, everyone. I'm excited to be with you today to provide an update on ATI-2138 regarding our plan to move into lichen planus or LP. As shown on slide 21, lichen planus is an ideal fit for this molecule for a variety of reasons, including mechanistic overlap, market size, available wide space, potential for cost-effective development, and the availability of regulatory pathways that may expedite development. I'll touch on most of these factors this morning. Let's start with the disease itself on slide 22. It's an unaddressed chronic inflammatory CD8 cytotoxic T-cell driven interface dermatitis. There are multiple subtypes, the three most common of which are erosive mucosal, cutaneous, and lichen planopilaris, which is a rare form of LP affecting the scalp and causing permanent scarring hair loss. Patients with LP experience sores, difficulty eating, severe itch, scales, plaques, permanent hair loss, and fatigue. Quality of life is also affected in most patients due to disease and symptom-related anxiety and depression. In fact, studies have shown that LP affects quality of life in up to 78% of affected individuals. As you see on slide 23, LP is a significant wide space market opportunity. There are currently no FDA-approved therapies for LP, so disease management has historically focused on immunosuppression and topical symptom control. Estimates of market size suggest that at least 0.1% and up to 1% of the population is affected in the U.S. Despite no targeted therapeutic intervention, up to 40% of patients with LP currently seek treatment. This percentage would likely increase with new, innovative, targeted, and effective oral therapies. The steroid failure rate in LP is also very high, as much as 60% in the moderate to severe population. We believe that new targeted therapeutics have the potential to dramatically increase diagnosis and treatment rates by providing rapid pain and itch relief and addressing multi-site disease involvement, in addition to minimizing flares and directly improving symptoms and potentially quality of life. In addition, oral agents are far more practical for the treatment of widespread or multi-subtype lesions than topically administered corticosteroids or calcineurin inhibitors. As a reminder, ATI-2138 is a highly potent investigational oral compound which interrupts T cell receptor, or TCR, signaling by inhibiting interleukin-2-inducible kinase, or ITK, and Janus kinase 3, or JAK3, signaling of common gamma chain cytokines in lymphocytes. Slide 24 further describes its mechanism involving dual inhibition of TCR-mediated and cytokine-mediated activation of CD8 cytotoxic T cells. ATI-2138 dual inhibitory activity results in a bispecific like effect that could be very powerful in certain diseases like LP. In fact, it is the first and only known JAK-based therapy that also inhibits the TCR. First, on the left side of the slide, it inhibits TCR signaling through potent inhibition of ITK, which inhibits autoantigen-mediated T cell activation, cytotoxic destruction of targets by CD8 T cells, and production of inflammatory cytokines, including interferon gamma. Second, on the right, it inhibits cytokine signaling via JAK3 inhibition, thus impacting cytokine-mediated T cell proliferation, activation, and survival. All in, on slide 25, you'll see that this provides the mechanistic rationale for broad and deep efficacy in LP. ATI-2138 is the only known drug in development that precisely targets these two signaling axes that are the defining pathological drivers of LP, potentially positioning it as the first mechanistically complete therapeutic candidate designed to address the root inflammation underlying lichen planus symptoms. This also aligns well with the clinical rationale and efficacy of ATI-2138 in atopic dermatitis, which was on display at the 2026 AAD meeting. It's understandable that the medical community is excited about this potential therapeutic innovation. As you see on slide 26, we intend to initiate a phase IIb basket study of ATI-2138 in LP, starting with the erosive mucosal and cutaneous subtypes in part A, then layering in lichen planopilaris in part B as the trial evolves. Our goal is to initiate this trial in the second half of 2023. We'll describe the trial design further as we approach initiation. We are also excited about the mechanism of ATI-2138 in other niche indications beyond lichen planus, such as the 10%-15% of asthma patients that are severe or refractory. With that, I'll turn the call over to Neal for some closing comments. Neal? Thanks to you, Jesse and Roland. Turning to slide 27, the PK and PD results with 052 provide a convincing surrogate for clinical effect and exceeded our expectations across the board. The results showed complete and sustained inhibition of both TSLP and IL-4R, providing an estimated half-life of approximately 45 days. The safety and tolerability profile is exactly what we wanted to see, if not better, as we proceed toward phase IIb, on slide 28 as you heard from Roland, ATI- 2138 is the only known drug