Aclaris Therapeutics, Inc. (ACRS) Earnings Call Transcript & Summary

Hello, and welcome to the ATI-052 Phase Ib POC results update. [Operator Instructions] Please be advised that today's conference is being recorded. It is now my pleasure to introduce Head of Communications, Will Roberts.

Thanks, Andrew. Good morning, everyone, and welcome to the Aclaris Therapeutics conference call to review the positive primary analysis results from our ATI-052 Phase I proof-of-concept trials in asthma and atopic dermatitis. The press release on these clinical results was issued this morning and can be found in the press release sub page of the Investors section of our corporate website, aclaristx.com. Please note that we've provided slides as a part of this discussion and are now available in the webcast window and is 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 foward 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 risks 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 and on our corporate website. Any forward-looking statements represent our views as of today, October 27, 2026. Joining me on the call are our CEO, Neal Walker, Jesse Hall, our Chief Medical Officer; Roland Kolbeck, our Chief Scientific Officer; and [ Michael Cameron ] from the Department of Dermatology at Mount Sinai in New York and an investigator in our atopic dermatitis trial. Hugh Davis, our President and Chief Operating Officer; and Kevin Balthaser, our Chief Financial Officer, will also be available for questions following their prepared comments. And with that, I'll turn the call over to Neal.

Thank you, Will. We are pleased to report that ATI-052 showed strong proof of concept in both atopic dermatitis and asthma. These results also demonstrate the art of the possible with a bispecific antibody showing that 1 compound may be able to provide not only rapid response, but also a broad response across indications and across diverse patient populations. They help validate the potential additivity or synergy of a dual mechanism targeting T-slip and IL-4R and as such, provide the compelling proof of concept we want to see. ATI-052 was well tolerated with no conjunctivitis and the efficacy signals emerged early and were consistent with the biology ATI-052 was designed to treat. As you see on Slide 4, ATI-052 targets type 2 inflammation at 2 important points in the pathway. T-slip is an upstream signal that helps start and amplify the inflammatory response while IL-4 and IL-13 are key downstream signals that drive many of the metastations of type 2 disease. Importantly, these pathways are relevant to the clinical features we are ultimately trying to improve. In atopic dermatitis that includes itch and overall disease severity and in asthma inflammation that can impair lung function. ATI-052 combined those 2 mechanisms in a single molecule blocking T-slip upstream and IL-4 and IL-13 signaling downstream through the shared IL-4R receptor -- the binding interface is multi-paratopic designed to deliver best-in-class potency and long target retention. A YTE mutation extends half-life supporting less frequent dosing. The goal is to achieve additivity or synergy of hitting both targets for broader control of the inflammatory response and ultimately greater impact on disease. A couple of contextual comments before getting into the results, Slide 5 helps clarify the importance of blocking IL-4, a question we often get, which ATI-052 does through its shared IL-4R receptor with IL-13. IL-4 as a mechanism is approved across 5 indications. And because it blocks both IL-4 and IL-13, it covers the biology that drives asthma and other TH2 diseases. By contrast, IL-13 stive antibodies are thus far, 0 for 8 in late-stage asthma and eosinophilic esophagitis programs. So blocking IL-13 alone hasn't been enough to match dupilumab with an IL-4 blocker T-slip adds complementary validation in EoE, asthma and CRS with NP and we believe will be validated in AD. That's the reason we believe blocking both targets in a single molecule has the potential to deliver a broader and deeper response in many indications. For additional context, an important point regarding severity and atopic dermatitis as described on Slide 6. When looking at atopic dermatitis data, not all patient populations are equal there are 2 ways to look at severity. EASI over 21 and IGA-4 status. IGA-4 is more reliable in dictating severity by largely taking its stent out of the equation. Patients who begin or severe disease like an IGA-4, for a variety of reasons, have further to go to reach the same clinical endpoint than more moderate patients like IGA-3. One can clearly see that the dupilumab and lebrikizumab data illustrate this well with stark differences between IGA3 and IGA-4 response even at week 16. It is clear that baseline severity should be taken into account when interpreting efficacy results from a given clinical trial. The next couple of slides show the results we'll cover in detail shortly. Starting with atopic dermatitis, we conducted this trial in a difficult-to-treat severe and diverse population. 78% of patients at a baseline IG-4. As you'll hear from Jesse, this is important as patients with severe AD have a higher baseline disease burden and therefore need a greater absolute improvement to achieve the same clinical endpoint as patients with moderate disease. At day 57 or week 8, after 5 weekly loading doses ending at week 4, we saw a meaningful placebo-adjusted reductions from baseline in EASI and PPNRS. As Jesse will describe later, we also saw an encouraging early indication of durability in atopic dermatitis with maintenance of response through week 16 or 12 weeks after the last load in dose in a severe patient population. And in the skin, we saw a pronounced reduction of established dupilimab biomarkers like TH17 and TH2 endotypes, while also potently suppressing the TH1 inflammatory endotype. Finally, we also saw a complete normalization of the skin Protea. These Cape strips analyses performed by Dr. Emma Guttman lab at Mount Sinai only increase our confidence in ATI-02, the role it and the underlying biologic rationale. With asthma, similarly strong results shown on Slide 8. These were heterogeneous patients with mild-to-moderate disease, including inclusion of high and low baseline FEV1 who received a single dose of ATI-052. The results demonstrated that the patients improved broadly and rapidly as measured by Pheno and FEV1with maximum improvement occurring in only 2 weeks. And in patients that have low lung function that meet a typical Phase Ib inclusion criteria, FEV1 demonstrated potential best-in-class improvements. The remainder of today's call will be as follows: First, Jesse will discuss the safety and efficacy results for the AD trial, followed by Roland, who will highlight the PD biomarker work Dr. Michael Cameron will then join us to provide his thoughts on the AD market, treatment gaps and his experience with ATI-052 as an investigator in this trial. Jesse will then return to discuss the results in asthma. And then finally, I'll be back at the end to conclude the call. I'll turn the call over to Jesse. Jesse?

