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

Good day and thank you for standing by. Welcome to the Aclaris ATI-052 Clinical Trial Update Conference Call. [Operator Instructions] Please note that today's conference is being recorded. I will now hand the conference over to your speaker host, Will Roberts, Head of Communications. Please go ahead.

Thank you, Olivia, and good morning, everyone, and welcome to the Aclaris Therapeutics conference call to review the positive interim results from our ATI-052 Phase Ia single and multiple ascending dose trial. The press release on these clinical results was issued this morning and can be found in the Press Releases sub-page of the Investor Relations section of our corporate website, aclaristx.com. Please note that we've provided the slides as part of this discussion, and they're now available in the webcast window as a downloadable PDF document. We'll reference the slide numbers throughout. As mentioned, the 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 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 Securities and Exchange Commission, which are available from the SEC or on our corporate website, www.aclaristx.com. Any forward-looking statements represent our views as of today, January 6, 2026. We also note that today's interim results are as of December 31, 2025, and the trial is ongoing. Joining me on the call today are our Chief Executive Officer, Neal Walker; Hugh Davis, our President and COO; and Jesse Hall, our Chief Medical Officer. Roland Kolbeck, our Chief Scientific Officer; and Kevin Balthaser, our Chief Financial Officer, are also available for questions following the prepared comments. With that, I'll turn the call over to Neal.

Thank you, Will. Good morning, everyone, and thanks for joining us on our call this morning. We are delighted to share the positive interim results for our lead bispecific antibody, ATI-052, which effectively binds both TSLP and IL-4R to block signaling of TSLP, IL-4 and IL-13. At Aclaris, our goal is to develop best-in-class therapies for people living with I&I disorders. There are options are limited at best and the need to improve tolerability and raise the efficacy ceiling is significant. Today's results take us one step closer to achieving this. As you'll hear, these results highlight ATI-052's strong safety, tolerability and PKPD profile, reinforce its potential best-in-class potency advantage to drive potential improvements in efficacy and provide support for the potential of an extended dosing schedule. ATI-052 is unique in that it provides the potential for improved clinical outcomes by inhibiting TSLP upstream and immune cells downstream in the Th2 cascade via IL-4R. The biology does not overlap, rather, it's additive and as such, has the potential to provide very strong efficacy in a variety of indications with infrequent dosing. The next several quarters are anticipated to be an exciting time for Aclaris and for ATI-052. We expect to initiate our first proof-of-concept trial in atopic dermatitis imminently, followed shortly by the start of our second POC trial in asthma this quarter. We expect both to read out in the back half of this year. Importantly, these results have enabled decisions to expedite development of the compound and planning is underway to initiate a Phase IIb trial in the second half of 2026 that would plan to assess multiple doses and a longer dosing schedule of ATI-052 that is supported by these Phase Ia interim results. Hugh Davis and Jesse Hall will walk you through an overview of the molecule and the trial results. I'll be back at the end to conclude the call. Hugh?