that hits the key modulators of interface dermatitis disorders like lichen planus, both TCR signaling and CD8 cytotoxic suppression, and as such, is an ideal mechanistic fit. This is a white space opportunity with an estimated U.S. market potential exceeding $1 billion, with an opportunity up to nearly $4 billion. We've had a productive first part of the year across the pipeline, including the new information we provided today, and we are looking forward to the rest of the year. As we show on slide 29, we expect to achieve numerous important milestones throughout the year. Thanks for your time today, and now let's open up the call to Q&A, though I'll remind you that we may be limited to what we can discuss beyond what we've disclosed. Operator, are there any questions? As a reminder, if you would like to ask a question at this time, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Our first question comes from Thomas Smith from Leerink Partners. Please go ahead. Good morning. This is Nat Charoensook on for Thomas Smith. Congrats on the data. We have two questions. First, the phase Ib asthma trial uses a single 480 mg dose, while the atopic dermatitis trial uses biweekly 480 mg doses. What drove that difference? Second, what are your expectation on the top line phase Ib data expected in second half 2026 from both asthma and atopic dermatitis indications? Any specific bar that you aim to clear before starting a phase Ib program? Yeah. I can start and you feel free to chime in. On the asthma dose, we're just mimicking the traditional pheno study to get an idea of dose response in patients in a pretty quick study, both on pheno and FEV1. You know, it's a typical study that most people do on the asthma side. In AD, it's a little different because usually with atopic dermatitis, you have a load-in dose, you know, just because you gotta get to the skin, the site of action. You know, we're trying to mimic that or at least use that as a surrogate in this study, and it also comps nicely and is a direct comparator to what we did in the healthy volunteer study. That's kind of the background rationale. Hugh, do you have any other comments? I mean, the goal with the AD is to really get to an exposure response profile that can be done successfully with five loading doses. We will also be able to do a pop PK analysis because we'll be able to combine the data from our healthy volunteers with that data set and really be able to hone in on any potential covariates. At the end of the day, we'll be able to look at true activity and efficacy profile in AD in these severe patients relative to established historical data from Dupixent, for instance, which has a four and an eight week monotherapy publication. We'll be able to get some really good understanding of actual clinical effect over time and a PK/PD analysis that we'll be able to take forward into the phase IIb. Yeah. W e'd like to see a 10% bump on the efficacy front. I think that that would be meaningful. You know, there's various ways to look at efficacy, whether it's speed of onset. For instance, in AD, you know, we'd like to see a rapid onset with this mechanism. That's why we're looking at a week eight, you know, kind of top line day 57, number four weeks after the last dose in the AD study. We're going to track those patients out another 12 weeks, so you'll get an idea of what the curve looks like. You know, rapidity of response in something like AD is important. Remember, AD is very different than psoriasis. It's a treat the flare disease. You know, in terms of, you know, a quick effect, that's important. We'd like to see obviously depth of response. There's a lot of efficacy being left on the table with current modalities, and we think hitting two inflammatory mediators makes sense. Got it. That's very helpful. Thank you. Our next question comes from Biren Amin with Piper Sandler. Yeah. Hi, guys. Thanks for taking my questions. Maybe to start on ATI-052. You know, your plans to move into phase IIb trials in asthma in the fourth quarter of this year, what's driving the priority for asthma compared to AD? Thanks. I can start if Roland or Jesse have any other comments. I think the key for us is we know 100% that tezepelumab works well in T2-low asthma. It's, you know, doing quite nicely in that indication. It's been well-received. We know that Dupixent also does quite well in T2-high asthma. If you look at our molecule, we're simply combining those two modalities. As you can see, we're doing so not only in a very robust way with 100% inhibition over an extended period of time, but then we have the advantage of a dosing interval on both. From our perspective, having a 1 +1= 3 in respiratory is very easy to understand and has a high probability of success. That's why we're prioritizing that out of the gate. Of course, we still like a number of indications in the TH2 family, including atopic dermatitis. Our next question comes from Jeff Jones with Oppenheimer. Good morning, guys, and thanks for taking the question. Congrats on the updated