Thanks, Neal, and good morning, everyone. I share Neall's excitement about these strong results in both trials. As Neal said, ATI-052 achieved proof-of-concept in AD with robust improvements in the extent and severity of disease as well as an itch in a broad and diverse population. This study evaluated a load-in dose format of 5 weekly doses of 480 milligrams of ATI-052 or matched placebo over a 29-day interval. We enrolled 14 AD patients, randomized approximately 3:1, and we followed them through day 57 or week 8. The data we're presenting today reflect everything available once all patients completed their week 8 visit. Patients then continued an additional 12 weeks for a total of 16 weeks of follow-up, there was no additional treatment provided after week 4. As Neal mentioned, we targeted a severe population requiring a baseline EASI score greater than 21. The study was conducted at multiple sites in the U.S. The primary endpoint was safety and tolerability, and we also evaluated efficacy using standard AD, including EASI and PP-NRS. I want to emphasize the work we did to identify a severe patient population. At screening, every enrollment subject had standardized full body and primary autographs taken. And those photographs went through central review by a dermatologist. The review helped ensure that each subject had the disease based on the target lesion and the extent of disease was consistent with the eligibility criteria. Turning to baseline characteristics on Slide 11, we enrolled a diverse range of patients. A high proportion had severe disease, 82% or IGA-4. We also in percentage of Black or [ Latin ] American and Asian subjects whose disease may have a greater TH17 and TH1 component. These patients are typically harder to treat with TH2 directed approaches alone. Given the underlying pathophysiology, it is also more difficult to detect improvement in the erythema component of Easy in patients with darker pigmented skin. Late-stage AD studies typically enroll 35% to 40% IGA-4 patients and a higher proportion of white patients than we did here. And we would expect our Phase IIb program to look more like that. To summarize, this was a diverse and difficult-to-treat population. Now the analysis population, all 4 subjects are included in the safety analysis. For efficacy, we will focus on the per protocol population, which was defined prior to unblinding. In the active arm, 2 subjects were excluded 1 received only 2 doses, so that patient received very well with an 81% improvement in EASI from baseline. The other did not meet eligibility criteria. Two placebo patients went on rescue medication early on and were also excluded. That is illustrative of the severity and extent of disease in this study. Two of the 3 placebo ex required rescue medication compared with none of the active subjects. Safety and tolerability exceeded our expectations. As you can see on Slide 12, and we're very pleased with the results. There were no SAEs, no grade 3 or 4 events and no discontinuations due to AEs. There were only injection site reactions, all transient and most or grade 1. And importantly, something that is beginning to differentiate this molecule. We have seen no cases of conjunctivitis in this study nor in any of our other clinical studies to date. Looking at efficacy on Slide 13. EASI improvement from baseline was our key exploratory efficacy assessment. At week 8, we saw 45% placebo-adjusted improvement from baseline, and that improvement continued through week 10. These are encouraging numbers, particularly given that this severe population only received loading doses. We also saw maintenance of response at week 16 and 12 weeks after the last loading dose, which speaks to the potential for durability. And as Neal mentioned, severity matters. As you'd expect, in the IGA-3 group, a more moderate population shown on the right side of the slide, we saw even greater reductions in EASI. Slide 14 provides additional context for week 8 EASI results, alongside published data from other biologics in AD. Neal highlighted earlier, please keep in mind the differences in baseline severity between studies. With that caveat, our early data compare well to the landscape. Other trials are different, and we have not controlled for those differences. On Slide 15, 78% of subjects who received ATI-052 achieved EASI-50 at week 8. Of those, among IGA-3 patients 100% achieved EASI-50 versus 71% in the most severe IGA-4 group, again, highlighting that more moderate patients are easier to treat. And 89% of ATI-052 patients achieved EASI-50 at some point during the study, which speaks to the breadth of response across the spectrum of patients. The other key outcome for this population is itch, which is shown on Slide 16. Itch is a major component of this disease so demonstrating a robust reduction in itch alongside the reduction in EASI is important. We know TSLP plays a role in driving itch, and Rowan will share biomarker data that explore that relationship further. We saw a rapid reduction in itch as early as week 1 and a robust absolute and placebo-adjusted 40% improvement from baseline at week 4, which was maintained through at least week 10. At week 8 specifically, patients on ATI-052 had a 43% placebo-adjusted mean improvement in itch from baseline. We've also included data from other biologics to provide context on the PP-NRS placebo-adjusted response at week. On Slide 17, at week 8 33% of ATI-052 patients achieved a 4-point or greater improvement in itch from baseline, known as PP-NRS 4. Again, we've included data from other biologics for context. On Slide 18, we want to show you visual examples of disease improvement in patients with ATI-052. These were selected as illustrative examples. The first patient had an IGA 3 at baseline with significant disease on the back of the neck. This was Dr. Cameron subject, who you'll hear them shortly. The baseline photo on the left shows erythema, scaling and licentification. By week 8, the disease had almost completely cleared. Below that is a second patient with severe disease, IGA 4 at Phase I. The first photo shows significant erythema. Those red areas are where the patient has been scratching, which experiences the skin bleeding. On the right, by week at the art has substantially improved, and there is a small catch of residual liquefication. These week 8 results leave us encouraged about the potential for further improvement with longer treatment. So these are 2 less certificates of difficult-to-treat disease where ATI-052 made a meaningful difference. Now I'll turn the call over to Roland to discuss pharmacodynamic results in AD. Roland?