A quick overview of the compound, its scientific rationale and why it represents such an exciting opportunity in a variety of indications. As Neal mentioned, ATI-052 inhibits TSLP upstream and immune cells downstream in the Th2 cascade by simultaneously binding both TSLP and IL-4 effectively and with high affinity. Antagonism of IL-4R blocks signaling of both IL-4 and IL-13 activity. We believe that ATI-052 has the potential to show superior activity in dermatological and respiratory I&I disorders compared to approved therapies and could also be efficacious in a variety of inflammatory immune diseases involving Th1, Th2 and Th17 inflammation. Referring now to the slide deck that Will mentioned, on Slide 3, you can see a diagrammatic representation of the molecule. On the right side, you'll see that ATI-052 has the same anti-TSLP ligand binding regions as our anti-TSLP monoclonal antibody, bosakitug. It retains the potential class-leading very slow dissociation kinetics, long resonance time and high potency advantages over tezepelumab and other comparator clinical stage assets. On the left, you'll see that it has 2 single-chain variable fragments that have high affinity to IL-4 receptor. Importantly, we added 2 Fc mutations: one, a YTE mutation to bind FcRn more tightly and as such, extend the half-life and the other, an AQQ mutation to reduce off-target binding and potential toxicity. We believe the results we are discussing today show the positive impact of these mutations. We've spoken at length about the potency advantage of ATI-052 over other compounds on the market and in development, most recently at our October R&D Day. Potency is the concentration needed to drive an effect. One way potency is driven is by maintaining high resonance time on TSLP. Since TSLP is an alarming with high potency itself, it requires a therapeutic that also has high potency in order to neutralize its pathologic effects. As you can see on Slide 4, ATI-052 has very slow dissociation kinetics, significantly better than comparators, which leads to a residence time on TSLP of over 400 hours, which is at least 30 and up to 116x longer than comparator antibodies. For example, compare the 416-hour residence time of ATI-052 to tezepelumab's 14.3 hours. This comparison shows that ATI-052 binds to TSLP target 30x longer than tezepelumab, thereby providing the potential for enhanced potency and efficacy compared to teze. On Slides 5 and 6, you will also see that ATI-052 can effectively bind 2 molecules of TSLP and 2 molecules of IL-4R concurrently. This means that all 4 binding sites are acting independently. Importantly, the effective binding of ATI-052 to one target does not alter its ability to bind to the other target. So not only do all 4 binding sites act independently, but they also maintain their same high affinity to their target. Functionally, all of this leads to a significant potency advantage. As shown on Slide 7, peripheral blood mononuclear cells from healthy donors produce CCL17, also known as TARC, when stimulated with both TSLP and IL-4. ATI-052 exhibits 4x greater potency in inhibiting CCL17 production than the combination of dupilumab and tezepelumab combined. The bispecific may be showing a synergistic effect that is more potent than the combination of the 2 antibodies. Slide 8 shows the functional potency of ATI-052, comparing to the lead compounds in modulating CCL17 by inhibiting TSLP, IL-4, IL-13, combination of IL-4 and IL-13 and then all 3 TSLP, IL-4 and IL-13. ATI-052 exhibits the broadest activity among those approved biologics, again, confirming its potency advantage. So to summarize these key attributes, ATI-052 effectively and simultaneously binds TSLP and IL-4 receptor, which is borne out by the clinical data I'll show momentarily. It is significantly more potent than comparator antibodies and its antagonism of IL-4 receptor blocks signaling of both IL-4 and IL-13. This is truly a unique compound. With that, I'll turn the call over to Jesse.

Thanks, Hugh, and good morning, everyone. I'm glad to be here to discuss these exciting SAD and MAD results. We had 4 goals in mind as we designed this trial, as you see on Slide 11. First, to confirm a favorable safety and tolerability profile of ATI-052 in a healthy volunteer setting. second, to confirm a pharmacokinetic or PK profile to support at least 1 month dosing. Third, to understand its pharmacodynamic response and the ability of the drug to achieve complete target occupancy. And finally, to clinically validate the compound's ability to efficiently inhibit both TSLP and IL-4R. I'm happy to say that we achieved or exceeded each of these goals. On Slide 12, you will see a schema of the trial design. The randomized blinded placebo-controlled Phase Ia portion of the first-in-human study was designed to evaluate the safety, tolerability, PK and PD of subcutaneously administered ATI-052 in healthy adults receiving single ascending doses and multiple ascending doses. In the SAD portion, 4 cohorts of 8 healthy volunteers each were randomized 3:1 to receive a single dose of ATI-052 of 30, 120, 360 or 720 milligrams or placebo. In the MAD portion, 2 cohorts of 8 healthy volunteers each were randomized 3:1 to receive 5 doses of either 240 or 480 milligrams of ATI-052 or placebo administered every 7 days. On Slide 13, we describe the baseline characteristics in the trial, which were generally balanced across cohorts with demographics and characteristics that are typical of a healthy volunteer population. Then on Slide 15 and 16, we describe the favorable safety and tolerability profile of the compound in this trial. And I'll preface this by saying that by all accounts and measures, we were very pleased with these outcomes. ATI-052 has shown to be well tolerated with a strong safety profile across all SAD and MAD cohorts with doses up to 720 milligrams. Looking at some important outcome measures, we saw a low rate of adverse events overall. And when they occurred, they were predominantly grade 1. The most common AE was injection site redness, which was self-resolving and generally mild or grade 1. We saw no serious adverse events across any of the clinical cohorts and no adverse events that led to study discontinuation. We observed no Grade 3 drug-related AEs.We followed the SAD cohorts out to day 113 and will follow the MAD out to day 141. Importantly, we have observed no conjunctivitis cases in any cohort to date. To conclude, ATI-052 was well tolerated across the SAD and MAD cohorts with a strong safety profile, including single ascending doses of up to 720 milligrams. And again, we know that conjunctivitis has been a concern for some who are watching the space. We have not seen it in any of our cohorts to date. I'll turn this back over to Hugh for his assessment of the PK/PD results. Hugh?

