Ladies and gentlemen, thank you for joining us, and welcome to Nektar Therapeutics analyst and investor event, to discuss Resolve AD maintenance data with atopic dermatitis experts. After today's prepared remarks, we will host a question-and-answer session. If you would like to ask a question, please raise your hand. If you have dialed into today's call, please press star 9 to raise your hand and star 6 to unmute. I will now hand the conference over to Vivian Wu, Investor Relations and Corporate Affairs. Vivian, please go ahead. Thank you, and good morning, everyone. Thank you for joining us today. Today you'll hear from Howard Robin, our President Chief Executive Officer, Dr. Jonathan Zalevsky, our Chief Research and Development Officer, and Dr. Mary Tagliaferri, our Chief Medical Officer. On today's call, we expect to make forward-looking statements regarding our business, including statements regarding the therapeutic potential of and future development plans for rezpegaldesleukin, the timing and plans for future clinical data presentations, and other statements regarding the future of our business. Because forward-looking statements relate to the future, they are subject to uncertainties and risks that are difficult to predict, many of which are outside of our control. Our actual results may differ materially from these statements. Important risks and uncertainties are set forth in our Form 10-Q available at SEC.gov. With that, I would like to hand the call over to our President and CEO, Howard Robin. Howard? Thanks, Vivian, and good morning. Thank you all for joining us today. We're very pleased to share the results from the 36-week maintenance period of our phase 2b Resolve AD study, which evaluated rezpegaldesleukin at monthly or quarterly maintenance dose regimens. These results build on our data already reported for rezpegaldesleukin and truly reinforce the promise of a first-in-class novel TREG mechanism to treat atopic dermatitis. In the induction part of the Resolve AD study that we reported in June of last year, we saw a rapid onset of EASI-75 response and itch relief. At the ACAAI conference, we reported, for the first time with a TREG mechanism, a significant improvement in self-reported asthma control in patients with comorbid asthma from the Resolve AD study. Now, patients with atopic dermatitis and comorbid asthma represent 25% of the overall population, so this was a very important finding for rezpegaldesleukin. Importantly, the combined data we've generated for RezPEG from both induction and maintenance showcase how a novel TREG mechanism, which addresses causal human biology, could offer compelling efficacy and safety advantages for patients. We're truly pleased today to welcome two experts in the treatment of dermatological diseases to our call today: Dr. Jonathan Silverberg, who is Professor of Dermatology at the George Washington University School of Medicine and Health Sciences in Washington, D.C., and Dr. David Rosmarin, who is Chair of the Department of Dermatology and Associate Professor of Dermatology at Indiana University School of Medicine. Following the review of results, they will share their thoughts on the data and take questions. We're planning to initiate phase 3 in atopic dermatitis in the second quarter of this year so we can advance this important potential new therapeutic modality to patients as quickly as possible. If our Phase 3 is successful, our goal is to submit a BLA in 2029. With that, I'll hand the call over to Jonathan. Thank you, Howard, and good morning, everyone. In today's presentation, Mary and I will highlight the very exciting 52-week results from the Resolve AD study of rezpegaldesleukin in patients with moderate to severe atopic dermatitis. During this call, we will show results demonstrating that ongoing treatment with ResPEG promotes maintenance of existing responses in patients that achieved EASI-75, EASI-90, vIGA score of 0 or 1, or itch NRS at the end of the 16-week induction, and maintained that response through to week 52. We will also present data showing new responses achieved for EASI-75, EASI-90, vIGA, or itch among patients that had achieved EASI-50 but did not have those responses at the end of the 16-week induction and then did achieve these responses with additional dosing by week 52. Mary will cover these data as well as our results for EASI-100, or 100% complete clearance of disease, shortly. To begin, we wanted to highlight the mechanism of ResPEG and how we believe this mechanism allows ResPEG to differentiate itself against the cytokine-blocking classes of therapies. Firstly, ResPEG is an agonist that drives the proliferation and activation of regulatory T cells, and it is then the collection of immune-resolving mechanisms employed by TREGs that drives the efficacy and resolves the symptoms and underlying pathology of the disease. Now, this is in contrast to cytokine-blocking therapies, which can only inhibit overactive pathways in the disease. For example, with such therapies, the aim is to target one pathway with a single agent or multiple pathways with bispecifics, with the goal being to turn off that overactive pathway in the disease, or essentially classical drug-based inhibition. On the other hand, ResPEG, through its TREG mechanism of action, can address the underlying condition by employing many of the immune system's natural pathways of immune resolution. For example, in our earlier clinical studies, we demonstrated this directly through serum proteomic analysis of atopic dermatitis patients treated with ResPEG. That analysis showed that ResPEG modulated multiple immunoregulatory pathways, including those involving TREG function, induction of immunosuppressive cytokines such as IL-10, ectodomain shedding of immunomodulatory proteins, antigen recognition and MHC binding, antimicrobial pathways, cell adhesion and migration, and antagonism of Th2 polarization. Overall, this immune remodeling property of ResPEG highlights the differentiation and importance of this first-in-class TREG mechanism of action and its potential to provide deep and durable responses in atopic dermatitis. In the phase 2b Resolve AD study, there were three key questions that we set out to answer with the trial. The first two questions were focused on the dose level and dose regimen for the induction portion of the future registrational studies for ResPEG. As you recall, we initially presented the 16-week induction results in June last year, and since then we continued to update the results of placebo-to-active drug crossover arm through additional presentations made through the year. I will briefly review these results and the key differentiating features of ResPEG in a moment. The third question asked in the Resolve trial was the very important question of could the low-frequency, monthly or quarterly, ResPEG dose regimens maintain existing responses achieved by patients at the end of week 16 induction, and could the ongoing dosing through week 52 promote new responses in patients that did not achieve a response at week 16. This exciting data, along with a thorough safety analysis, will be presented by Mary in a moment. Let's briefly review what we have learned to date from the first part of the Resolve AD trial. The results from the 24 microgram per kilogram arm dosed Q2 week have shown us a number of key points for ResPEG. ResPEG has a rapid onset of action for efficacy, and especially for EZ75 and itch relief. Many patients see these effects after just one or two dose administrations, and this is especially important for itch relief, which is the major driver of quality of life associated with the disease. Helping patients feel better quickly is a critical feature and a highly desirable property of a potential therapy. ResPEG also showed a significant magnitude of itch relief as a single agent without the need for combination with topical corticosteroids. It showed equal efficacy in patients that had either moderate or severe atopic dermatitis at baseline, and besides dupilumab, ResPEG is the only agent that has demonstrated control of self-reported asthma and atopic dermatitis. This population was 25% of our population in the Phase 2b and representative of the 1 in 4 patients who have atopic dermatitis and comorbid asthma. From our placebo crossover cohort after induction, we have seen that extended dosing beyond week 16 to week 24 results in further deepening of efficacy across key efficacy endpoints, and from these analyses, we have established 24 microgram per kilogram Q2 week for 24 weeks as our induction dose regimen to be evaluated in Phase 3. This is a slide we presented