Thanks, Jesse. I'm glad to be here this morning to discuss the former dynamic markets we investigated in this trial. -- clinical efficacy data Jesse presented are supported by pronounced changes in the skin proteom and in key systemic biomarkers. In collaboration with [ Dr. Amar Gutman, ] Laboratory at Mount Sinai, we collected tape strips provisional and nonlesional skin at baseline and week 8 and analyzed more than 300 proteins using Olin proteomics. We also evaluated endogenous serum biomarkers, including CCL17 or TAR IL-5 and Poladiosynophils. Together, these analysis provide evidence of the broad biological activity of ATI-052 and the potential additivity or synergy of simultaneously targeting our 4 receptor alpha and TSLP. Slide 19 summarizes the pharmacodynamic profile we observed a broad pathway modulation across TH1, TH2, TH17 and TH22 fibrosis and its associated biology. We also saw an almost complete normalization of the lesional skin proteom at week 8 with the treated lesional profile coming to closely resemble nonlesional skin. This included pronounced reductions in established biomarkers modulated by dupilumab, together with additional suppression of TH1 biology. These results are consistent with the combined activity expected from targeting both Telit and alpha-receptor alpha. On Slide 20, the heat map visually shows the skin protium changes. At baseline, lesional skin was clearly distinct from non-lesional skin. At week 8, the lesional skin of patients treated with ATI-052 shifted toward a pattern that closely resembled nonlesional skin. The solutional profile in the placebo group remained comparatively similar to baseline. Quantitatively, ATI-052 produced a 95% overall improvement in the lesional versus nonlesional podium relationship by week 8. For context, the published dupilumab data set shown on the slide, reported a 66% improvement by week 16. The depth of normalization observed with ATI-052 supports the potential for additive or synergistic biological activity from dual IL-4 receptor alpha and tip inhibition. Slide 21 examines the breadth of that response in more detail. Genset variation analysis showed down regulation of TH1, TH2, TH17 and TH22 and pruritus associated signatures in lesional skin. The slide includes representative remediators within these signatures. I want to particularly highlight the reductions in the TH1 associated markets, [ 69 and 6-10, ] which are not modulated by our 4 receptor alpha blockade alone. This broad pathway modulation is consistent with the contribution of this slip inhibition to the drill mechanism of ATI-O52. The systemic biomarker data tells a very consistent story with what we saw in the skin. I would particularly highlight the reductions in IL-5 and peril eosinophils with ATI-052 which are consistent with the inhibition of the TSL pathway and differentiate ATI-052 from alpha receptor alpha blockade alone. With [indiscernible] IL-5 is not reduced, and peripheral eosinophils can transiently increase. So when we look across both the skin and blood, we see broad and pathway modulation that is consistent with engagement of both components of ATI-052. The point specifically about slip. The question we have received often is whether Tslip has an important role in atopic dermatitis. The ATI-052 results add to the emerging evidence we observed clinical activity in a patient population enriched for severity, together with broad modulation of TH1, TH2 and TH17 and TH2 biology. Marked normalization of the lesional skin podium and reductions in our 5 neonate. These findings support the role for T slip in the broader inflammatory biology of AD. In summary, -- this trial evaluated loading doses without a maintenance regime. ATI-052 achieved the safety tolerability and clinical efficacy [indiscernible] dynamic results support the proposed dual mechanism and provide evidence of the potential activity synergy of targeting to T slip together with Alfreceptor alpha. We believe ATI-052 this molecule potential applicability across type 2 diseases. With that, I'll turn the call over to Dr. Michael Cameron, Assistant Clinical Proffice and the Department of Dermatology and Mount Sinai for his thoughts on the market opportunity and his experience with ATI-052 to Dr. Cameron.