data. Could you expand a little on how you're thinking about the lichen planus trial design? You mentioned erosive first, the drivers there to expand and how you're thinking about endpoints and bars for the bar for success. Thanks. Yeah. Thank you, Jeff. Yeah, it's pretty exciting. You know lichen planus is in my mind very similar to where hidradenitis was many years ago. It's a disease that is a lot more prevalent than the numbers would suggest. That's why we provided that range of like 0.1% to like 1%. In fact, I've seen some that say it's, you know, upwards of 1.5%. It is a spectrum of disease. That's kinda one of the things I like about this category is the pathophysiology is the same. It's an interface dermatitis, it attacks the mucosa. You can get mucosal LP, which would manifest in the mouth, the esophagus, also in the general area. The severe extension of that is erosive, and these patients sometimes need tube feeding. That's how painful and distressing it is. Then you have cutaneous LP, which has its own issues with the burden of itch, etc. The next layer in the spectrum is lichen planopilaris, which is a pretty devastating scarring alopecia, which we heard about recently from a competitor. Why I like that is we can design a basket study where we step through these indications. We're gonna start with mucosal and cutaneous, and we're gonna test two different doses, 10 mg BID, 20 mg BID. As a reminder, we tested 10 mg BID in the atopic derm study. Once we see the effect there, then we'll take that kinda winning dose and move forward into the next layer, which is lichen planopilaris, which is a little bit more difficult to treat. We really feel strongly about the mechanistic fit here. You know, Roland alluded to it, but just to reiterate, there's kinda two pieces. One is the JAK-driven inflammation, but there's also an antigenic stimulation, which fits perfectly with inhibiting the TCR. The easiest way to think about this is ATI-2138 has the efficacy of a cyclosporine by hitting the TCR with the efficacy of a JAK3, which is a highly selective way to inhibit the JAK milieu. Basically, we get a three for one here in terms of the indication set, and there are opportunities for, certainly opportunities for orphan designation within that category. Great. Thank you. Our next question comes from Roger Song with Jefferies. Hey, team. Thanks for the update. Very helpful PK/PD data today. I have two from us. This is Nabeel Nissar on for Roger Song. Thanks for taking our questions. One on the translation. On the biomarker, was thinking if you could help us better understand the predictive value of TARC suppression in magnitude and durability, and if you feel this is equally informative across asthma and atopic derm, or do you also look at other biomarkers in those indications? A follow-up. Hugh, do you wanna start? Yep. Sure. Yeah, the way we think about this is, we have two sides of the molecule. We wanna make sure both sides are equally active in contributing to the potential efficacy downstream. By doing an assay where we have this target engagement, it really shows the value of the molecule. We had 500, even up to 1,000 times, higher concentration than what you would expect in disease with TSLP and IL-4 at the concentrations we used. If we can inhibit 100% of these targets that are added into this natural milieu of cytokines and cells and chemokines and the like, if we can inhibit it at these concentrations with the doses that we used, then we're going to be able to show complete impact of both the 240 mg and the 480 mg dose, where we're seeing 100% inhibition, out, you know, with TSLP, out to 20 weeks. It really shows the potency of the TSLP arm, as mentioned through the structural interface with TSLP and not releasing. On the IL-4R side, same thing. IL-4 is 10 times more potent than IL-13 in driving downstream chemokine secretion in PBMCs. If we can inhibit IL-4 at 2 ng/ mL, which is 1,000 times higher than normal and even greatly higher than AD or asthma subjects, then we're gonna be able to have a molecule that's gonna be able to take these targets and this pathway down to homeostasis. It'll translate, but there's not a direct mechanism showing that if you inhibit TSLP generated TARC, that you'll be clinically effective. Clearly, the molecule is able to shut these pathways down completely for the, you know, the complete dosing that we did. It's gonna translate to both asthma and AD. In fact, I'm not sure why we don't use a loading dose in asthma to have an even greater earlier effect in patients. At the end of the day, this will translate well not only to AD and severe asthma, where, but other indications as well that follow on behind that. Thank you. Would you be sharing any updated, like any additional biomarker data in the later months? For the healthy volunteer study, you know, we don't have that. Jesse, do you wanna speak to the Ib? Thanks, Hugh. What we're going to be doing is we're going to be looking at endogenous levels of all of these biomarkers in both the asthma