in June 2024, the top-line presentation for the 16-week induction data. From that portion of the trial, we established the therapeutic validation of the Treg mechanism of action, the PK/PD profile of ResPEG, as well as the efficacy and safety of the 24 microgram per kilogram Q2 week regimen, which was the only dose level and regimen that met statistical significance across all primary and key secondary endpoints. This slide also, from the June top-line presentation, demonstrates the rapid onset of efficacy for the 24 microgram per kilogram Q2 week regimen, which is the red line in the chart shown in this slide. Importantly, note the upper left EASI-75 and lower right Itch NRS charts to see the rapid separation from the placebo after just a few administrations of ResPEG. As we reported multiple times last year, we have also observed that ongoing treatment of the placebo crossover cohort at 24 microgram per kilogram Q2 week beyond week 16 to week 24 resulted in further deepening of responses beyond the 16-week period. This is seen importantly in the key registrational endpoints of EASI-75 and IGA. Now that we've reviewed what the Resolve AD questions 1 and 2 have taught us, I'll turn the call over to Mary to cover today's exciting data presentation and a deep discussion of the maintenance portion of the trial. Mary? Thank you, JZ. Our goals for the 36-week maintenance period from Resolve AD were very straightforward, and it was designed similar to other 52-week studies which evaluated maintenance periods after induction. We assessed monthly and quarterly maintenance regimens with ResPEG to examine the durability of responses across key measurements and to evaluate new and deepening responses with longer-term dosing. Extending the Phase 2b trial to 52 weeks also allowed us to evaluate long-term safety with 52 weeks of dosing. Our ultimate goal was to show that less frequent ResPEG dosing sustains clinical responses through to 52 weeks of treatment. When we started the trial, we knew that less frequent monthly or quarterly dosing could establish a more patient-centric regimen for optimal long-term chronic treatment of atopic dermatitis. Our goal was to maintain a high response rate with less frequent dosing while also deepening responses and converting non-responders to responders by the end of 52 weeks. And of course, we wanted to further demonstrate that ResPEG has a favorable safety profile with up to one year of treatment, which is now supported by data from over 1,000 patients treated with ResPEG. You could see that our 381 patient years of ResPEG exposure at the end of Phase 2 far exceeds most agents, including the amlitelimab, which had about half the number of patient years of exposure prior to advancing to Phase 3. Shown here is the design of the Phase 2b study with three ResPEG induction regimens compared to placebo. Following induction, patients who achieved at least EZ50 in induction were re-randomized to receive the monthly or quarterly maintenance dosing at the same dose level they received in induction. Unlike historical phase 3 trials that re-randomized patients achieving an EZ75 and/or IGA response, we intentionally used a lower EZ50 threshold for re-randomization. We made this decision so we could evaluate ResPEG's ability to deepen responses, which was a core hypothesis based on the T regulatory mechanism of action Jay-Z just described. For today's presentation, we have color-coded the treatment arms. Red represents 24 microgram per kilogram Q2 week induction to monthly or quarterly dosing and maintenance. Blue is the 24 microgram per kilogram monthly induction to monthly or quarterly maintenance, and green is 18 micrograms per kilogram Q2 week in induction to monthly or quarterly in maintenance. As was done in all other trials evaluating maintenance regimens, a placebo arm was included in maintenance only to preserve the double blind from induction for the monthly and quarterly dosing maintenance arms. This arm included patients who achieved at least an EASI-50 in the placebo arm in induction. Because the arm is only used to preserve the blind, it is excluded from the efficacy analyses in an identical fashion to other reported trials with maintenance periods. On the left side of the slide, you could see patients entering maintenance with a response of at least EASI-50 in the top two induction arms, which are shown in red and blue. All patients randomized in these two cohorts received the same dose of 24 micrograms per kilogram on either a monthly or quarterly regimen. This allows us to pool the efficacy analyses for all the EASI-50 or higher responders, which increases the sample size for these two important planned Phase 3 monthly and quarterly dose regimens. To evaluate efficacy at 52 weeks after 36 weeks of maintenance dosing, we utilized the same measurements as seen in other trials with maintenance arms. Specifically, we evaluated the percentage of patients who could maintain their responses of EASI-75, vIGA, EASI-90, and itch from week 16 to week 52. Again, these are key measurements used in other trials to evaluate the drug's ability to maintain durability with continued dosing. Second, and unique to Nektar, our study was designed to quantify the conversion of new patients to responses on the endpoints of EASI-75, vIGA, EASI-90, and itch who were non-responders at re-randomization, and also look at patients who deepened their responses during maintenance. Finally, we're very excited to share with you today an analysis of patients who converted to an EZ100 response from week 16 to week 52. EZ100 represents complete clearance of disease, so it is an incredibly important endpoint for patients. With that introduction, I will now review the first new maintenance data, which assesses rezpegaldesleukin's ability to sustain responses they achieved in the induction period. Summarized here are the overall durability data by individual maintenance arms. Importantly, these are the same type of maintenance data included in product labels for other approved biologics for atopic dermatitis. Each column shows one of the six re-randomized cohorts, and the four data rows display maintained responses at week 52 for EZ75, EZ90, vIGA, and itch. At the top of each cell, you could see the percentage of patients who maintained the response at the end of one year. The lowercase n between each percentage is the number of responders for each endpoint at re-randomization before they entered maintenance. All of the monthly and quarterly maintenance arms showed excellent durability of responses over the 36-week maintenance period. As an example, for EASI-75, you can see 74% of patients re-randomized to the 24 microgram per kilogram monthly regimen maintained their baseline response at study end. And what you can see from all the fields is very encouraging for patients: irrespective of dose or dose frequency, responses were maintained and durability was achieved. As I mentioned earlier, we pooled the monthly dosing cohorts and quarterly dosing cohorts for EASI-50 responders at week 16 who received the same high dose of ResPEG, 24 micrograms per kilogram, in the maintenance portion of the study. This is the dose that we intend to evaluate in our Phase 3 study and the dose that performed the best on the key efficacy endpoints in induction. Above each bar, you can see the number of patients included in each analysis. Now, looking at the left graph, you could see the percentage of patients on the monthly dosing regimen who maintained responses. On the right, the same data are shown for the quarterly dosing regimen. As an example, 80% of patients who received the monthly dosing regimen maintained an EZ90, while 78% of the patients who received the quarterly regimen maintained an EZ90 response. As we look closely at these data, it is clear that both the monthly and quarterly dose regimens provided great benefit to patients in the 36-week maintenance period. So the next logical question is how these data compare with the current standard of care, dupilumab, and the next novel MOA, the amlitelimab, that is expected to advance to BLA filing. So let me walk you through our results in context of the benchmark data. The data on the next few slides for dupilumab is from the SOLO-CONTINUE Phase 3 trial, where they conducted a 36-week maintenance period following 16 weeks of induction. For amlitelimab, we compared the 36-week maintenance dose from the Phase 2 STREAM-AD study that was moved into Phase 3. There has been no reported maintenance data yet from the Phase 3 trials of amlitelimab. On the left side is a side-by-side comparison for maintaining EASI-75 