Thanks, Jesse. The next set of slides describe the potential best-in-class PK profile observed in this trial. On Slide 18 and 19, the concentration time profile of the 30, 120, 360 and 720 milligram SAD cohorts and the 240 and 480-milligram MAD cohorts are shown and summarized. The dose range of 120 to 720 milligrams showed dose proportional increases in PK for both Cmax and AUC. Linear PK was observed for a prolonged period above the threshold concentration for target-mediated drug disposition known as TMDD, which in the case of the IL-4R receptor is approximately 1 to 2 microgram per mL. As the concentration in blood approaches the TMDD threshold, enhanced clearance will occur. Duration of drug concentration above the TMBD threshold was observed for 6 to 8 weeks following a single dose and at least 8 weeks after the lower MAD cohort of 240 milligrams. The higher MAD cohort dose of 480 milligrams shows a higher Cmax than the 240-milligram cohort and as such, would be expected to exhibit a longer duration above the TMBD threshold concentration. This was a very well-behaved molecule from a pharmacokinetic perspective in this trial. These PK results provided an effective half-life of at least 26 days, roughly 2.5x that of dupilumab. And considering the strong dose proportional PK profile, along with the sustained PD effect I'll describe momentarily, ATI-052 has the potential of up to 3-month maintenance dosing interval. We plan to explore this potential for extended dosing in the Phase II program, which is already in planning for later this year. Moving to the compelling PD results, starting on Slide 21. We converted the typical buffer-based PBMC CCL17 TARC assay that I previously described to a human whole blood assay. This assay better reflects the human biologic environment since it now includes a milieu of cells, cytokines, chemokines and the like in whole blood, where we also have endogenous levels of TSLP, IL-4, IL-13 and CCL17. We then stimulated the whole blood sample containing 052 with either TSLP or IL-4 and determine the percent of inhibition of CCL17 secretion by the drug. The results of these analyses are shown on Slide 22. The collection points for the PD analysis were on days 1, 4, 8, 22, 43 and 113. First, with IL-4 stimulated CCL17 at the top of the slide, even the 30-milligram cohort showed strong inhibition of IL-4 stimulation of CCL17 production. As mentioned, 30 milligrams was intended to be a sub-pharmacologic dose and yet the level of inhibition seen was quite strong even at approximately 100 nanogram per mL of ATI-052 that's present on day 4. As the dose increases to 360 milligram, we saw strong inhibition of IL-4 stimulated CCL17 out to at least day 43, including complete inhibition that was observed out for at least 3 weeks. When we assess inhibition of TSLP stimulated CCL17 in the bottom panel of the slide, for those same cohorts, we saw an even more impressive level of inhibition. Even in that 30-milligram cohort, we saw greater than 50% inhibition. And in the 360-milligram cohort, we observed complete or near complete inhibition out to day 43 and continued partial inhibition beyond that. These data are more compelling given the high concentrations of the stimulants that were used in these assays. ATI-052 was shown to bind, occupy and neutralize the effect of these stimulants on both sides of the molecule effectively with 100% inhibition of both targets at pharmacologically relevant doses for an extended period of time beyond even the PK profile. So we saw a sustained effect beyond what the concentration would have predicted. As mentioned, the combination of the effective PK duration and the sustained and strong PD results support the potential for up to every 3-month dosing. These results allow us to help clinically validate the binding and potency attributes I described earlier. They also provide 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 an extended dosing schedule of up to every 3 months with the potential for best-in-class activity. I'll now turn the presentation back to Neal.