study as well as the AD study. We think we're going to be able to have a nice understanding of the exposure response, as Hugh mentioned, over the time course of the treatment as well as off therapy. If you recall from the AD study, for example, we're going to be following subjects for up to four months after the last dose. I think this gives us a really good opportunity to understand the duration of response and the ability to suppress these PD biomarkers for a sustained period of time. Got it. Thank you. Congrats on selecting your lead indication for your ITK molecule. I was wondering if you could share any more updates on the ITK selective program. Thank you. It's all on track. ITK selective is due for IND in the second half of this year. We're very excited about that. You know, with the onboarding of that into the clinic, we'll have 4 clinical stage assets. Thank you for taking our questions. Our next question comes from Adam Vogel with Craig-Hallum. Great. Thanks, team. Great to see a clean and support PK/PD profile emerge here. Just a couple questions from me. Maybe first, beyond the biologic rationale, and to as much as you can disclose, have there been any early insights from the ongoing phase Ib studies that increase your confidence in clinical translation in asthma over, say, atopic derm? I have a quick follow-up from that. Yeah, I mean, those are ongoing studies. You can't really talk about those, but we're excited about both. I mean, we obviously had a lot of this PK/PD data, you know, particularly the 720 and 240, for a little while. We were just waiting for the 480. Can't get much better than 100% suppression, and these are in isolated systems. I think the whole promise of bispecifics is a 1 + 1 = 3 approach. I mean, I think we saw that with the Pfizer disclosure. To us, it's tremendously exciting. There's a reason we're looking at eight weeks as a primary top line in the AD study. You know, traditionally, biologics will look much later, at week 16 or so. We're looking at week eight because we truly believe we're gonna see a rapid response there based on the totality of the data that we've observed. On the asthma front, you know, we're expecting to see robust effects on FeNO and FEV1. I think there's always a little doubt about TSLP and AD, but remember, like, we have a whole slew of indications on the respiratory side, you know, vis-a-vis everything that Dupixent and Tezspire's in that we can go after and kinda claim first line therapy. Atopic dermatitis for us is an extra added bonus, and there's great biologic rationale for TSLP there. Super excited about the phase Ibs and, you know, I think enrollment's going well, that augers well. It means investigators are excited. Great. Maybe in the context of LP being a wide space of high unmet need, how should investors think about 2138 versus the next gen ITK selective, development strategies? Thank you. I think it's great question. I mean, you know, the next gen ITK, we think is more applicable to the traditional mass market, you know, indications like AD as an oral with a very clean target product profile, kinda no, you know, JAK overhang, if you will. Although, you know, that hasn't really played out in the market. You know, docs are pretty comfortable with that. The mechanistic match here, it's important, right? We hit the T-cell receptor with ITK, but then we mop things up with the JAK3, and the literature's pretty clear about going after the cytotoxic CD8 lymphocytes and going after an interface dermatitis. This is a much better hammer to hit this disease pretty hard. This is a devastating disease. I mean, if you see. Just look at the pictures. I mean, you can imagine these patients, like if you wake up and you have mucosal involvement, you know, all around your mouth, pain, the effect on eating, and this lasts for quite a long time, and, then you layer in the cutaneous aspect and of course the hair loss piece. T his indication is deserving more of a hammer approach rather than a more elegant approach to hitting ITK. Got it. Thanks, team. Our next question comes from Michael King with Rodman & Renshaw Hi, this is Jillian Weiss on the line for Michael King. Just to follow up on the TARC discussion for 052. The ex vivo whole blood data show TSLP stimulated TARC fully suppress out to about week 20, whereas IL-4 stimulated TARC is maintained only to roughly week 12 at 480 milligrams. Based on what you know from the assay design and your prior TSLP and IL-4, IL-13 work, can you share your working hypothesis for why TSLP inhibition appears more durable in the IL-4, IL-13 in this setting, and whether you think that difference will meaningfully impact clinical efficacy or your ability to dose every three months? I'll start and then hand it to Hugh. No, we don't. First of all, this is 100% inhibition for 12 weeks over the course of the dosing interval. Actually, as we noted in our prepared comments, we didn't assay at week 14, but our simulations 100% support continued 100% inhibition. Somewhere between week 14 and week 16, it