from week 16 to week 52. You can see that the ResPEG quarterly dose cohort is the same, if not better, when compared to the labeled weekly or every two-week dose of dupilumab from SOLO-CONTINUE. When compared to DUPI's Q4 week and Q8 week maintenance regimen, the difference is even more pronounced. On the right side of the slide are the proportion of patients who maintained a vIGA from week 16 to week 52. Here, the ResPEG monthly regimen showed excellent durability with 85% of patients maintaining their vIGA response compared to 54% on the weekly and every two-week DUPI regimen. When compared to DUPI's monthly regimen, ResPEG's monthly regimen maintained responses in more than double the patients. On this slide, you can see the comparison for maintaining EZ90 for both DUPI and amlitelimab and for achieving an itch NRS response by week 52 for DUPI. There were no analogous itch data reported for amlitelimab from the 36-week maintenance period of their Phase 2 study. Again, the appeal of ResPEG's longer dosing regimens is clear when viewed side by side to DUPI and amlitelimab. There were four additional analyses published from DUPI's SOLO-CONTINUE trial measuring itch and IGA results. These analyses are not available for amlitelimab. On the top of the slide are two graphs showing improvements of itch and IGA where a higher% score is more favorable. On the bottom part of the slide, you see worsening of these two measurements where a lower% score is more favorable. Now, starting from the upper left, you can see ResPEG is slightly better than DUPI on maintaining an itch NRS response of three points or better from baseline to week 52 among EZ75 or VIGA responders. On the upper right, ResPEG is highly effective at maintaining the VIGA response within one point of the week 16 value. On the lower left and right graphs, fewer patients treated with ResPEG experienced worsening of their itch and VIGA scores. These endpoints highlight how ResPEG differentiates from Dupixent. On the Dupixent eight-week dosing regimen for worsening itch and worsening VIGA, roughly 1 out of 2 patients worsened. Whereas on the ResPEG quarterly dosing regimen, roughly 1 out of 14 patients for itch and 1 out of 25 patients for IGA worsened. These results for ResPEG are highly favorable and underscore the important clinical benefit that this novel MOA could offer patients. Now that we've reviewed ResPEG's ability to maintain responses and how that compares to standard of care, we will now shift focus to ResPEG's ability to achieve new and deepening responses in the patients who were re-randomized to maintenance regimens following induction. Here, we are showing the 6 dose cohorts in columns with four rows highlighting the proportion of patients with new responses. On this table, the new EZ75 responders come from those patients who were EZ50 to EZ74 at week 16. Below that row are the new EZ90 responders, the new VIGA 0 and 1 responders, and the new itch responders. The lowercase n's in each of these fields are the denominator, which equals the total number of non-responders for each endpoint at the time of re-randomization following induction. What you see is impressive. ResPEG is able to generate new responses and deepening of responses to the existing ones. Now, looking at the pooled monthly and quarterly dose cohorts for 24 micrograms per kilogram that we're going to advance into phase 3, we present here the results for new and deepening responses as bar graphs. Above each bar are the number of non-responders at baseline, and the percentages show the proportion of patients who became new responders. Patients on the monthly regimen are displayed on the left and those on the quarterly regimen on the right. You can see that of the non-responders at maintenance baseline, 41% and 40% treated with the monthly and quarterly regimens, respectively, converted to become vIGA responders at the end of 52 weeks. These data show that patients treated with ResPEG continue to derive clinical benefit over time beyond the first 16 weeks of therapy. This slide shows both the full population of patients in maintenance who were EASI-50 or higher at baseline, as well as a subset of those patients who were EASI-75 responders at baseline, which will more closely mimic the design of our maintenance population for the Phase 3 studies. On the left, you can see all patients entering maintenance with EASI greater than or equal to 50, where roughly one of every two achieved a vIGA response. This means their disease was clear or almost clear. On the right are all patients entering maintenance with EASI greater than or equal to 75 and/or vIGA 0 and 1 response. And you can see that 58% and 61% achieved a response on monthly and quarterly maintenance after one year of treatment. As I mentioned earlier, EASI-100 is an exceptionally important endpoint because it represents complete clearance for patients. When we look at the same two populations to assess the deepest EZ response of 100% at the 24 microgram per kilogram dose, you can see that the monthly dosing regimen had a five-fold increase in complete clearance of the disease for the total population and for the planned Phase 3 population as well. While just 6% of patients with an EZ greater than or equal to 75 and/or VIGA response at maintenance baseline had achieved an EZ100, by the end of the 52 weeks, 30% had complete clearance of their disease. This degree of clearance is impressive and consistent with what we'd expect with an immune-modulating mechanism that leverages Treg biology. Across 52 weeks of treatment, RezPEG's safety profile in both the maintenance and escape populations remained consistent with previously reported data. The discontinuations for adverse events were low at 3.5%, and this rate is within the range observed in contemporary Phase 2b studies. Importantly, there was no imbalance to suggest an increased risk for infections compared to placebo. We have not observed a safety signal for conjunctivitis, facial swelling or erythema, oral ulcers, myocardial infarction, pulmonary embolism, deep vein thrombosis, or malignancy. The most common adverse events were injection site reactions, and nearly all were mild to moderate and self-resolving. Treatment discontinuations due to an ISR were very rare at 0.7%, and the ISR frequency decreased with longer maintenance dosing. We were very pleased with the safety dataset, which continues to show the regimen is favorable for patients. Now, speaking further to the ISR rate, you could see on the top the frequency of ISRs across all dose administrations from the induction part of the study, and this is what we presented in June. On the bottom, the same data are presented for the maintenance portion of the study. You can see these data show that the frequency of ISRs decreased in the maintenance period compared to induction. And with that, let me highlight the key takeaways. As you know, this past year, Dr. Sakaguchi and two others were awarded the 2025 Nobel Prize in Physiology or Medicine for their groundbreaking discoveries for peripheral immune tolerance with T regulatory cells. In our study, we were able to validate the Treg mechanism of action for deep and durable efficacy in patients with moderate to severe atopic dermatitis with extended dosing out to 52 weeks. Both the ResPEG monthly and quarterly maintenance dosing regimens achieved durability and demonstrated a deepening of responses, which supports the evaluation of both regimens in our Phase 3 program. You saw that extended dosing regimens with ResPEG compared favorably to historically reported long-term maintenance data across other Phase 2 and Phase 3 trials for biologics. And on a very exciting note, extended dosing regimens with ResPEG resulted in new and deepening of responses achieved from week 16 to week 52, including up to a five-fold increase in patients who achieved EZ100 or complete clearance of their disease. And finally, our long-term safety profile was consistent with previously reported results with no new safety concerns, and we now have over 1,000 subjects who have been treated with ResPEG, establishing a very robust safety package as we head into our Phase 3 trials. Shifting focus, let me share with you our phase 3 trial design for our registration program. We completed our end-of-phase 2 meeting with the FDA, and we plan to start this study next quarter. We will run two global phase 3 monotherapy trials, and each study will randomize approximately 650 patients, ages 12 and older, with moderate to severe atopic dermatitis. Patients will be randomized 2:1 to receive subcutaneous treatment with ResPEG 24 micrograms per kilogram