Thank you, Hugh and Jesse. These PK and PD results provide a potential surrogate for clinical effect. Relative to the competitor data that has preceded these results, we observed complete and sustained inhibition of TARC at very low doses. The results showed inhibition of both TSLP and IL-4R with both arms effectively and simultaneously with this bispecific. Beyond that, the safety and tolerability profile is exactly what we want to see. We have made the decision to expedite the clinical program for ATI-052. First, we expect to initiate the Phase Ib POC trial in atopic dermatitis imminently. That trial will be followed in short order by a second Phase Ib trial in asthma, which we now expect to start later this quarter. We plan to provide more information on each of these as they initiate. As Jesse and Hugh alluded to, we are planning a Phase II trial in atopic dermatitis to initiate in the second half of this year, in which we'll plan to assess the extended maintenance dosing schedule supported by these results. As noted by others, ATI-052 could be efficacious in a variety of inflammatory immune diseases involving Th1, Th2 and Th17 inflammation. So the potential is vast. This is expected to be an exciting year for Aclaris with multiple milestones and data readouts expected from across our pipeline. Today's readout is an important first data point for the year. We're building a next-generation biotech company with a broad and deep pipeline and a world-class preclinical and discovery team in an effort to continually deliver innovative new compounds to the clinic. Thanks for your time today. Let's open up the call to Q&A. So I'll remind you that we may be limited to what we can discuss beyond what we've disclosed. Operator, are there any questions?

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

Maybe I could start off with -- on the PD data across both IL-4 and TSLP stimulated CCL17 assays, it seemed like the TSLP inhibition was a little bit more pronounced. In your view, what was driving that? I mean you clearly saw IL-4 inhibition as well, but it seemed like TSLP inhibition was slightly better?

Sure. So Hugh, do you want to address that, please?

So you're right, Biren. What we saw was the TSLP inhibition was definitely a little stronger. And I think this speaks to the way the molecule has been designed. It's meant to completely bind and inhibit with that long retention time and really take TSLP out of the equation at the top of the Th2 cascade. And I think that potency that we've seen with bosakitug has translated very well into the 052 molecule here. And then the IL-4, our binding sites were designed to have roughly the same affinity as dupilumab, and we were expecting that would be additive and in some cases, potentially synergistic. So your observation is accurate due to the potency of the TSLP side of the molecule, I believe.

Got it. And then maybe just a follow-up. I think you mentioned that the Phase II AD trial would potentially evaluate every 12-month dosing. But I wanted to ask on the Phase Ib, if you could tell us a little bit about the dose selection and the frequency of dose administration in both the Phase Ib trial for atopic dermatitis as well as for asthma and the endpoints that you're hoping to evaluate and I guess, the time course as well for both of those studies.

Yes. Just to clarify, we're anticipating up to 3 months, not 12 dosing. But Jesse, do you want to just comment on the Phase Ib study designs?

Yes, sure. Thanks, Hugh and Neal. So the plan will be to conduct 2 Phase Ib studies. The initial study will be in an atopic dermatitis study. We're going to be utilizing the same dose that was utilized in the high-dose MAD cohort, the 480 milligrams. We'll be dosing that over a 28-day interval. So the drug will be dosed a total of 5x over that 28-day interval. The primary endpoint for that clinical study will be at day 57. And from a design perspective, we want to make sure that we're studying the same dose from the healthy volunteer study into the AD patient population so that we have equivalent PK and PD comparisons. To further elaborate our dosing selection in the subsequent Phase IIb clinical study. And then finally, we'll be utilizing the same dose in the asthma study that will be administered a single time with the primary endpoint at day 28. Does that address your question?

That's perfect.

