Good day, and thank you for standing by. Welcome to the Nektar Therapeutics Q4 2024 Financial Results Conference Call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during this session, you will need to press star 11 on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star 11 again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Vivian Wu. Please go ahead. Thank you, Crystal, and good afternoon, everyone. Thank you for joining us today. With us on the call are Howard Robin, our President and Chief Executive Officer, Dr. Jonathan Zalevsky, our Chief Research and Development Officer, Dr. Brian Kotzin, our Interim Chief Medical Officer, and Sandra Gardiner, our Chief Financial 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 drug candidates and research programs, the timing of initiation of clinical studies and the availability of clinical data for drug candidates, the timing and plans for future clinical data presentations, the formation, future development plans, or success of our collaboration agreements, financial guidance, and certain other statements regarding the future of our business. Because forward-looking statements relate to the future, they're 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 10Q that was filed on November 8, 2024, which is available at sec.gov. We undertake no obligation to update any of these forward-looking statements, whether as a result of new information, future developments, or otherwise. A webcast of this call will be available on the IR page of Nektar's website at nektar.com. With that said, I would like to hand the call over to our President and CEO, Howard Robin. Howard? Thank you, Vivian. Thank you all for joining us today. 2024 was a productive year for Nektar, and I'm very proud of our team for executing on important clinical development milestones for our lead autoimmune pipeline program, Rezpegaldesleukin, also known as REZPEG The achievement of these clinical development goals prepares us for meaningful data catalysts for REZPEG in 2025. Earlier this year, we announced the enrollment completion for both our Nektar-sponsored Phase 2b studies. Our 400-patient Resolve AD trial in atopic dermatitis opened enrollment in October of 2023 and completed enrollment in just 14 months. Our 90-patient Resolve AA study in alopecia areata opened in March of 2024 and completed enrollment in roughly one year. Both studies were completed on schedule in highly competitive clinical trial landscapes for both indications, which I think demonstrates the enthusiasm from patients and physicians for REZPEG's novel mechanism of action and for the data that has been generated to date. J Z will discuss in a minute some of the unique operational features of our studies that are designed to minimize clinical operational risk. We look forward to data from both trials in atopic dermatitis and alopecia areata in the Q2 and Q4 of this year, respectively. Now, in the U.S. alone, there are over 15 million people living with moderate to severe atopic dermatitis. We know that less than 10% of those patients who could receive biologic treatments for this chronic skin disorder are actually receiving treatment. New mechanisms are the key to growing this underserved market. This belief also extends to alopecia areata. According to the National Alopecia Areata Foundation, nearly 7 million people in the U.S. alone have or will develop this disease, and a treatment market that is estimated to reach $5.2 billion in the United States and Europe by 2023. This disorder significantly affects the quality of life for patients, and the approved JAK inhibitor therapies, with their high relapse rates, are not durable and can carry significant potential safety risks. With REZPEG, we hope to offer a more durable treatment option in the form of a novel immunomodulating mechanism. Moving on to type 1 diabetes, we recently announced the clinical trial agreement with TrialNet, an international clinical trial network at the forefront of diabetes research, in which they will conduct and fund a Phase 2 clinical trial to investigate REZPEG in 66 patients with new-onset type 1 diabetes. We're proud to support TrialNet's mission of advancing innovative mechanisms aimed at slowing or stopping the progression of this disease. Nearly 2 million people in the U.S. have type 1 diabetes, and the disease incidence continues to rise at a rate of 3-5% per year. Brian will talk more about this later in the call. Now, turning to the progress we've made with our preclinical programs, over the past year, we expanded the company's preclinical pipeline in immunology and inflammation. First, we continue to advance our novel TNF-R2 agonist antibody program, Nektar 0165. IND-enabling studies are ongoing with the goal of preparing for an IND submission in the second half of 2025. Last year, we presented the first preclinical data at EULAR, showing that this antibody demonstrated selective enhancement of Treg cell function. Given the importance of TNF-R2 agonism in a number of autoimmune diseases, Nektar 0165 could potentially be developed in autoimmune diseases such as multiple sclerosis, ulcerative colitis, and vitiligo. We are also designing a pipeline of bispecific molecules that pair TNF-R2 agonism with other antibody targets. We are planning for the first bispecific in this program to be ready for IND-enabling studies