every 2 weeks or placebo in the 24-week induction period. For the maintenance phase following induction, patients on ResPEG with an EZ75 and/or IGA response will be re-randomized 2:2:1 to receive ResPEG monthly, ResPEG quarterly, or withdrawn from ResPEG to receive placebo for an additional 28 weeks. This design is similar to the Phase 3 designs conducted for the approval of other biologics, as is standard in those studies. Placebo responders from induction will continue on placebo to preserve blinding and will be excluded from the maintenance efficacy analyses. Our co-primary endpoints are EZ75 and an IGA-related endpoint. We are currently finalizing the target patient population to be enrolled in the Phase 3 trials, which is expected to include patients who have not received prior biologics, the biologic-naïve patients, and could also include patients who have received prior biologics or JAK inhibitors. Now, before opening up the call for questions, I'd like to summarize our upcoming milestones over the coming year. As Howard stated earlier, we plan to start the Phase 3 study in atopic dermatitis in Q2 of this year, which will allow us to target a BLA filing in 2029. For data milestones, we plan to present data from Resolve AD, including new translational data, at a medical meeting in the third quarter of this year. The 52-week off-treatment part of the Resolve AD study will complete in early 2027, and we will announce the data in Q1 2027. In the second quarter of this year, we will announce the data from the 52-week follow-up period in our Phase 2 study of ResPEG in patients with alopecia areata. With respect to the ongoing study of ResPEG in patients with type 1 diabetes, which is being sponsored and funded by TrialNet, we expect to have initial data from that study in 2027. For our next immunology program in the pipeline, NKTR-0165, which is our TNFR2 agonist antibody, we are planning to present new preclinical data at a scientific conference in the second half of 2026. And finally, for NKTR-255, our IL-15 agonist in oncology, our collaborator Merck KGaA will present data from the JAVELIN Bladder Medley study at ASCO GU at the end of this month. And with that, let me open the call to questions from our experts for our experts from you. We will now begin the question-and-answer session. Please limit yourself to one question and one follow-up. If you would like to ask a question, please raise your hand now. If you have dialed into today's call, please press star 9 to raise your hand and star 6 to unmute. Please stand by while we compile the Q&A order. Your first question comes from the line of Yasmeen Rahimi with Piper Sandler. Your line is open. Please go ahead. Hey, this is Shannon on for Yaz. Congrats on this awesome data, and thank you so much for taking our question. For the docs on the call, we would love to get your perspectives on the ResPEG data package and how you would expect to use this in practice. David, do you want to go first, or should I take a crack at it? Happy to answer. So first of all, I'm happy to use ResPEG, assuming consistency in the Phase 3 program, as first-line treatment. I think it's a strong overall package. There are patients who would love to have a Q12-week dosing. I think there are patients who are going to be very excited by this mechanism as well. And the fact that it treats comorbid asthma, the fact that it works in patients who have Alopecia areata, are bonuses on top of that, and it possesses some advantages that we don't see with other assets currently available. So I expect it to use it both as first-line as well as later-line treatment in my patients, and again, there are great results here. Jonathan? Agreed. I think what we're seeing here in terms of the data package is very competitive results compared to Dupixent other type 2 blockers that are out there, but I think really probably going to shift the conversation and advance the field as we start thinking about the deepening of responses over time over that 52-week period. We were talking about it a lot theoretically for the OX40 and OX40 ligands previously, but I think that conversation has changed drastically over recent current events with the OX40-OX40 ligand class. And even with that conversation, I'm not sure it ever fully made sense the way it was being discussed there, but looking at these data, I think there really is a very strong argument in that maintenance period, again, for the maintenance of response, but also for the deepening of responses. Importantly, you have a very large safety pool at this point in time, which reassures us. Obviously, you need even more data. You want to study even more, all right? That's why we're moving into phase 3. But I think based on what we know right now, we're quite reassured on the safety. And I think based on that balance of safety and efficacy, this really can be a first-line contender and certainly has a real positioning for the preferred second line as well. Great. Thank you so much. Your next question comes from the line of Julian Harrison with BTIG. Your line is open. Please go ahead. Hi. Thank you for taking the questions and congratulations on the data. Maybe first to the dermatologists on the panel. You were just asked a similar question, but to get more specific, assuming these results in Resolve AD are replicated in phase 3, what fractions of your biologic-eligible atopic dermatitis patients would you expect to eventually be on ResPEG? Jonathan, do you want to go first? I hate those questions. I mean, they're hard questions to answer. I mean, there's so many factors with access and other issues. I mean, from a medical perspective, I mean, it's almost impossible to answer this right now, but I think from a medical perspective, I'm a big believer in shared decision-making. I don't think there's ever going to be necessarily a single treatment path in this disease given disease heterogeneity. So I'm optimistic that you're going to have a nice-sized chunk. I could throw out a random number of 25% or more, but I honestly don't know yet because there's a lot of other variables that sort of have to sort out. And there's this rapidly evolving world of access with other drugs, and they're changing and changing patent likes and biosimilars and other things. So I think it's hard to answer that specifically, but I can just give sort of a high-level optimism that this is something that's going to be used a lot in my practice. And I'll say even with my own referral bias, I see a tough-to-treat patient population who've already, if you came into my practice, you think everyone fails Dupixent. And I know that that's not the case. I'm not trying to suggest that, but it's just the nature of what I'm treating. So I need to turn to alternate drugs, alternate mechanisms. And so I have sincere enthusiasm about using ResPEG. Yeah. I concur with what Jonathan is saying that, first of all, you can't divorce the use of a medicine from access or from the shared decision-making process with patients. We both practice in a similar way. I can assure you that we will both be using this medicine quite a bit in our patient population. All right. Thank you for that. And then just as a follow-up, to what extent can you entertain the possibility of progressive efficacy in asthma in light of these strong results in atopic dermatitis? And maybe for management too, is there a relevant ACQ-5 subgroup analysis we could expect maybe later this year for the long-term data? Yeah. I'll start off by saying I think that's a really great question. And given the fact that we're seeing this deepening response here, I think it should have us more optimistic that we would see it in the asthma population as well as other populations as well in general cross-inflammatory disorders. So I think it should have us all very optimistic. But again, you can't say it for sure until you prove it. But again, I certainly am optimistic about seeing it in other inflammatory disorders. The second part of your question, though, in terms of the subgroup analysis, I'll let the Nektar team answer. Yeah. So Julian, in our Phase 3 program, we are definitely going to be including the ACQ-5. And as we shared before, unfortunately, 25% of patients who have atopic dermatitis have a comorbidity of asthma. And outside of Dupixent, none of the other approved agents or the OX40s have shown any benefit for those patients who have a comorbidity of asthma and atopic dermatitis. So we feel like this is a highly differentiating element to ResPEG and look forward to collecting those data now, as we showed you, we're going to have roughly 650 patients in each one of