weans off. Remember, these are isolated systems, and I mentioned this previously. You know, I think anybody in bispecifics that is developing bispecifics or combo therapy is expecting not just an additive approach but a synergistic approach. You know, I think we easily get to three months, if not longer. You know, these data certainly support that. Hugh? Yeah. I would say, you know, on the TSLP, as I mentioned in my comments, the potency of the TSLP binding sites on 052 are just, you know, off the charts, due to that complete enveloping and binding to TSLP and not releasing with that low dissociation I think that that effect is just carrying through to the 20 weeks and maybe longer. On IL-4R, you know, we already have drug bound to cells in that whole blood sample. At the end of the day, adding more IL-4 to be able to inhibit it 100% for 12 weeks while it is already bound to receptor is pretty amazing. Whereas the TSLP components of the bispecific, even if it is bound to receptor, can still bind additional TSLP because we have the four active binding sites that can be achieved simultaneously on the molecule. I think it is a bit of high potency and also a bit of the dynamic of the assay itself. Okay. Thank you so much. Our next question comes from Seamus Fernandez with Guggenheim Securities. Oh, thanks for the questions. Just a first one. What are you guys we know [inaudible] had at least a successful, you know, data set in asthma, you know, but really more of a monthly profile asset there. You know, interested to just know what you'll be looking for in that data set and then what you're hoping to see from a differentiation perspective. Obviously, the sort of failed effort on their part in AD, you know, sort of sets up a different opportunity for 052. The second question is just, you know, what, if any challenges, were there to selecting lichen planus over alopecia? What new learnings did you guys gain, from the start of the year to kind of really move as aggressively as you are, into LP and its subtypes? I know, Neal, you've explained, you know, quite a bit about the sort of T-cell dynamic, but it seems like there was a bit of a push and pull that you needed to kind of work your way through on the decision of alopecia versus LP. It seems like obviously LP rose to the top, but wondering if there are some new learnings outside of just the competitive landscape in alopecia that really drove you to LP. Thanks. Sure. I'll let me take the question about [inaudible] first. You know, it's I think everybody has seen there wasn't much disclosed there unfortunately. You know, I think we've always maintained that to maximize efficacy, it's logically better to hit IL-13 and TSLP rather than just going after two inflammatory mediators and potentially leaving IL-4 unsuppressed. I think the things we don't know about that program are, you know, what is the potency of that IL-13, what's the potency of that TSLP and that construct. We don't even really know the dosing interval there either. Certainly, so far in the bispecific space, I think we're kinda class leading in terms of the dosing interval potential here, which is important. More importantly is the ability to max out the efficacy by hitting three inflammatory mediators, which I think we got a glimpse of that with the Pfizer data. You know, it's hard to understand the totality of their data with the disclosure that was out there, you know, basically alluding to a signal with EASI-75 and IGA, yet mean change from baseline, I guess, didn't hit the mark. You know, we really just don't know a lot there. You know, we're happy with our decision to go after three inflammatory mediators rather than two. Just remember, we have the ability with this molecule to go after the breadth of indications across the respiratory landscape, anything that Dupixent and also AD. AD is just kind of one leg of the stool, if you will. Hopefully that answers that question. On the LP front, you're right. We took probably more time than I'd like to go through this. You know, it's important because all these areas, everything in I&I is pretty competitive. You know, we're seeing more people jump into the alopecia space. I like going after white space opportunities. You know, we produced phenomenal data in Angela Christiano's lab with our mechanism, which is a tribute to hitting ITK at the T-cell receptor level and hitting cytokine CD8 lymphocytes, and also mopping up JAK3. Very strong mechanism. It just boils down to what do we wanna lead with. We will certainly cycle back to alopecia at some stage, but I also wanna be able to just own a category and own a category that I know very well, you know, is a strong mechanistic fit and also has kind of three shots on goal within the same indication. That's what really drove that decision. It wasn't easy. There's probably. You know, if you just look at what ritlecitinib, which is our closest comp, is studying, they've got, like, 20 studies ongoing, y ou know, there's a lot to choose from. You know, if we were a bigger company, I'd