Well, thanks, Roland, and thank you, Aclaris for involving me in this conversation. As I mentioned, I had the esteemed opportunity to be involved in this clinical trial and see some of my patients really benefit from it. And as has been discussed, there's a lot of mechanisms of action in the pipeline for atopic dermatitis. But really, this is a massive, massive market that's growing year-over-year. And unfortunately, we have not seen much movement in terms of increased efficacy in our commercially available therapies. You look lab toxin, which has been out for close to 10 years. And the primary endpoint around 37%, 40% getting an IGA response, 48%, 50%, 55% getting an EASI-75 response non-placebo adjusted, we haven't really seen incrementally much movement from there. And the vast majority of my patients that are on DUPIXENT are either partial responders have a tolerability issue or lose response over time. And so there's just a massive need for new mechanisms of action. We look at all the different endotypes of atopic dermatitis -- and it really is driving that need. Not only do we need things with higher bar efficacy, both in terms of skin clearance and Italia, but we need new MOAs to target those various endotypes. So that really is what makes me excited about this Aclaris asset is we're really excited about bispecifics just because you are not only going to target exclusively the TH2 pathway. You're going to introduce, for an example, here, T-slip which is a really important pruritogen for atopic dermatitis. And that's what I saw with my patients was you're getting that skin clearance via the IL-4 receptor inhibition, but you're also getting really immediate itch relief in additional anti-inflammatory effect by targeting T slip. And so I had a patient that was actually presented in this slide deck. That was my patient. And -- she had been through numerous previous biologics, and she had a very rapid and very, very deep skin clearance and intra-lease with this IP. And interestingly enough, close to a half year out even while off therapy, she continues to have a very, very durable response and almost a remit effect. And so that really gets me excited about this asset. And I think more and more mechanisms of action are going to be needed over time, and that's what gets me excited about the bispecific. So for me, in terms of looking at atopic dermatitis as a whole, like what are the big gaps? Obviously, we want an oral medication that does not require lab monitoring. It is going to have to be like efficacy or better ideally. But in addition to that, I'm seeing for my patients that more and more patients want injectables as opposed to orals. I think that Wall Street and investors often think that oral is better. And I don't think that's necessarily the case. I think we've seen that with the TYK2 inhibitor in psoriasis and throughout the immunology space. And I think the innovation behind the GLP-1s and the tens of millions of Americans are taking GLP-1 has gotten even more and more people comfortable with injectable cations. I think dermatologists have a lot of prescriber inertia. And they oftentimes they get used to 1 way of doing things, and they've gotten used to providing their patients for atopic dermatitis with biologics, with injectables. And so that's what really gets me excited about something like this asset where we can potentially raise the bar in terms of 1 action for its relief and skin clearance, and we can target more potential endotypes for atopic dermatitis. So thank you again, Aclaris for involving me in this trial, and I'm really excited to hopefully be involved in the Phase II trial as well.