within the second next quarter. We look forward to providing more color on our early pipeline as these programs progress, and Jay-Z will discuss more on this later. Now, before I turn to the R&D discussion, I want to reintroduce Brian Kotzin, who we announced last month would be returning to Nektar to lead the development of REZPEG as Interim Chief Medical Officer. Brian has over 40 years of expertise in immunology and has extensive development and management experience. He has also been supporting the clinical development of REZPEG in various capacities since 2017, and his intimate familiarity with this program has provided a seamless transition. Before I hand the call over to Brian, I want to highlight that Nektar remains in a strong financial position with a cash runway that extends into the Q4 of 2026, ending 2024 with $269 million in cash and investments on hand. I'm going to ask Brian to share a few comments on his enthusiasm for REZPEG and also comment on our recent announcement for the program in type 1 diabetes before we turn it over to Jay-Z to review more details on REZPEG's ongoing Phase 2b studies and our early pipeline programs. Brian? Thank you, Howard. It's great to be back at Nektar. As Howard mentioned, I've had the great pleasure to work on REZPEG since 2017, even continuing as a strategic advisor since retiring in 2023. When Howard and Jay-Z called me with the opportunity to work on this program with my colleagues at Nektar again, I was very enthusiastic to help. I have a great passion for the potential of boosting regulatory T cells in autoimmune disease, and REZPEG is the most advanced IL-2 Treg stimulating mechanism in the field. Having closely worked for several years on its clinical development, I believe it has the potential to truly address unmet needs for safe and durable therapeutic options for patients battling atopic dermatitis, alopecia areata, and now type 1 diabetes. As Howard mentioned, we recently announced a collaboration agreement with TrialNet to evaluate REZPEG in a Phase 2 placebo-controlled clinical trial in patients with new-onset type 1 diabetes. I have had great interest in pursuing REZPEG in this indication since it first entered the clinic, and I'm very excited to work with some of my colleagues at TrialNet on this new clinical study. In type 1 diabetes patients, there is a dysregulation of the balance between regulatory T cells and pathogenic autoreactive T cells, which leads the autoreactive T cells to destroy insulin-producing beta cells in the pancreas. Studies in mouse models and early human research of low-dose IL-2 and other agents have shown that boosting Tregs can lead to the preservation of insulin-producing beta cells. This preservation of endogenous insulin secretion is key to improving long-term health outcomes and quality of life for patients with this disease. This is why I am so excited about the work that TrialNet is recommending for REZPEG. The proposed placebo-controlled TrialNet study will enroll approximately 66 patients while they still have partially preserved beta cell function and insulin production. We will start evaluation in adult patients and move to pediatric and adult patients in different phases of the study. TrialNet's goal is to initiate the study later this year. With that, I'd like to hand the call to JZ. Thank you, Brian. It's exciting to be working with you on a daily basis again. As Howard mentioned, we announced in January there will be completed enrollment in the Resolve AD Phase 2b trial in patients with atopic dermatitis in just under 14 months. We are grateful to the patients and physicians whose strong interest in this novel mechanism and proof-of-concept clinical data led to enrollment completion of this large Phase 2b study. We look forward to reporting the top-line data from the 16-week induction period in June of this year. In February, REZPEG was granted fast-track designation by the FDA for the treatment of adult and pediatric patients with moderate to severe atopic dermatitis. This designation allows us to collaborate closely with the agency on the design of the registrational program for REZPEG and will be leveraging it as we work on our phase 3 registrational strategy in atopic dermatitis. As a reminder, the Resolve AD study randomized approximately 400 biologic naive patients with moderate to severe atopic dermatitis across three different dosing regimens of REZPEG or placebo. Guided by our scientific advisory board of industry-leading dermatologists, we designed this study to ensure high-quality sites were used and implemented criteria with the goal of addressing some pitfalls in operational execution from past trials. Patients were recruited from approximately 110 sites globally to ensure adequate geographic representation. Patients were stratified based on geographic region as well as baseline disease severity. 67% of patients were enrolled in Europe across Poland, Bulgaria, Germany, Czechia, Spain, Croatia, and Hungary. 