put up five indications. Neal, would part of the, you know, sort of evolution be this basket study approach that you're taking, or was that kind of planned all along? I'm sorry. I missed that last part. I think you. Just was the basket study approach kind of planned all along, or is that a new evolution to the strategy for LP? It was on the list. W e've seen, you know, as an example, there's been an IL-17 basket study out there. I think it's smart. You know, it allows us to basically do a little dose ranging within the different categories. What we would envision is starting a study that includes mucosal, which includes the most severe forms, erosive, in that category, along with cutaneous, and then look at two doses, 10 mg BID, 20 BID, so we double the dose. You know, we look at how that does, and then we can basically, in an adaptive way, pick the higher dose, move forward with that. You know, get into a phase IIb design that would be, you know, because there's orphan potential, I think, you know, very seamless into a phase III. It's very capital efficient for us and answers a lot of questions in a very quick amount of time. Awesome. Thanks, guys. Appreciate it, and congrats. Thank you. Our next question comes from Martin Fan with Wedbush Securities. Hi, everyone. Good morning. Thanks for taking our questions and congrats on the progress. Wanted to follow up with the last question on lichen planus trials. I think you mentioned 10 mg- 20 mg BID for lichen planus. Any reason not to go higher with the dosing, given what you've seen with the atopic dermatitis trial? Then to follow up on that, curious about number one, how large do we think a phase I or phase II program might be, and whether or not we might have any estimates on timing for conducting those trials, how long those trials might take to go through. Thank you. Yeah. Just to clarify, we're starting the phase IIb in the back part of this year. second half and, you know, obviously, we need to start it before we guide to a completion. I would say that, you know, back part of 2027 is a good marker to keep in mind. We think this is gonna enroll, you know, pretty quickly. In terms of the dosing, this molecule is so potent, you know, we can dose up to 40 BID according to the MAD, but, you know, the 10 mg BID showed really strong results in AD across both clinical and pharmacodynamic measures. We just don't think we need to press dose that much higher, and we are doubling the dose. 10 mg-20 mg, you know, I think keeps you in that window of not kind of begging for problems on the safety side, but driving, you know, incremental efficacy. That was informed through a pretty extensive analysis of all the PD biomarkers, looking at kind of effect on natural killer cells and kind of everything in between. We're doing ILC2 work, we've got a lot of data to support all that. To your point, can we go higher? Yes. I don't think we need to, given this mechanism in LP. We think that, you know, 20 mg will give us that dynamic range, double the dose. Great. Thank you. Then in terms of estimates on how long it might take to run a phase III program, I guess we'll see how long it takes to first do the recruitment for the phase II. Is that right? Yeah. We think it's gonna be pretty quick. I mean, there's, when we went to the AD, it was very evident in talking to a handful of KOLs in this space that there's a lot of pent-up demand, particularly on the mucosal side, in addition to the cutaneous. Look, LPP, I've seen patients with LPP for years when I was practicing, and I would say the prevalence is a lot higher than people imagine. These patients have nothing. I mean, there's just nothing that they can turn to. You know, stopping, putting out the fires is step number one, and then, you know, re-healing the mucosa and also growing hair is kinda step number two. Perfect. Thank you. Thank you. Our next question comes from Raghuram Selvaraju with H.C. Wainwright. Thanks so much for taking my questions. Congratulations on this exciting data with ATI-052 and the plans on moving forward with ATI-2138. With respect to ATI-052, I was just wondering if you could comment a little bit on where in the overall indication panoply you expect the extended dosing interval to be the most significant competitive advantage. If you could also comment on how you see the relationship between ATI-052 development and bosakitug development evolving going forward. I think, you know, previously you have commented on, you know, the possibility of effectively regarding bosakitug as kind of a feeder club, as it were, for ATI-052. I was just wondering, you know, kind of when we might expect bosakitug clinical development activities to ultimately wind down, or if you do see potential applicability for bosakitug as a standalone asset going forward. With respect to ATI-2138, I know there's been some questions around, you know, this basket trial approach in phase IIb. How do you see that potentially feeding into a registrational program? Do you anticipate that a registrational program