our Phase 3 studies. So we'll have a very large dataset on this patient population, which could also be a major driver for decision-making for people like David and Jonathan and other dermatologists to select ResPEG over an alternative biologic. Very helpful. Thank you and congrats again. Thank you. Your next question comes from the line of Jay Olson with Oppenheimer. Your line is open. Please go ahead. Oh, hey. Congrats on these impressive results. We had a couple of questions. Are there any differences for patients who maintain their response versus those who did not in terms of biomarkers such as Treg levels or other patient characteristics? And then as a second question, as you had previously shown benefits in asthma control for atopic derm patients with concomitant disease, are you also tracking asthma benefits during the maintenance setting, and should we expect the asthma benefits to deepen over time as well? Thank you. Daisy, you want to start? Yeah. Mary, I can start with the first one. So Jay, thank you for the question. So this is top-line data. And the kind of additional sort of translational and molecular analyses for patients that maintain their response versus new responders is some of the work that's ongoing. But I can sort of highlight we mentioned that we will be presenting translational data later this year. And I could give a little bit of the color around that. That really is the same kind of translational analysis for patients in the induction where, if you recall, we had roughly 20% of patients that responded very rapidly after just a single dose of ResPEG and achieved an EASI-50 or deeper response after just one dose. So we will be doing translational analysis to look at some of the features of that population. That's going to be one of the subjects of later this year. And then as far as the maintenance portion, that's ongoing translational studies that we'll be reporting in the future. And then, Mary, I'll turn it over to you. Yeah. Yep. And so we did not evaluate the, excuse me, the ACQ5 in the maintenance portion. But again, as I just mentioned, we'll have a very large dataset from our Phase 3 program, and we're very eager to see the consistency with that data in the Phase 3 program because, again, as we've highlighted, because the OX40s and because every other biologic aside from Dupixent has run Phase 3 trials and have not shown efficacy in patients with asthma, we're really excited to show this level of differentiation. So we've built it into our Phase 3 program, and the next time you'll see data from the ACQ5 will be from the registrational studies. Great. Thank you so much for taking the questions. Congrats again on these results. Thank you. Your next question comes from the line of Roger Song with Jefferies. Your line is open. Please go ahead. Great. Again, congrats for the data. So I got quite a few questions from investors related to the placebo arm of the maintenance cohort performance. Understanding your design is unique compared to others. You don't have the placebo withdrawal arm. So just can you confirm with us how's the placebo arm performed? Have you ever analyzed the data, and then did that in line with other AD maintenance trials? Have any of those trials reported the same placebo arm performance? And I have a follow-up. Thank you. Thanks, Roger. I could fully appreciate people who don't have experience with this indication not understanding the placebo arm when patients move from induction, have a response, and go into maintenance. It is standard, convention, and we've done what every other trial has completed. When those patients move from induction with a response into the maintenance phase and stay on placebo, those patients are never analyzed for efficacy. They are purely there to ensure you maintain the blind so that the investigators don't know who's on placebo and who's on drug, and the patients don't know who's on placebo and who's on drug. That's critically important for the integrity of the dataset. No one analyzes the efficacy of those patients. However, there are placebo patients who will be analyzed in our Phase 3 program identical to what has happened in other biologic studies. This is a completely different patient population I want to explain. When in the Phase 3, you're randomized to a high dose of ResPEG for 24 weeks. After the 24 weeks, when you move to maintenance, we will rerandomize those patients in a 2 to 2 to 1 fashion where you will be randomized to the monthly regimen of ResPEG, the quarterly regimen of ResPEG, and then a placebo arm. In that case, those placebo patients have now been withdrawn from drug. And so we will analyze those placebo patients in the Phase 3 program. We did not have an analogous population like that in our Phase 2B. In the Phase 3 program, those data looking at the two different maintenance doses versus placebo will go into the label. So for your investors, Roger, who have any confusion, I would direct them to look at the labels and the published literature for Dupixent and lebrikizumab, and they will very clearly see this laid out that that placebo to placebo population was purely maintained for the blind and never analyzed in any other trial. I can understand and appreciate it may be confusing for people, but the convention and the standard for this group is eminently clear when you look in the labels and you look in the literature. Excellent. Thank you so much for the clarification. Just quick follow-up. For the ISR, the report, the data, can you comment on those patients? They are the same or different patients during the induction versus maintenance? And then how frequent of the ISR for those patients different between the induction versus maintenance? Because I remember during induction, you have 70% people, maybe more than that, only have two or less ISR. Thank you. Yeah, sure. So we actually looked at the number of patients who did not have an ISR in induction and had it in maintenance. And there are only about 6 or 7 new patients out of the total population that entered maintenance that had an ISR in maintenance and not in induction. We also then looked at, just like we did in the induction phase, what proportion of patients had 2 or fewer ISRs in the maintenance phase. And it turned out to be roughly 73% had 2 or fewer ISRs. And you saw from the data that we just presented, when we looked at the ISRs per injection, the incidence rate of ISRs goes down. I think it's really important for you to hear from Dr. Rosmarin, his experience with a patient who took ResPEG and the ISRs because the feedback we receive from the investigators is really what we see in the data. 0.7% of patients actually dropped out due to an ISR. In the maintenance portion, 0% of patients had a severe ISR. These are largely erythematous areas that are not painful that patients experience, and they don't have any impact on the patient's ability to continue on treatment. But Dr. Rosmarin has actually treated a patient, and so we'll let him weigh in on what his personal experience has been. So my patient experienced an ISR redness every time, and it didn't bother him at all because it wasn't painful. And I think that's consistent with my experience treating a lot with a lot of different biologics is that what patients truly care about is they don't want to be hurt. They don't want pain. And I think that having some redness is not bad to them. But again, they really don't want to experience frequent, painful injections. And so that's been my experience with my patient, and that's what we're seeing with the data. I'd also highlight some other experiences, particularly with psoriasis biologics, that have higher rates of ISR that over time, they tend to decrease. And we're seeing the same here, that we're seeing a decrease in incidence of the ISRs. Thanks, David. And Jonathan, as a practitioner, can we have you weigh in on a risk-benefit balance of a drug that causes ISRs but then doesn't have an association with conjunctivitis or ulcers? And just even what it takes for you to manage a patient that has a severe case of conjunctivitis, do they have to go off treatment? Do you have to refer them to an ophthalmologist? Can you share a little bit more with us about the management of a patient on Dupixent with the side effect profile that we're aware of? Sure. I think from the way trial data report out using safety reporting, we lump everything together as just under this broad bucket of safety. But to me, I would consider ISRs really more of a tolerability issue than a safety issue. And I think it's something I mean we're not dealing with something that's going to be