Thanks, Dr. Cameron, and thank you for all you do for patients with this disease. Now on to the asthma results. The short version is that this was another trial with encouraging results. After a single dose of ATI-052, patients responded rapidly. We saw changes in Pheno, a marker of airway inflammation and in lung function within the first 2 weeks. The speed and breadth of that response gives us confidence in this molecule's potential in asthma. As you can see on Slide 23, we enrolled 16 patients and randomized them 3 to 1. This was a single injection at baseline. Active subjects received a single 480-milligram dose of ATI-052 and the others received matched placebo. The assessment period was 29 days, followed by an additional 6-week follow-up period for a total of 10 weeks of follow-up. The majority of sites were in the U.S. with 2 sites in Germany. Summary endpoint was safety and tolerability. We also evaluated key efficacies that matter for asthma patients, including pheno reduction and FEV1 improvement. Slide 24 shows the patient population. To be eligible, patients needed a baseline pheno of at least 35 parts per billion. For eosinophils, eligibility required a current or historical eosinophil count to be at or above 150 cells per microliter. Interestingly, the population included subjects with eosinophils less than 300 cells per microliter. A population of patients for whom the benefit is smaller with dupilumab compared to those with an eosinophilic phenotype above 300. The other point I'd like to highlight is baseline FEV1. We set a minimum of 60% of predicted but no maximum. As a result, half of the enrolled had a normal FEV1. So the improvements I'll show were achieved in patients with limited room for improvement. In a more typical Phase IIb or Phase III population, FEV1 balance are typically set up to 80%. So patients with considerably more room for improvement in lung function. Turning to safety on Slide 25. ATI-052 was well tolerated, consistent with the AD study and the healthy volunteer study. There were no SAEs in any patient. It was a sync treatment-related adverse event in the 052 group, a mild injection site reaction. And consistent with the rest of the program, we observed no conjunctivitis. Now to pheno suppression on Slide 26. This highlights the rapidity and breadth of response to ATI-052. Patients who received a single dose of ATI-052 experienced a 59% reduction in Pheno for baseline, an absolute reduction of 45 parts per billion. Our goal going into the study was about a 40% reduction with 50%, representing a particularly strong result. Given the 59% reduction, we were pleased with both the magnitude and the speed of the response. On Slide 27, we've included published dupilumab and tezepelumab pheno data to illustrate the broader treatment landscape. Slide 28 shows responses in the subset of patients with eosinophils below and at or above 300 cells per microliter. This threshold is commonly used as a marker of type 2 inflammation and dupilumab has shown benefit in clinical trials in eosinophilic phenotypes above 300 cells per microliter. At day 15, we observed a 58% reduction in pheno among patients with fewer than 300 eosinophils and a similar 60% reduction among those at or above 300. That is a consistent response in both groups, which speaks to breadth of response in this study. Also at day 15, looking at another outcome measure for disease improvement, 58% of ATI-052 patients reached a Pheno at or below 25 parts per billion, a level generally considered low. We also saw FEV1 improvement in both eosinophil groups. On Slide 29, we show FEV1 results. At day 15, we observed a placebo adjusted improvement of 200 microliters which increased to 260 microliters at day 29. As a reminder, we enrolled patients who generally had normal FEV1, meaning at or above 80% are predictive. On the right is a post hoc exploratory analysis, a subset of ATI-052 patients with baseline FEV1 below 80%, which is more typical of a Phase IIb population. In this subset, activations improved by an absolute 350 mls at day 15 compared with a 140 ml worsening among placebo patients. On Slide 30, we show the absolute and placebo-adjusted FEV1 change in that subset, alongside published data for context. Finally, Slide 31 shows an outcome from osylometry, which measures resistance in the large and small airways. The small airways matter most in asthma and particularly for exacerbations. Patients with severe small airway disease are at substantially higher risk of exacerbation. In the same subset of ATI-052 patients as on the prior 2 slides, we saw a reduction in small airway resistance, consistent with improved small airway function. This is the kind of signal you want to see in a POC trial in patients with asthma. So to bring this together, a single dose of ATI-052 was well tolerated with a safety profile consistent with the AD trial. We saw rapid responses in both Pheno and I with benefit visible at the earliest time point measured, and the response was consistent across a heterogeneous population, including both eosinophil high and eosinophil low patients. I'll turn the call back over to Neal for some concluding comments. Neal?