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

Congratulations on this data. I was wondering if you could comment on specifically the plan to explore 052 in asthma and how this fits into the overall clinical prioritization of indications for this asset, particularly in the context of what you previously had indicated regarding preference for dermatological indications versus indications within respiratory disease. And also, if you could comment on what you see as potential advantages in either the asthma or atopic dermatitis indications from a competitive landscape and competitive positioning perspective. Also wanted to see if you could provide us with some additional color on what you anticipate to be the commercial implications of a once every 3-month dosing schedule, which was indicated in the press release as being a possibility for 052.

Yes. Thanks, Ram. So yes, clearly, we're interested actually in both dermatology and respiratory indications. And that's why we have 2 Ibs that will be kicking off very shortly here in both atopic dermatitis and asthma. And we think that the opportunity to expand into virtually all the similar indications that dupi is currently either approved in or being studied in is quite likely. I mean that's the big vision. And I think given the data that we showed here where we're getting complete inhibition at very low doses, this way exceeded our expectation, particularly for a healthy volunteer study. So I'm really excited about the potential in both derm and respiratory. And I think atopic dermatitis is a very fast-growing market. We still have not maxed out the efficacy in that indication. And so I think it's a great time, particularly with those of us who have bispecifics. And now we're -- we show that the art of the possible there with an IL-4R TSLP. So we think that from a competitive positioning standpoint, we're well positioned to show potentially best-in-class efficacy, just extrapolating all the data we have from our TSLP MAD, all the in vitro data and then the data we just presented here today. And then on the respiratory front, I think there's similar opportunity. Obviously, we're still hitting efficacy ceilings. That's why everybody is so interested in hitting multiple targets now. And I think the dosing interval, it's interesting. If you're talking about dosing intervals that involve Q2-week administration that then go to Q3 month or longer, I think that's a meaningful jump. I don't necessarily think that going from 2 to 3 months really matters or 1 to 3 months really matters all that much when -- if you're driving superior efficacy, right? So we do think we can get out to 3 months based on all the data we showed. But if it was 2 or 3, so long as we're showing, again, complete inhibition of chemokines like TAR and we will be continuing our work on this study, generating additional biomarker data. So we're really excited about it. I mean I think if you go back and you look at this and just from a practical perspective and show the progression from 30 to 120 to 360, just beautiful dose response and not just complete inhibition, but sustained. Imagine what we're going to be showing with the MAD dosing.

And then can you just briefly comment on the immunogenicity profile of 052, particularly as this pertains to potential circulating neutralizing antibodies as well as the possibility of specific subcutaneous presentations of this asset, for example, in the context of non-needle visible subcutaneous delivery pen, like, for example, what is currently available in the case of dupilumab.

Yes. Thanks for that. All that work is in flight. We test all the samples in the study at the same time at the end of the MAD and SAD cohort. So we're using an in-study cut point using the baseline samples for the ADA. I think you can extrapolate from looking at our data so far, both on the PK and PD side that we're not really worried about that at all. We showed obviously nice -- really nice results in both PK and PD, and that would likely be reflected in those curves. So more to come on that. And in terms of just future development, certainly, we'll be looking at those sorts of things as we look at a to-be-marketed commercial presentation.

Our next question coming from the line of Roger Song with Jefferies.

Congrats for the early but very exciting data. Maybe a couple of questions related to the PD markers. So pretty clear, this is a very deep inhibition sustained. Can you just contextualize the assay you use for the ex vivo compared to other monoclonal antibody or the bispecifics in the similar context? And then also, when I see those other competitive trials or the assay around 20%, 30% inhibition, any evidence to support the correlation of the level of the inhibition eventually can translate to the clinical results?

Yes. Why don't I hand that off to Roland to just talk about that assay compared to what others do. And I think the punchline is I think there's been pretty good data to support that this is why people use these biomarkers. When you look at the aggregate of them, they certainly are a guiding light to what one might expect in the clinic. And I think that's why we all try to incorporate that into our early decision-making. Roland?