life-threatening. We're not dealing with something that's malignancy risk, severe infection risk, opportunistic infection risk, right, which is clotting risks like that. These are the safety concerns that we deal with with other drugs in the class or not in the class, I should say, in the field. So we're dealing with something that's really more of a nuisance side effect and something that in the derm world, we deal with. I mean, we deal with this. I manage sometimes ISRs for neurologic medications in patients who are taking it for Parkinson's or other things like that, right? So this comes up, and I think we're comfortable with this. And to David's point, we see this with other biologics. So I don't think it's something that scares us or intimidates us in any way. And we already have good guidance from the company and what the trialists have used throughout the trial that has worked quite well to keep patients in the trial. In the grand scheme of things, I don't see it as really being a deal breaker in the slightest. I think it's something we'll work through. We have the conjunctivitis issues and the facial erythema and some of the rare safety concerns that come up with the type 2 blockers like arthralgias and myalgias, etc. And that may be also a safety signal. It even comes up with omalizumab as well. Those are real concerns. Again, I'll be the first to disclose my referral bias. If you came to my practice, you'd think every patient who went on Dupi has conjunctivitis. I know that's not true. I'm not trying to say it is. It's just the reality of what we deal with, and it's not easy to navigate through. We're sterile compounding eye ointments and trying other things and switching medications. Sometimes once the cat's out of the bag with the facial erythema with Dupi, we can't get it back in no matter what class we switch to. I can throw clobetasol ointment at it, and I can't shut it down. I don't know if those are deal breakers for those drugs either. But the point is that they really are a nuisance to deal with in clinical practice, and I don't think something that should be trivialized. And here, if we're trading off or we're getting to injection site reactions, which, just of note, right, we're talking about ISRs more so with ResPEG. But the truth is, right, even you look at any of the data for Dupi, Lebri, etc., you have a substantial ISR rate there as well. So I think it's something that is going to be easily enough managed. And I think it's going to be part of that shared decision-making conversation that comes up. There's a lot of patients, whether sometimes I don't even think it's justified, but what they pick up on social media, they're scared they're all going to go blind from Th2 blockers. And it's like I'm trying to convince them they're not. But to have something that doesn't have this conjunctivitis concern, even in theory, is a big deal for a lot of patients. I've never had a patient ask me, "What's the ISR rate of a certain drug?" I mean, people care about the cancer risks that you may see or some other very serious side effects, but I've never had somebody really follow up with injection site reaction. I think it's an advantage here that it's such a clean profile. I think we're focusing on the one thing that we are seeing, which is, again, ISR rates. But to me, if they're not painful for patients, I don't view this as a problem in my population. I don't expect to get calls from patients several after their injections that they're really scared of this. I think if we counsel them that you're going to experience some redness, that's part of how the drug works. I don't think this will be an issue. I think patients, when they get that initial itch relief, which is very rapid, they're going to be really happy with their outcome. I want to actually just add two points to Dave quickly if we have time. One is just counseling. I think if you educate the patient, "This is not an allergic reaction. There's no reason to come off drug," that's really more important than anything else. But two is keeping in mind, we're seeing some really nice data for the Q12 week maintenance. That obviously offers that opportunity to tailor to the individual patient because if the patient is doing fantastic clinically but is getting some ISRs, well, that might be the perfect patient to go to a Q12 week maintenance dose on. Then I don't have to worry about those ISRs nearly as much. So I think that's something that's going to be very nice as much as you might argue, "Well, just keep everyone on Q4-week long-term." But the Q12-week data looks so good. It really offers that opportunity to balance on the ISRs. Yeah, I completely concur, John. I think that the Q12 week dosing here, I think, is going to help a lot of people, and that's going to be very attractive to my patients. In the psoriasis space, having a medicine like Skyrizi or Ilumya that you only dose four times a year to be able to do that in maintenance for this medicine is very, very attractive for people. And I think it also mitigates any concerns over the ISRs as well. Thank you so much, David and Jonathan. Those insights are incredibly valuable, both to us as a company, to patients, and to the investors and analysts on the call. So we really appreciate all your commentary here. It's very, very helpful. Yeah, I really appreciate that. Congrats again for the great data. Thanks, Roger. Your next question comes from the line of Arthur He with H.C. Wainwright. Your line is open. Please go ahead. Hey, guys. Congrats. Really happy for you. And I believe for the ADs, it's like a horse race. It's not who jumped off the first at the gate, right? It's about who finished at the finish line, right? So I guess for two questions, one for the team, could you clarify regarding the data on slide 14, why the IGA 0/1 is about significantly high in the Q12W for the Q4W induction co-arm? And I had another one for the docs. Can we start out with the docs, Arthur, and then we'll put up the slide? Sure. For the docs, I guess, yeah, for the docs, my question is more about the remittive effect of the RezPEG. So given the phase 1b data, we see about 36 weeks of off-drug treatment efficacy and also today's maintenance data. So how should we think about the data upcoming for the 52-week follow-up we're going to see next year? And on the therapy side, how should we see these impact for the alopecia indication there? Thanks for that. Jonathan, you want to start? Sure. I mean, I think we always have to be very precise and careful when we use terms like remittive effect because I think they've been tossed around way too loosely in the conversations around OX40 and OX40 ligand. But I think what we can be comfortable from what we're seeing, especially with the Q12-week maintenance data, is a nice persistence of effect, whether that's the longer half-life or is that a biologic effect because of persistent Tregs that's driving that or both. I think is a very nuanced translational question that obviously we need more data for. But my expectation is that we're going to probably see overall good stability clinically over time, whether that's with continued dosing. And probably there will be a subset where you could eventually stop, and they're going to be able to maintain that response over time. I think all of us clinically are going to be a little cautious to do that in the real world because even if I have a drug that shows a high subset of patients where they could have "remission," I have no way of really predicting who that patient is, usually on an individual patient level. So my expectation is I'm going to continuously dose for a good period of time before I really even entertain that conversation. That may be subject to change. Maybe the phase 3 data will look so good that it'll blow my mind, and I'll change my entire practice philosophy. But I'm just guessing that that's how I would approach it. But I think that there's something real there. And I think that's really one of the cool parts of the science of Tregs. And I think it's definitely something we want to watch. I think the same concept you asked about alopecia areata, I think we already have an indication that there's a longer-term persistence in terms of the benefit for alopecia areata. So it's something that we definitely are going to keep an eye on for, but that definitely is one of the value propositions of this drug. Yeah. So regarding alopecia areata, I'm certainly more optimistic that there are going to be at least a cohort of patients that are able to hold their response, especially again, we only should have more confidence given the current data. In terms of the