17% enrolled in the U.S., and the rest were enrolled in Canada and Australia. We had a goal to balance U.S. recruitment due to the recent phenomenon in the last several years of a rising placebo effect observed in the U.S. We are very pleased with the 17% ultimate U.S. recruitment figure, which aligns more closely with the recent winning atopic dermatitis studies in terms of site distribution. Other important criteria that we used in the study include requiring that most of our sites be board-certified dermatologists or immunologists with prior experience participating in other atopic dermatitis studies. We also required that patients enrolled met a strict EASI threshold that was consistent in both screening and randomization, unlike some other trials that have only required EASI measurement at screening. Reconfirming that the patient's disease severity has not changed significantly between the screening and baseline time points allows us to reduce the potential for enrolling patients with flaring or episodic disease into the study, patients with unstable disease, or with a significant change between screening and randomization or screen test. After randomization, patients receive either REZPEG at 24 micrograms per kilogram twice a month, 24 micrograms per kilogram once a month, and 18 micrograms per kilogram twice a month or placebo for a 16-week induction treatment period. After the induction period, patients that meet an EASI 50 or better efficacy threshold to advance from induction to maintenance are re-randomized into one of two maintenance regimens at their original dose level to receive that dose on either a once-a-month or once-every-three-month regimen. The maintenance portion of this study is 36 weeks, which will in total provide 52 weeks of treatment duration for patients in this study. We are following participants for one year after the conclusion of the 52-week treatment period, enabling us to evaluate REZPEG's potential for long-term remittance effect. As I just mentioned, we anticipate top-line data from the 16-week induction period of this Phase 2b study in June, and we expect data from the 36-week maintenance period of the study in the Q1 of 2026. Now, turning to Resolve AA study, alopecia areata is a dermal disease in which the patient's immune system mistakenly attacks the hair follicle and disrupts the body's normal ability to keep and grow hair, leading to hair loss. There is strong rationale for REZPEG in this indication based on the role of Tregs to either prevent or downregulate the underlying pathology of the disease. Last month, we announced enrollment completion for our 90-patient Phase 2b study in alopecia areata. The trial recruited patients across approximately 30 global sites. Patients had to present with severe to very severe disease defined as SALT 50 to SALT 100 for at least six months in order to be eligible for inclusion. 62% of patients were enrolled in Poland, 24% in Canada, and the rest in the U.S. Randomized patients will be treated for a period of 36 weeks and observed for up to 60 weeks in total. Our primary endpoint for this study is mean percent improvement in SALT or the Severity of Alopecia Tool for week 36. We will also be looking at a number of other secondary endpoints, including the proportion of patients that were observed to have varying degrees of improvement in SALT score, including the regulatory approval endpoint SALT 20. We expect top-line data from the 36-week treatment period in the Q4 of this year. Turning to our preclinical programs in immunology, I'll start by talking about our novel TNF-R2 agonist antibody program, Nektar 0165. TNF-R2 agonism has been shown to potentiate Treg function as well as maintenance of Treg linear stability, especially in the non-lymphatic tissue compartment. Genetic studies show that if TNF-R2 is absent, the phenotypic effect is autoimmunity as well as other conditions that resemble a FOXP3 loss of function. In contrast, its presence and activation of its signaling has been associated with immune regulatory function and tissue protective effects. The first preclinical data from this program presented last year at EULAR demonstrated that Nektar 0165 has a very high specificity for signaling through TNF-R2 on Tregs and enhancing immunosuppressive activity. It also showed that the agonists we discovered are able to signal through the TNF-R2 multimeric receptor's single-arm monovalent antibody, which is a very novel finding for a TNF-R2 agonist antibody. We are very excited with Nektar 0165's unique and differentiated profile, and we believe it has the potential to become a first-in-class treatment for various autoimmune diseases, including multiple sclerosis, ulcerative colitis, and vitiligo. We are rapidly advancing this program into the clinic with plans to submit an IND in the second half of this year. Since the TNF-R2 agonist antibody specificities we discovered are active as single-arm antibodies, we have leveraged this to design a pipeline of TNF-R2-containing bispecific molecules that pair TNF-R2 agonism with other specificities. The first of these is known as Nektar 0166. These assets take advantage of multiple mechanisms to bring about novel molecules to target autoimmune diseases. We will nominate the first development candidate, Nektar 0166, from this pipeline in the Q2 of this year and look forward to providing more color around this in the future. Overall, we have observed growing interest for a selective TNF-R2 agonist like Nektar 0165, and as we move forward with our IND-enabling studies and develop the bispecific pipeline, we remain open to opportunities to work with companies interested in these areas strategizing the best path forward. Before turning the call over