Thank you, Jesse, and thanks, everybody. The POC data gave us several key learnings. We saw signs of additivity and synergy across clinical and PD measures, along with breadth and depth of response. Activity against all 3 inflammatory endotypes in severe atopic dermatitis and improvements in both Pheno and FEV1 in T2-high and T2-low asthma patients. In atopic dermatitis, we saw strong evidence of T-slip involvement, including complete normalization of the skin proteome and reductions in IL-5 and eosinophils. Early durability in atopic dermatitis was encouraging with responses maintained through at least week 16 so far. Tolerability has also been strong and potentially differentiated with no conjunctivitis seen to date. Overall, we see a real opportunity to raise the efficacy ceiling for patients with type 2 diseases. Together, those markets represent hundreds of millions of patients. Having demonstrated these proof-of-concept results consistent with our development strategy and disciplined capital allocation, we intend to move to Phase IIb, where we will prioritize eosinophilic esophagitis. This is a great opportunity for this molecule for a variety of regions, including a growing global market, ample open white space and a strong mechanistic fit for ATI-052 given the disease biology and the efficacy demonstrated with targeting IL-4R and T-slip alone. We expect to start this study early next year with the intent of designing it as a seamless Phase Ib/III. We are also evaluating the potential for 1 additional indication, and we'll provide updates shortly. And as promising as these POC results are, this is just the start of the catalyst calendar for us. In addition to the go-forward plan for ATI-052, we expect the top line data readout from our tslip-mabvosacatug and atopic dermatitis later this quarter, which we hope will further demonstrate the value of T-slip and AD. We have a slew of catalyst with our oral small molecule program, including monzatinib. As a reminder, we received Fast Track designation for this program earlier this year. We expect to kick off the like and planet trial in the coming couple of weeks. Once we have data for 60% of patients in the mucosal cohort, we plan to conduct an interim analysis, which is expected later in '27. And if the data are supportive, we plan to engage with the agency regarding potential to convert into a registrational study as allowed by Fast Track. And lastly, we expect to file the IND for our ITK inhibitor, ATI-9494 this quarter as well, which will then kick off a series of catalysts in '27. Thank you for your time and your interest. We'll now take your questions.

[Operator Instructions] Our first question comes from the line of Biren Amin with Piper Sandler.

And congrats on all the data across both the AD and asthma trials. Maybe to start on the AD studies, how many patients in the AD trial had prior biologics. So that's the first question. And the second question is, what led you to prioritize EoE for the Phase IIb and then for the next indication -- there is a second indication of either AD or asthma, what are key considerations that you're thinking about as you choose that second indication for 052? And does the data from Bosecatag and AD at all faint that decision-making?

Thank you, Berin. I appreciate it. So in terms of the prior biologic use, we did have about 4 of the patients in the active group were on previous biologics, including drugs like lunsicamig and some IL-18 inhibitors and -- so there is definitely an experienced population that was part of the study. On a percentage basis, that was about 40% or so of the active cohort. In terms of prioritizing EoE I think between the last time we provided an update and getting this obviously elumab generated really strong results in EOE kind of validating the T-slip side in the pathysiology of usinophilic esophagitis. And clearly, knowing that Dupi is approved, this is, again, kind of like asthma, a spot on mechanistic match, and we obviously believe we have best-in-class T-slip side of that molecule. So I think that is a key consideration. I think the other key consideration is the ability to take an indication all the way to the finish line. And I think EOE is obviously, less capital intensive there. Studies are a little bit smaller than asthma or atopic dermatitis. So I think for a small company like us, it makes sense just like we're doing with LP on the oral small molecule side to engage in indications that perhaps have a little bit less competitive intensity and that we can take all the way. In terms of the second indication, we're in that evaluation mode. Fortunately, we've done a lot of the work already on all 3 indications. We're just shifting capital over to EOE. I think in the coming weeks, we'll -- these -- both of these studies are ongoing. So we'll collect the remaining amount of data there. And I think you bring up a reasonable point that the efficacy that we saw in AD was -- exceeded our expectations, gives us confidence in posacatug, but we want to see that data read out, and that would certainly I think, put the final nail in the story of T-slip involvement in AD. So more to come on that, but full steam ahead on EoE.