remittative effect, that has never been so I completely agree with Jonathan. We have to be careful how we're using the terms. To me, that's not as important as it may allow for the infrequency of dosing because this is a chronic disease. Patients are going to still need treatment. Three years later, they're not going to be off drug. They're going to need something. So the fact that we can go to potentially Q12 week is, again, very meaningful and impactful. If we see in a phase 3 those patients who are doing well, going on to placebo, maintaining their effect for even longer, that's great. But again, I still recommend patients really hold on to that regular dosing so that they don't flare, which is just par for the course for AD. Thank you so much, David. Thank you so much, Jonathan. Then, Arthur, to address, I had to pull up slide 14 for myself to address your question about the field and cell where you see n=13 for VIGA. Just to let you know, we did stratify our re-randomization from induction into the maintenance portion on three factors, and they were all based on the EASI. So we did EASI 50-74, EASI 75-89, and then EASI 90-100. And so therefore, you can see well-balanced populations based on the EASI but not on the VIGA. Thank you. Thank you very much. Yeah. Sure thing, Arthur. Thank you. Your next question comes from the line of Mayank Mamtani with B. Riley Securities. Your line is open. Please go ahead. Yes. Good morning, team. Thanks for taking our questions, and congrats on this study, yet again, delivering an impressive dataset. And I like the Skyrizi analogy. So on the EASI-50 versus 75 cutoff, this responder decision that you made to go into maintenance, and you showed some EASI-75 and VIGA comparisons on slides 16 and 17 versus peers. If you were to do an apples-to-apples comparison for the 75 cutoff, do you expect that delta to even further grow? Just also putting in context the phase 1b study where you just discussed that off-treatment, you have the best responders earlier on. And if you can also comment on what the peak 24-week efficacy you're assuming in the phase 3 study, what delta you're hoping for. And then I have a quick follow-up. Yeah, Mayank, I do believe when we go into maintenance in the phase 3 program, and we are looking at patients that are the EASI-75 and the vIGA 0/1 responders as opposed to EASI-50, I do believe that we will see those patients doing better. And so that is certainly very exciting as well. And then in terms of your second question, JZ did show you slide 9, which had the increased efficacy from week 16 to week 24. And you could see, for example, on the EASI-75, 58% of those patients at week 24 were responders. And for the vIGA, you see that 36% were responders at week 24. I believe these data, if they continue into the phase 3, these are nice benchmarks because they're based on our own data for rezpegaldesleukin. Just to let you know, in the phase 3 study, these are not like oncology trials where you are powered just enough to see a difference between one treatment group versus a second treatment group where you're adding on a third medication to two already active ones. This is a phase 3 trial compared to placebo that are very well-powered, 99.99% powered to see a difference between placebo and drug. And the reason for that is you could run smaller phase 3 trials to evaluate efficacy. But of course, because this is a disease that hits 10 million people in the United States, we do need to have a robust safety dataset. And therefore, these trials are overpowered to be able to really detect and determine the safety profile, not so much efficacy. These trials are extremely well-powered to detect the difference between the EASI-75 and the vIGA, between placebo and drug, just to provide you the level of confidence about the design of these trials and the robust power that exists to detect differences. Yep, yep. Thank you. Maybe for Dr. Rosmarin and Dr. Silverberg, just the importance of the EASI-100 complete skin clearance dataset. There's not a whole lot of data for biologics. I think maybe there's a couple. But maybe can you put in context what we've seen there with JAKs or even JAKs, what numbers we are seeing here? And do you expect this to also improve given the phase 3 will go beyond that 52 weeks? And at the end of the day, do you think this could be a reason why, on top of other reasons you've identified, phase 3 enrollment could actually go faster than you would think, induction, less frequent dosing, and then obviously deepening in terms of EASI-100, all that? What's your sort of feeling on the phase 3 enrollment rates? I mean, I'll jump in. I'm happy to because there were a few questions there. So maybe I'll answer the last one first. I think that's a great point. I mean, I think that it's a busy trial landscape. And so investigators are somewhat selective. And so when you're dealing with early phase studies, there's often a preference towards going towards a later phase study where you have a drug that's got a proven safety and efficacy profile. There's a few things more frustrating than putting a patient doing all that work, and then drug doesn't do anything. So here, having these data, I think, are going to be very positive in that respect. And also the 2:2:1 in terms of the randomization rates means patients are going to be likely to get drugs. So I think you're going to have a good setup there. I think that's going to incentivize sites and patients to want to participate. And I do think that's going to help enrollment. So I think that's a very good point. There were a few other questions. I don't remember what the other questions were. Sorry. EASI-100, important. Oh, yeah. I mean, there's no doubt EASI-100 is a big deal. We don't even talk about it. I mean, there's a reason why you haven't heard about it with the other biologics is because we generally don't get there. So it's not something we're thinking about very much. This would be a paradigm shift to start talking about it in the biologics space. We do think about it a little bit more, address a little bit more when you're dealing with the high-dose JAK inhibitors. But that's a whole different beast when it comes to the safety profile and the risk-benefit ratio. So to have for a clean biologic, the ability to start discussing this really is a paradigm shift potentially in the biologics space. Yeah, I completely agree with both comments. First, the EASI-100, I mean, we don't talk about it because it's so hard to achieve with past biologics. So the fact that we're achieving this now is incredibly impressive. And again, you've totally taken away the disease from a patient. That's incredible. And in terms of the trial design, I completely concur with and trial enrollment, I completely concur with Jonathan that it's very competitive. There's a lot of AD trials. Knowing that you have a drug that works very well in frequent dosing, has all these benefits, and will be a long-term trial with a long-term extension, will significantly help with enrollment. Having more patients on drug compared to placebo, again, helps with enrollment. There's so many studies for AD right now that matters and for keeping patients in the studies as well. Yeah. Thank you, David and Jonathan. I think the other point is, again, we mentioned a couple of times on this call that the Nobel Prize in Physiology or Medicine was awarded for the discovery of what T cells can do. I do believe the population that we're recruiting and the investigators who are participating in this trial, they're interested in science, and they will be eager to participate in a study that's based on the Nobel Prize-winning medicine. Yep, got it. And maybe just one quick one for Howard. We haven't heard from him. Just maybe talk about just the pedigree of science and the clinical validation, all that that we have here, just how you're thinking non-dilutive versus dilutive in terms you want to underwrite this phase 3 program, I'm sure, to its full course. And obviously, we have the Lilly trial back on docket. And any updates you can share on that, that would be great. Thanks for taking our questions. Well, sure. Good question. Look, we expect to start, as we've said a number of times, phase 3 program in the not-too-distant future. And of course, we're looking at a number of ways to raise capital to do that. We were talking about potential collaborations. We're also talking about synthetic royalty-structured arrangements to help fund the trial. So I think you'll see that coming, hopefully, in the near future. And of course, I can't comment on the Lilly litigation. The trial date has been set