Yes. Thanks, Neal. Great question. So CCL17 for our molecule is just a perfect biomarker because it's regulated by IL-4, IL-13 and TSLP. So we could use the same readout to really look at PD effects in our whole blood assay. And as you were pointing it out, I mean, the results are really outstanding. It's very complete and very robust inhibition. Now what others have done is, for example, also look at STAT6 phosphorylation as an alternative readout, which is triggered by IL-4 and IL-13 or you could also look at IL-4 receptor occupancy. But I would argue that readouts like CCL17 or TARC are really downstream of the TSLP cascade and the IL-4 receptor cascade. And it's a very well accepted and very robust biomarker. So we feel very good about our data.

Yes. And the way we did the assay looking at human whole blood, I think, is important because it more accurately reflects the kind of milieu in which we'll be operating. But yes, I mean, look, Roger, this was something where I was anticipating something a lot lower just as a signal. And again, just to highlight, we're seeing this at our lower doses. So I always like complete inhibition rather than partial.

Absolutely. A quick follow-up on the -- I understand this is the good assay for you. Have you tested any other PD markers beyond the POC? And then lastly, just on the clinical, you seems to want to accelerate the development path. Would you -- do you plan to start the Phase II without the Phase Ib data? Or you want to look at at least atopic dermatitis Phase Ib data before you will start the first Phase II?

Yes. Of course, the Ib will complete prior, but we're going to do all the spade work to get it going so that we can literally press the button this year on it. And we're pretty confident now given the totality of the data that we've seen. We are doing additional biomarker analysis. This was kind of the first cut and more to come on that as we evolve throughout the year.

Our next question coming from the line of Alex Thompson with Stifel.

This is Charles on for Alex. Congrats on the initial data. I think maybe a couple of questions from my side. Maybe first, is there anything you can say on the MAD portion that you're observing so far, either from a safety or PK/PD perspective? Does it seem consistent with what you've seen from the SAD side? And then I guess on AEs, I understand these are mostly ISRs, but anything else that was notable would be great.

Thanks, Charles. Yes. No, there was really nothing else notable. It was very clean. Of course, like everybody else, we look for things like conjunctivitis, infections, things like that. And so far, so good. We haven't seen anything related to that. And the ISR profile is actually quite limited and quite mild and even through the MAD portion. And you'll see that in the slides that we aren't seeing anything different in the MAD. In fact, it's just the curves are getting better. You can see that in the PK profile. We're out to 480 now, and we're going to continue to follow that data out through day 143 or so. But yes, still -- that's why we're so excited about the SAD data because, again, just showing the PK and PD in particular, up through 360 and you're seeing the numbers that you're seeing with complete inhibition. And usually, the general rule is with these biologics that as you go up in dose, it's pretty predictable. And so we expect to see even better at 720 on the SAD and then even better on the 240 MAD and 480 MAD.

Awesome. That makes sense. And maybe just a quick follow-up. Have you commented at all on how you're thinking about like trial site location for your Phase II study in atopic dermatitis potentially?

We have not. We will going forward. And certainly, it behooves one to do global studies there. I will say that some have talked about placebo effects that are actually greater in the U.S. versus elsewhere in the world. There's really no basis for that. It doesn't actually make sense either if you think about it. The key thing you have to do in atopic dermatitis studies is actually screening patients with pictures to make sure they not only have disease, but also adequate disease. That's the single best way to exert control over the study to make sure you're getting the right patients in.

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

Congratulations on this update. Maybe just quickly on the injection reactions. I know it is only injection redness, but maybe if you can talk about the ISRs in general, what you're seeing? And then on the Phase I atopic dermatitis trial, maybe if you can remind us about the rationale for testing weekly doses in the Phase I, given the long half-life you are seeing with the bispecific?

Okay. I'll hand the Phase Ib to Jesse, but the ISRs, we really just didn't see much. The majority of it was mild, just self-resolving. If you look at across the cohorts, there wasn't any sort of increased incidence as dose went up. In fact, when you look at the 480 MAD, 2 placebo patients had some mild redness. So it was really unremarkable. So -- which I was really happy to see because as we all know that, that can be problematic down the road and I think gives us a lot of confidence in the program moving forward. And on the Ib, my initial comment would be like we're trying to show in a proof-of-concept study in AD in a very short study, kind of a max effect to help inform decisions as we move to the Phase II. And so that's why we're going to dose aggressively there. And Jesse, do you want to maybe comment as well?