to Sandy, I'll make a few comments on Nektar 255, our IL-15-based oncology program. Last year, we presented data on Nektar 255 that highlights its potential to augment the response and patient outcomes of a variety of cancer treatments in both solid and liquid tumors. Data published in Blood, the peer-reviewed medical journal of the American Society of Hematology from Stanford's IST, demonstrated that Nektar 255, when combined with Stanford's CD19/CD22 bi- CAR T-cell therapy, doubled the 12-month relapse-free survival rate for patients with B-cell acute lymphoblastic leukemia by 67% compared to 38% of Stanford's historical controls treated with the same CAR T-cell therapy. At ASH, we shared supporting data showing that Nektar 255 enhanced complete response rates following CD19-directed CAR T therapy in patients with relapse-refractory large B-cell lymphoma. 73% of the Nektar 255 treatment group achieved a complete response at six months compared to 50% in the placebo group. This clinical benefit surpasses the published historical benchmark data from multiple pivotal trials and real-world meta-analyses of currently available commercial CD19 CAR T-cell therapies. Finally, interim data presented at SITC from Dr. Steven Lin's Phase 2 study suggests that Nektar 255 has the potential to confer clinical benefits in patients with locally advanced non-small cell lung cancer. Results show that Nektar 255, in combination with durvalumab, demonstrated a statistically significant improvement in the eight-week absolute lymphocyte count compared to historical control data. These data strengthen our belief in Nektar 255's therapeutic potential as a new application in combination treatment with checkpoint inhibitors. The growing body of evidence showcases its broad applicability to be combined with a variety of therapies across cancer indications. Looking ahead, we'll continue to collaborate with AbelZeta to evaluate Nektar 255 in combination with their tumor-infiltrating lymphocytes in patients with advanced non-small cell lung cancer who do not respond to anti-PD-1 therapy. We continue to work with Merck KGaA to evaluate Nektar 255 in combination with Bavencio in their Phase 2 Javelin Bladder Medley study, with the first potential PFS readout expected in the middle of this year, as this is an event-driven analysis. As we continue to generate supportive data in these combination studies, we continue to explore the best areas for continued development of this drug candidate in partnership with collaborators. With that, I will turn the call over to Sandy for a review of our financial guidance. Thank you, JZ, and good afternoon, everyone. We ended 2024 with $269.1 million in cash and investments, with no debt on our balance sheet. On December 2, 2024, we completed the sale of our Huntsville manufacturing facility for consideration of $64.7 million in cash, net of transaction costs, and approximately 20% equity ownership in the new portfolio company, Gannett BioChem. Turning to the income statement, our revenue was $29.2 million for the Q4 of 2024 and $98.4 million for the full year 2024. Our R&D expenses were $28.7 million for the Q4 and $120.9 million for the full year. Our G&A expenses were $17.1 million for the Q4 and $76.8 million for the full year. In connection with the sale of our Huntsville manufacturing facility, we recognize the gain of $40.4 million. Our non-cash interest expense for the Q4 was $10.2 million and $28.1 million for the full year. Our net income for the Q4 was $7.3 million or $0.03 basic and diluted earnings per share. For the full year 2024, our net loss was $119 million or $0.58 basic and diluted loss per share. I will now review our 2025 financial guidance. We remain strong in our financial position and still expect our cash runway to extend into the Q4 of 2026. We plan to end 2025 with approximately $100 million in cash and investments. Our revenue for the full year of 2025 is expected to be between $40 million-$50 million, which primarily includes non-cash royalties. As a result of the sale of our Huntsville manufacturing facility, we will no longer have product revenue and cost of goods sold. We anticipate full-year R&D expense will range between $110 million-$120 million, including approximately $5 million-$10 million of non-cash depreciation and stock-based compensation expense. We expect R&D expense to remain consistent with 2024 levels as we continue our Phase 2b studies in atopic dermatitis and alopecia areata. We expect G&A expense for the full year of 2025 to be between $60 million and $65 million, including approximately $5 million-$10 million of non-cash depreciation and stock-based compensation expense. Our full-year non-cash interest expense is expected to be between $15 million-$20 million. As I stated earlier, we expect to end the year with approximately $100 million in cash and investments. With that, now we'll open the call for questions. Operator? Thank you. As a reminder, to ask a question, please press star 11 on your telephone and wait for your name to be announced. To withdraw your question, please press star 11 again. In the interest of time, we do ask that you please limit yourself to one question at this time. Please stand by while we compile the Q&A roster. Our first question will come from Yasmeen Rahimi from Piper Sandler. Your line is now open. Good afternoon, team. Thank