for September. So we'll have to wait and see how that goes. But really, probably best not to comment on that now. But thank you for the question. Thank you. Your next question comes from the line of Samantha Semenkow with Citi. Your line is open. Please go ahead. Hi. Good morning. Thanks very much for taking the question. Congratulations on the data. Let me add mine as well. I have a couple of questions. One is a follow-up on the Q12 weekly regimen and how it performed quite well, better than we had expected. For the team, what is driving that mechanistically, do you think? Then just if there's any additional things for the physicians and how you would think about choosing between Q12 weekly versus Q4 weekly in actual practice, I think that would be helpful to hear. Sure. Hey, Sam. Happy to take the first question. So one of the things that, remember, we learned in the phase 1 study was that even though it was a very small study, we had about 17 people enrolled to 24 microgram per kilogram dosed Q2 weeks. And after only 12 weeks of treatment, we withdrew the drug completely, and we saw a substantial durability of response, right? So we had 80%, roughly, maintenance of IGA response from that study and around a 72% maintenance of EASI-75 after only 12 weeks of treatment without any additional dosing. And so that kind of was a phenomenon. It replicated studies we did preclinically in mice, but that's not something an effect that had been seen before in a disease setting in people. So when we looked at this data from this study, the first thing that we saw when Mary presented the maintenance portion of the study was that we already knew you could stop dosing altogether. And the continuation of dosing looked highly durable, right, and very consistent with what we saw in phase 1. So either a monthly or a quarterly regimen was both were effectively equal, almost equally effective at maintaining the responses that were achieved by patients at the end of the 16-week induction. What we saw that was new and different than the phase 1 was that the continuance of dosing caused new responses and deepening. And it drove to the discussion we just had about EASI-100. That's not something we saw in the phase 1. We saw maintenance. But with additional dosing, we saw additional responses in depth added to the maintenance. So that was a big extension to us from what we learned from that early study of drug withdrawal. When we kind of think about what could be driving it mechanistically, I think it really takes me back as an immunologist to what a Treg can do based on all of the first principles and all of the experiments that have been done through the decades since Shimon first discovered these cells in the mid-1990s. We know that they can have a very long lifespan in tissue. It's a little controversial because, as you can imagine, it's hard to measure cell lifespan in a distal tissue in an organ. But some studies have reported that Tregs can live as much as 10 years in tissue. We know that they don't like inflammation. When there's high inflammation, they tend to have a short lifespan. When the inflammation is low, they can live even longer. We see that we're getting disease resolution. We're clearly fixing the inflammation in the skin. Then there could be a very long-lasting lifespan of the Tregs. That can help explain to me why a once-a-month or once every 12-week regimen still maintains and allows the deepening to be seen. Also, for us, the Q12 week was important because our hypothesis was that there should be a true drug holiday on a once-every-12-week regimen. That is indeed what we saw. We only expect about 8 weeks of exposure from a single dose. On a Q12-week regimen, again, you're really treating very infrequently. It truly is the promise of an immunomodulatory drug. Its PD substantially outlasts its PK because this PD is driven by cells. The cells are active long after the drug is gone. That's great. So I'll start by saying that when am I going to use the Q12 week? Well, if I have a patient who's doing well. So if a patient said an EASI-75, for example, and again, there is some shared decision-making there, they're going to want to go to Q12-week dosing. And I'm going to be happy to oblige them. And they're going to be, I think, very satisfied with that. I also want to highlight another part of the study that we haven't really touched much on is that the data on the worsening of itch, which was extremely low in the maintenance phase and significantly higher for other medicines like in the dupilumab studies. And for me, I have plenty of patients who, before their next dose of dupilumab, of any of the biologics, and particularly even the JAK inhibitors, right, before they're taking the next dose of their JAK inhibitor, they're getting itchy again. And the fact that there's such a significant difference from what we're seeing here with ResPEG, even at the 12-week mark, hardly any worsening of the itch in patients is extremely meaningful to me. Also gives me significant confidence that we can give that Q12-week dosing, especially that's this most sensitive signal is the itch. So that's what I would have you focus your attention to, that we can have real confidence in that dosing schedule. And again, to me, that's particularly impressive data. And I'm through the roof for that particular piece. Yeah. Clinically, I agree completely. I think from that medical decision-making perspective, I think David's points are spot on. I mean, I would say some of it will probably depend on what that final label shows, right? Because in the phase 3, if the Q12 looks just as good as the Q4 maintenance after a longer 24-week induction, then we may have a label that says after 24 weeks, decrease to Q12. And that is our dose. And that's it. Alternatively, it could be that the Q4 week the Q12 looks great, but the Q4 week looks a little bit better for certain endpoints, in which case, maybe we have the option to use both. For me, bottom line is, as long as the axis is available to use continuing Q4 week in that subset, probably small subset who continue to need it, as well as the option in the larger subset to use the Q12 week for maintenance, I think we're going to be in great shape. And the derms are going to be able to easily figure out where to do that. So I think we'll be. It's great if, personally, I'd love it if you have the option. But obviously, in the labels, it's always a little bit different how you deal with that. But medically, we should be able to navigate that situation very easily. Got it. That's super helpful context. I have one quick follow-up as well. It's on the response curves, particularly for those that showed a deepening of response. I'm wondering in the data, if you have it, if you're able to see a plateau at patients achieving a maximal response, or if there's a suggestion that with longer-term therapy, which I know we're not doing in this phase 2 study, but with longer-term therapy, could you have achieved greater responses approaching more patients in EASI-90, more patients in EASI-100? Thanks very much for taking the questions. Yeah. We do see a gradual uptick from week 16 to week 52 on almost all the endpoints, Sam. So Jay-Z and I have looked at these data very closely. I think we shared them with Jonathan and David as well. We do believe there is a possibility for ongoing benefit for these patients. We'll have two opportunities to look at that. In the phase 3 program, we are looking at additional dosing in a long-term extension study. And then, of course, even with the phase 2b, we'll be able to follow these patients to see if, with Jay-Z's biology here, with the Tregs in the skin for a longer period of time, do people end up having even improved benefit off treatment? So we'll have two opportunities to look at additional benefit for patients beyond 52 weeks, one off treatment, looking at the remittive effect and potential enhancement of efficacy over time, and two, in the phase 3 program, looking beyond 52 weeks. And the kinetics of the curves that Jay-Z and Jonathan have reviewed really do show that there could be ongoing benefit beyond 52 weeks on these endpoints. So thank you for asking. There are no further questions at this time. I will now turn the call back to Howard for closing remarks. Thank you. I want to thank everyone for joining us today. I want to thank our employees for their hard work and commitment in moving this molecule forward in the clinic. We look forward to starting our phase 3 studies in the near future. Please stay tuned. Thank you very much. This concludes today's call. Thank you for attending. You may now disconnect.