And our next question comes from the line of Raghuram Selvaraju with H.C. Wainwright.

Congratulations on this data. I wanted to drill down a little further on what you see as a key safety advantage for ATI-052, specifically with respect to lab and if you believe that based on the mechanism of action of the drug and the profile that you have observed so far, that additional safety advantages for istepilumab could emerge beyond the absence of conjunctivitis.

Yes. Thanks, Ram, for that question. Appreciate it. It's something that certainly doesn't get asked a lot. And I think as a former practitioner, I'm sensitive to those because all safety issues matter, right? And I think certainly, conjunctivitis is a key differentiator could emerge as that for us. And we've seen varying rates going up as high as 18%, 20% with other molecules and 10% with dupilumab. And we know that with Dupi in general, when you're taking down the TH2 side of the house that sometimes you get a TH17 skewing and those patients can sometimes get so negative arthritis. We also know that oftentimes, there could be a TH1 where you get eruptions of erythema and rash on the head and neck area. So there are some things, I think, that 1 has to be mindful of. And maybe the beauty of 052 as we clearly show today, we're not just taking the TH2 side down, but we're also firmly compressing TH17 and also roping in TH1. So I really -- that was 1 of the most exciting thing to me is not only do you pick up the heterogeneity piece, but importantly, as you point out, I think you check many boxes on the safety side.

And with respect to dose and convenience, is there some way for us to be able to assess what you ultimately expect to be achievable with 052 that could constitute a sustainable competitive advantage. As we all know, lots of other folks have attempted so far to demonstrate a profile that would reflect meaningfully improved convenience versus the twice a month injection schedule with dupumab. But -- in other context, we've seen particularly yesterday in psoriasis, the prospect of the possibility of a once a year doing, et cetera. So what do you think is ultimately achievable here in between sort of the twice a month and the once a year dosing administration?

Yes. It's a good question. I think everything is kind of indication dependent, psoriasis, as you well know, is a much different market. But I think from my perspective, again, having practiced for many years, I think quarterly dosing is, to me, a sweet spot when you're managing these I&I diseases that tend to vary over time. And certainly, there's a lot of room between what you just mentioned twice a month and yearly. So what we've consistently messaged is that we believe we can get up to quarterly dosing and we're going to test a variety of dosing regimens in our go-forward study. And there's -- as you know, in atopic dermatitis as an example, there is induction dosing that usually occurs through 16 weeks and then you go to maintenance. And -- so we'll be testing a variety of factors there. But I think from my perspective, we've always kind of leaned in a lot more on efficacy and certainly believe that dosing interval and convenience is important, but you have to [indiscernible] that first box first.

Our next question comes from the line of Seamus Fernandez with Guggenheim Securities.

Just a couple of quick clarifying points. Can you just remind me how many patients -- we're in the final analysis and the placebo side. It's just a little bit unclear in the sort of final analysis, how that played out. Second question is, as we think about the EOE opportunity, what is that path forward from Phase II to Phase III, this sort of seamless approach when should we anticipate seeing the EoE data. It does -- and I take your point on efficacy with a certainty, but weekly dosing with Dupixent seems like an easy bar to move past for bispecific and the EoE setting. So is it kind of an underlying assumption that monthly is kind of a base case for your program in EoE that offers potential optionality to a longer dosing profile in EoE, in particular. And then the last question, as it relates to your like in planets advancement in the next couple of weeks. Can you just highlight for us a little bit more of the sort of clinical trial design, specifically the endpoints that will be used in that study the patient population that you'll be approaching initially? And then what that path rapid path forward to Phase III could include in the ligand Planet setting specifically?