you so much for all the great updates. We're very much looking forward to the data across both of the studies for this year. I guess the first question is, you guys have shown in the earlier stage really phenomenal dose responses in the EASI scores. We'd love to understand how you're thinking about dose response across the three dose arms. Secondly, if you could just maybe remind us, what is the criteria or responder analysis defined for patients to be eligible to go from the induction phase to the maintenance phase? I'll jump back in the queue. JZ, you want to take that call? Does that answer the question? Sure. Yeah. Thanks, Yas. The first question about the dose response. We addressed that with three different cohorts that addressed both dose level and regimen. Two of our dose cohorts evaluated the 24 microgram per kilogram dose. One of those evaluated that dose twice a month. The other cohort at once a month. We changed the frequency there because that was sort of designed to model the pharmacodynamic profile of the Tregs that we measure in the blood. That is why we wanted to have the same Cmax one time, the different exposures in the once a month versus twice a month setting. That was the goal there, to assess that based on the PK/PD knowledge. We also selected 18 micrograms per kilogram dose twice a month. That dose is higher than the 12 microgram per kilogram that we used in the Phase 1B study. We felt that that dose 12, while it did separate a little bit from placebo, was a little bit on the lower efficacy side. We wanted to evaluate a higher dose level than 12 micrograms per kilogram in the Phase 2b. That is why we chose 18 micrograms per kilogram, halfway between 12 and 24 from the Phase 1B study. That is our expectations around the design of the Phase 2b. In terms of the criteria for patients moving from the induction to the maintenance arms of the study, at the end of the 16-week inductions, patients that have an EASI 50 or better response are eligible to be re-randomized to enter into the maintenance. In the maintenance, they are re-randomized to stay on the same dose level that they were on in the induction portion of the study. But now the regimen is either once a month or once every three months. We use that EASI 50 criteria for advancement from induction to maintenance. Thank you, JZ. Thank you. Our next question will come from Julian Harrison from BTIG. Your line is open. Hi. Thank you for taking my questions. First, on the Phase 2b atopic dermatitis data expected next quarter, I'm wondering if you could talk about what kind of efficacy bar, either on EASI or IGA, you think would be commercially viable and worthwhile to advance REZPEG into pivotal development? Yeah, that's a good question. I think we've done a lot of homework in that area, especially recognizing that Amgen just released its data on OX-40. I'll let JZ give you a more thorough answer on that. Yeah. Thanks, Julian. We definitely see at least two different versions of activity. Obviously, there are ranges of EASI that are active and that are desirable to achieve. Also, the separation from placebo, both features are very important. We like what we saw in our Phase 1B study, right, which showed both a dramatic separation from placebo in terms of placebo-adjusted and also an 83% change from baseline. We are looking to replicate that kind of data in our Phase 2b. We also acknowledge that as a drug with a novel mechanism and an agent that has already shown a remissive effect, as we have shown in the Phase 1B, even efficacy in the range of Dupixent, the standard of care currently, would also be a very successful outcome for us. We are definitely aware of the recent results in the field, including Amgen's ROCKET data. I think that data is probably considered a little bit underwhelming by some of the folks that have addressed and looked at that data. We think that we're in a great position to replicate the Phase 1B results that we had with respect. Always remember that it isn't a zero-sum game. It really is a quite underserved market with a very serious disease. Having a novel mechanism is certainly going to be appreciated by patients and physicians, I'm sure of that. Got it. Thank you. That makes a lot of sense. One more, if I may. I'm curious how you're thinking about your rights to Dupixent in light of the recent litifilimab royalty monetization. Are there any differences compared to litifilimab that are worth noting? JZ, you want to comment on that? Yeah. There There are different mechanisms of action, of course, right? One is the BDCA2 inhibitor that's targeting more of the plasmacytoid arm. And of course, that drug has shown activity in both systemic lupus and cutaneous lupus. It seems like it has maybe even more potential in the cutaneous form of the disease, whereas Dapi, right, is a CD40 ligand targeting agent, right? It addresses different mechanisms of action. Mechanistically, both of the drugs have demonstrated, I think, impressive results in Phase 2. Obviously, Dapi has positive phase 3 data as well. All right. Excellent. Thank you. Thank you. Our next question will come from Jay Olson from Oppenheimer. Your line is open. Oh, hey, congrats on all the progress. Thank you for providing this update. Maybe another question on the top line, Phase 2 atopic dermatitis results in the Q2. Can you just talk about