Yes. Thanks, Neal. So with regards to the design of the Phase Ib, as mentioned, we'll be dosing a total of 5x over that 28-day interval. So very similar to the design of the MAD cohort, the 480 MAD cohort. As Neal mentioned, one of the rationales is to make sure that we get adequate drug concentrations over that short 28-day interval. And then the other component is we really feel strongly that we want to match the dose that's utilized in the MAD Cohort 2 into the patient population with atopic dermatitis because that really aids our ability to design and develop POPPK models for our subsequent doses in the Phase IIb study. So that's the rationale is getting adequate drug concentrations and then secondarily, to continue to build out our robust POPPK modeling.

[Operator Instructions] Our next question coming from the line of Thomas Smith with Leerink.

This is Pujan Patel on for Tom Smith. So a couple from our end. With the encouraging Phase Ia data so far that we saw with 52 on hand, how do you guys plan to prioritize internal resources between both and 52 programs moving forward? And then regarding the Phase Ib proof-of-concept design for AD, can you provide a little more detail about your patient enrollment strategy? Is there like a target mix between biologic naive and biologic experienced patients that you have in mind?

Yes. Thanks for those questions. Could you repeat the first one, please?

Yes, sure. So with the encouraging data that we saw today, how do you plan to prioritize the internal resource like between both end, 2? Could we potentially see like a strategic shift in capital R&D focus? Or is that something we'll see more so after the Ib?

Yes. No, it's a good question. And so we think both have places in the market. Clearly, the AD study is going to read out in the second half of this year. We're excited about that. I think this bispecific data just provides further evidence of the potency of our compounds. And so we do think that a tezepelumab has a place in the treatment armamentarium of dermatologists who want a nice background therapy. We know there's polypharmacy out there with AD. And we already had kind of messaged earlier in the year that we won't be allocating our own capital against respiratory indications there. We'd be looking at partnerships. I think given the bispecific data that we have now, obviously, we're going to be prioritizing this a lot more. And that's why we messaged today about getting into a Phase IIb in AD at a minimum. So I think that's where you'll see us putting our dollars. We're really excited about the bispecific. We think we've shown quite a compelling profile so far. And in all likelihood, we'll partner the tezepelumab. And I would say that folks talk about combo treatments a lot, and we definitely have a best-in-class potential on our tezepelumab with our residents' time and think that, that would be a unique opportunity to combine with a variety of other constructs. On the -- what was the second question because I was having trouble hearing you.

Sorry, no problem. I can repeat it. Let me get off -- can you hear me better now? I'm off speaker.

Yes. Perfect.

Yes, apologies for that. Yes. So the second question, for your -- the Phase Ib proof of concept in AD, can you provide more detail like on your patient enrollment strategy? Like is there going to be a target mix between biologic naive and biologic experience specifically dupi, obviously? Or anything on that would be great.

Jesse, do you want to comment on that?

Happy to, Neal. Yes. So as we look at that Phase IIb study moving forward with the bispecific, we're still in discussions internally the appropriate mix between bio-naive and bioexperience. And clearly, there's an advantage to both. The bioexperienced patient population, there's a number of patients out there that have failed dupi or just unsatisfied with the every 2-week dosing. So we do think that there's a good opportunity in that patient population. I would just say that we're still working from the mix perspective, what proportion of patients will be bio-naive and which will be bioexperienced in that Phase IIb.

And I'm showing no further questions in the queue at this time. I will now turn the call back over to Dr. Neal Walker for any closing remarks.

Thank you, everybody, for joining us on the call today. We're really excited about these results, not just because it helps validate 052 specifically, but it continues to build the storyline of what our multi-specific antibodies can do for patients. More to come on this throughout the year, and we'll see many of you at JPMorgan in a week. Thanks for your time today and speak again soon. Thank you.

Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.