would be sort of pan LP in focus, or that you would anticipate effectively moving forward with ATI-2138 in specific subpopulations within LP for registration in a more sequential manner? Yeah, all good questions. Maybe on the first one. You know, these are evolving markets, right? I think the market, in my opinion, over-indexes on extended dosing intervals like to us. It's always been about trying to max out the efficacy first. You know, particularly in diseases like AD, where you're trying to treat flares. That's why we're trying to look at an early endpoint in the phase Ib study at eight weeks. You know, we think, you know, a strong result there would augur well. You know, I think it just depends how the landscape evolves. You know, as a former practitioner, I think, you know, anything more than quarterly, quite frankly, just doesn't make a lot of sense in diseases that wax and wane. You know, we've seen instances where, you know, longer dosing intervals than that in certain diseases, you know, might be problematic, right? We saw GSK get a CRL with Exdensur and CRS with NP and the FDA flag, you know, issues of what happens if the treatment effect wanes after, you know, up through six months, right? I think the most important thing for all of us is to be thinking about how we max out efficacy. Then the dosing interval question is on a case-by-case basis, and it is very, you know, indication driven, right? Like, psoriasis is a much different market than AD, much different market than asthma. It remains to be seen. I think if you develop a drug that at the end of the day, docs and patients want the thing to work, and they want it to be safe. That's what we tend to over-index on. On bosakitug, you know, look, we got to see what the data shows, right? We're excited about it. We feel like the trial is going very well. We've gotten good feedback on it. There is a place just like there might be a place for, you know, mechanisms like Nektar or OX40 for a TSLP, mAb TSLP is exceedingly safe. You can envision background therapy of that, particularly in a disease that skews young. You know, AD is always about polypharmacy and rotating therapies. You know, that being said, you know, if the bispecific continues to move along as we've seen, you know, there's a thought that that might cannibalize things. You know, we're super excited about it. You know, we'll have to make capital allocation decisions. Maybe TSLP is something you out-license, right? To a bigger player that can, you know, maximize that across indications. We'll see. We'll see when we get the data. That data will read out, by the way, after the bispecific phase Ib. It'll be interesting, you know, to see how that all comps. On the LP front, it's a very good question. I'll bounce that question to later. I could see constructs where I go after a pan LP. It's the same exact pathophysiology, histologic kind of process. you know, I could make an argument to that, to, you know, get a global label there. A little too early to comment on that. If I get the opportunity to click off a couple of those because they're more orphan-esque very quickly, I'll take it, you know, and get it on the market. That remains to be seen. The beauty of the strategy that we've come up with is, again, it's a three-for-one, and I have, you know, good. In one construct, I have good short-term visibility on getting on the market quickly. Thank you. Our next question comes from Alex Thompson with Stifel. Hi. Congrats again on the data, and thank you for taking our question. This is Charles on for Alex. Maybe just one on ATI-052. I was curious as to whether suppression of STAT6 signaling was measured. If so, how long did that last? If not, is that a biomarker that'll be measured in the phase Ib studies? Thank you. Thanks, Charles. Appreciate the comments. So we'll certainly be measuring a spectrum of biomarkers in the phase Ib's. We don't have data for that for the healthy volunteers. You know, as we said before, healthy volunteer data has a lot of limitations in terms of just variability, and they're healthy, right? You know, I think the construct that we put out today is kind of unambiguous. It's super high levels of both stimulation on TSLP and IL-4R, and I'm not sure how we can get much better than 100% inhibition. Thank you. I'm showing no further questions in queue at this time. I'd like to turn the call back to Neal Walker for closing remarks. Thanks, everybody, for joining the call. We're tremendously excited. We feel like we significantly de-risked the 052 program, and we have great visibility on 2138 in terms of getting closer to phase III and thinking about how to get a great molecule like 2138 in the hands of patients. Took a little while to get there on the indication, really like the white space opportunity. We're a clinical stage company with 3 active clinical programs with a fourth to onboard at the end of the year. Really appreciate your time. Thank you. This concludes today's conference call. Thank you for participating. You may now disconnect.