the scope of data that you're planning to share in that top line release and maybe some of the secondary endpoints we should be looking for? Also, what do you think the profile would be that would help you capture meaningful market share in a first-line setting? Yeah. I think good questions. I think we haven't discussed a lot about the exact secondary endpoints at this point. I think clearly, as a novel mechanism and a completely different approach than IL-13, I would like to see a drug that's similar in activity to Dupixent with a very different biologic profile. I'll let JZ talk a little bit more about that. Go ahead, JZ. Yeah. Sure. Thanks, Jay. Yeah. Just to reiterate how I said, we haven't sort of guided on the specificity of the top line. Obviously, the majority of the data we would need to present at a medical meeting. We would intend to focus, obviously, on the 16-week induction data, as we've described, and to give at least a minimum directional, right, understanding of the performance of the drug. I think that's a bare minimum. We can cover that more later. In terms of the profile, I mean, it's pretty obvious that the greatest way to impact the share in the front-line setting is with efficacy, right? If we are able to replicate the Phase 1B results that were really quite marked, right, quite notable, obviously, that's one of the strongest ways to impact the first-line treatment space. Even all that aside, we're a completely different mechanism. We're not another IL-13. We're not a depleting antibody like RocA is. We're really providing a completely different mechanism of action. We are providing the data set that has already demonstrated the potential for really durable responses, which could translate into a very, very low-frequency dosing regimen, which would, at minimum, be highly convenient to patients. We think there are really a number of ways that we can impact this market. We are very excited that being a novel Treg mechanism gives us these additional avenues for it. I think it is also important to point out that while Dupixent is certainly an excellent drug, no debate on that, there is a high percentage of patients who fail Dupixent therapy over time. As JZ just said, having a novel mechanism that works in a completely different fashion is something this market desperately needs. When we wind up comparing our results to Dupixent results, certainly, I'd like to see similarities, but recognize that you're dealing with a completely different way of approaching the treatment of this disease. Thank you. That's super helpful. If I could sneak in a question on 255, can you just talk about any updates on timing or expectations for the interim PFS results from the Javelin Bladder Medley study and what we should be looking for there? Thank you. We should be seeing results from that middle of this year. JZ, do you want to comment a little further? Yeah. That's exactly right. It is event-driven, right? You need to accumulate PFS events. Merck gave us some guidance at the middle of the year, like summertime is about the kind of time where we might expect to see that. In terms of PFS events, obviously, our goal is to improve, right, on the PFS and potentially maybe even the OS of single-agent Bavencio in this setting, right, in the post-chemo setting. That is obviously the objective of the study. That is what we'd like to see. That is what Merck would like to see as well. I mean, that is how the study has been designed, with Bavencio as an active comparator to directly test the combination of 255 plus Bavencio versus Bavencio alone. Thank you. That is super helpful. Thanks for taking the questions. Thank you. Our next question will come from Roger Song from Jefferies. Your line is open. Great. Thanks for the update and taking our questions. I have a quick one related to the Phase 2 atopic dermatitis. Given the enrollment you have completed compared to the recent atopic dermatitis trial, what's your expectation in terms of the patient baseline? What is your expectation there? Thank you. JZ or Brian, you want to take that one? Yeah. Sure. Yeah. Thanks, Roger. One of the things that we'd really like to see is the baseline EASI to be in the range of like 25, 25-30, right? Because as we've seen other studies historically, those kind of baseline EASI scores for the entire population have generally been linked with lower overall placebo responses and also better studies. There is more dynamic range to measure from patients that are having higher EASI scores. That is one of the things that we'd like to see in the study, something in that kind of range for baseline. In terms of setting expectations for placebo, I mean, we do not know. I mean, this is a blind study. Certainly, we would like to see much, much lower placebo response rates than have been reported recently for some of the studies, including the studies that were reported last December, such as from Q32, where the placebo rate was very, very high. One of the things that we did in our study that I tried to cover earlier in our call was that we really had a number of prospective features that we built into the study, such as limiting the U.S. footprint geographically. We only had 17% of our sites in the U.S., focusing on board-certified dermatologists and immunologists that had demonstrated experience working in atopic dermatitis studies, as