Sure, no problem. I think I got all that in my head. So thank you for the questions. I'll answer the EOE first. You're right, Seamus. I think the bar there is certainly lower and Q monthly would be at a minimum and obviously strive for greater, but I think it's a little bit easier hurdle on the convenience side and indication. So thank you for bringing that up. On the atopic dermatitis study, so 14 patients in there were 3 of those were in placebo grew. Two patients in the placebo group had major protocol violations at day 35, I believe, both of them were put on high-potency topical corticosteroids. And that basically meant there out of the analysis because now you're no longer comparing to placebo, you're comparing to high-potency topical steroids. So there was 1 patient in the placebo group that was going forward from about 43 or so on. And then on LP, in terms of activities there, we're initiating that study in about 2 weeks. And so you'll start seeing things on clintrials.gov from us there. On trial design it's a -- as we mentioned in the past, it's a basket study, but we're doing it cohort by cohort. We're going to spend most of our time on mucosal LP, which predominantly will involve the oral area. And that will be a 16-week study endpoint -- primary endpoint will be ODSS which is the oral disease severity store. We'll also have a variety of other endpoints, including IGA. And then we're going to take an interim look. When we get about 60% of those patients, 50% to 60% of those patients through week 16 and what we anticipate to see is a pretty rapid response. And if that is the case, then I think what Fast Track allows us to do is to go have some conversations with the agency and then what we would strive to do is to convert that particular phenotype into a registrational study. So we're not going to wait for the whole entire basket study to finish. We're going to do it cohort by cohort. So that's, I think, what it looks like. And hopefully, that answers your questions.

Our next question comes from the line of Prakhar Agrawal with Cantor Fitzgerald.

Congrats on these data sets. Maybe in the asthma trial, the kinetics of the pheno reduction for the bispecific at day 15 versus day in 19 is a bit different than Sanofi's lens acumen, which targets the T-slip cetane. So maybe if you can elaborate on why this may be happening? And what does it mean from a dosing perspective, especially for the EU trial as well as we think about induction versus maintenance? Secondly, on planets, Neal, you talked about or mucosal and DSS has been the endpoint. Like what's the good result on that endpoint? And will the trial be powered to show statistical significance given it's a smallish trial?

Sure. Sure. Thanks for the questions, Prakhar. On the Pheno kinetics, right out of the gate, we were down to 50 then to 59% and then at the end, 40%, which even when you compare 40 to the competitive set is still quite strong. And what you're dealing with there is a single dose kinetics versus multi-dose kinetics. And now with this molecule single dose with TMDD, behaves a little bit differently. And we clearly showed in the atopic dermatitis study. We mentioned this a couple of times that we have quite long durability in terms of clinical -- both PD and clinical effect. So it is, I think, a loading sort of phenomenon there, and we only tested single dose in that study. On the LP front, on the endpoint, I'll hand that over to Jesse in terms of what we're looking for on ODSS, Jesse?

Yes. Thanks, Neal. So just with regards to ODSS and Bocar's question, so that's the primary endpoint that we'll utilize in the oral like plaintiffs study. So that was something that was originally developed for oral pemphigoid and then subsequently adapted for oral liken planes. If we look at that score, it's a really nice scoring methodology for these smaller trials and that it's very sensitive to change. So it goes from 0 to greater than 116 and you can imagine you would see a benefit of change in a smaller patient population with a continuous variable, such as that. We haven't disclosed externally exactly what we're doing from a goal perspective, but you'll hear more about that in the future. But I would anticipate that that's an excellent outcome measure to evaluate disease change in a small patient population.

Our next question comes from the line of Michael King with Rodman & Renshaw.

Yes. Sorry for any background noise. Just wanted to ask, again, I also have a question about the demographics of the AD patients in addition to the 2 drops, it looks to me that the -- 052 group was fairly about 10 years younger and also weighed a fair bit less. So I don't know if that had any influence on the outcome. I don't know if Dr. Cameron can -- I don't know still on that if you can talk about whether the heavier patients respond better or worse than lighter patients, younger versus somewhat older patients, but I just wonder how you want us to think about that.

Yes. I don't -- I can take that, Mike. I don't think -- I mean, certainly, overall, if you have a meaningful difference in weight, I suppose, that can help from an exposure standpoint. I don't think it was really a factor at all in this study, I mean, across all the patients. I mean that was the beauty to me of these results is that even in a very severe and diverse population, although small end, there was just a remarkable amount of consistency across the board when you think about close to 80% of patients getting to an easy 50 level after just a load in dose and just maintaining that out for so many weeks, I think that's quite remarkable. And and not necessarily what I expected. So I don't -- I really don't think that, that delta play much of a role.

All right. And then is this the last data that we'll see here? Are you going to present this so we can see more about the durability -- and I know other questioners have asked about the response rate by prior therapy. Will those kind of details be made public at some point in the future just to get some idea of the pharmacodynamics, 052 and AD?

Yes, certainly. So both studies are still ongoing. And so we will provide an update likely at a medical meeting in the future. So stay tuned on that front.

Are the patients allowed to go on subsequent therapy after the 12-week follow-up.