well as measuring the EASI score multiple times before drug was administered and patients were randomized. All of those things we did prospectively in order to protect the study and ensure that ideally, we do not have a very, very high placebo response rate. Obviously, when we present the results of the top line later this year in June, we will show what that is directly. Thank you for the question, Roger. Thank you. Thank you. Our next question will come from Mayank Mamtani from B. Riley Securities. Your line is open. Yes. Good afternoon, Dean. Thanks for taking our questions. Glad to see the progress here. Could you touch on just a related question to the last comment, JZ? Anything you can touch on the screen failure rate you have seen on this extra stringent criteria you are using and how that may compare to some other studies that have been done around screening and then randomization? I have a quick follow-up. Yeah. That would be the kind of information we would share in the future when we present the results of the study. Okay. Okay. Got it. And then the escape arm piece in the protocol, how patients go on the escape arm, could you just remind me how that's kind of structured for induction and maintenance? And then lastly, just high-level, the read-through from AD data set to the Resolve A study, any translational markers you're looking at would be helpful to know. Thanks for taking our question. Sure. Yeah. In the way the study is designed, which was one of the expert pieces of advice also given to us by the steering committee, is that when patients reach the end of the 16-week induction, if they are not better than EASI 50, then they have the option to enter into an escape arm. The escape arm is the 24 microgram per kilogram dose of Rezpegaldesleukin given twice a month, particularly good for patients, for example, with blind study, but that might have been randomized to a placebo arm, right? It gives everyone a chance to have access to drug. That is how that escape arm works. The primary entry point is at that 16-week time point at the end of induction for patients that fail to meet the EASI 50 or better rerandomization criteria to enter maintenance. The other way that patients can enter into the escape is during the maintenance, if for one reason or another, people lose activity or lose response, then they have a second chance to enter into the escape arm. That is really the way that it works. It is really very standard to these kind of studies that offer an escape arm therapy to patients that are in the study. In terms of other kind of questions you asked about sort of read-through, I mean, we selected alopecia really because it is a key dermatological indication, right? As you know, with REZPEG, we've seen activity in multiple dermatological inflammatory conditions ranging from skin manifestations of lupus, psoriasis, atopic dermatitis. Also the underlying knowledge about the biology of immune privilege and the role that Tregs play in helping to maintain and sustain that immune privilege state. We will be looking at biomarkers across both studies. As you saw from our publication in Nature Communications in October of last year, a number of biomarkers that we measure are induction markers because our drug is an agonist. I expect we'll be able to measure those kind of induced pathways independent of underlying disease etiology of the patient. Those will just be based on the signaling of our molecule onto Tregs, for example. Those will be some very important correlative biomarkers that we'll be collecting in the future. We're looking forward to the readout of both of these studies. As we discussed, the first one, atopic derm, is coming in June for that induction. For alopecia areata in the Q4 of this year, we expect to be reading out the 36-week treatment data from that study as well. Thank you, JZ. Thank you. Our next question will come from Arthur He from H.C. Wainwright. Your line is open. Hey. Good afternoon, Howard and team. Thanks for taking our question. JZ, thanks for the additional color on the dose regimen for the AD study. I just want to follow up a little bit on the rationale to pick those three regimen arms. Why not go for a higher dosing regimen than the 24 microgram per kilo Q2W? Yeah. I had a follow-up on the trial as well. Yeah. Across the clinical program, we've evaluated various doses, both weight-based dosing, such as what we're using in the study, and also flat dosing as was used in other studies like the lupus study. Really, when you look at it, that gives you a range of different doses that we've established. We've gone well above and well below. Actually, the 24 microgram per kilogram is really an optimal dose level. It gives us all the things that we want to have from a PK/PD relationship. We engage the target very effectively. We get very robust Treg expansion. You can dose for a very long time at that dose level without seeing any cessation or any hysteresis in any of the pharmacodynamic responses. From the biomarker data that was asked earlier and that we published, you can also see a very robust induction of immune pathways that we see at that dose level. That is really an optimal dose level that we are really focused on. Thanks for that. The second question is also regarding probably both AD and the AA study. Could you remind us how the stratification in both.