Good morning, and thank you for joining the Nektar conference call to review the 16-week induction data for the phase IIB study of REZPEG in patients with atopic dermatitis. At this time, all attendees are in a listen-only mode. A question-and-answer session will follow the formal presentation. To our analysts that are joining us live to ask a question, please use the raise hand feature to indicate you have one. As a reminder, this call is being recorded, and a replay will be made available on the Nektar website following the conclusion of the event. With that, I will now hand the call over to Corinne Franklin in Investor Relations at Nektar Therapeutics. Please go ahead, Corinne. Thank you, and good morning, 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; and Dr. Brian Kotzin, our Chief Medical Officer. Later in the call, we'll be joined with Dr. Jonathan Silverberg from the Department of Dermatology, George Washington University School of Medicine, and Dr. David Rosmarin from the Indiana University School of Medicine. 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 REZPEG, 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 10Q that was filed on May 9, 2025, 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. Good morning, and thank you, everyone, for joining us. Over the past several years at Nektar, our strategy has been to advance innovative therapies for serious autoimmune and inflammatory conditions, with a focus on driving a paradigm shift in treatment through immune system rebalancing and an ultimate goal to achieve immune homeostasis for patients. Our focus on regulatory T cells as a modality has been driven by early proof-of-concept data signaling to us the potential for this first-in-class mechanism to treat a range of autoimmune and inflammatory conditions, particularly dermatological diseases. With these phase IIB studies' results in atopic dermatitis, REZPEG, which is a first-in-class Treg stimulator based upon IL-2, has now also been validated as a best-in-class approach. While other approaches to access IL-2 agonism have focused on the design of muteins, which we believe hindered their development, we instead took an elegant approach with a native sequence IL-2 and a validated technology, pegylation, which has led to the approval of over two dozen biologics over the past several decades. Today, we're excited to share positive and statistically significant results across primary and secondary endpoints for REZPEG in the 16-week induction phase from our phase IIB trial in atopic dermatitis. These data potentially pave the way for a differentiated and novel treatment option for patients. The trial met its primary endpoint of the mean improvement from baseline in EASI score at week 16 for all three arms of REZPEG versus placebo, with a p-value of less than 0.001. All three dose arms also achieved statistical significance at week 16 for the key secondary endpoints of EASI 75, EASI 50, and BSA, and the Q2 week arms achieved statistical significance at week 16 for the key secondary endpoints of vIGA and Itch NRS. In addition, at week 16, the highest REZPEG dose of 24 micrograms per kilogram, Q2 weeks, achieved statistical significance on the EASI 90 endpoint. We saw a rapid onset of response for all three endpoints, and especially for EASI 75 and Itch NRS, separating from placebo quickly within a few doses of receiving REZPEG, and JZ will talk more on that later. This is a key differentiator from other immune modulation approaches, such as OX40 pathway inhibitors. Safety was consistent with our previously reported results, and importantly, we saw less than 1% of patients discontinue because of an ISR. Additionally, we saw no increased incidence of conjunctivitis and infections, such as oral herpes, as compared to placebo. This is another key differentiator compared to approved agents and to those in later stage development. The compelling efficacy findings are further boosted by the translational data, which show for the first time that REZPEG also reduced key TH2-related inflammatory markers of atopic dermatitis. With this validation, we eagerly await results in the fourth quarter of this year, evaluating REZPEG in patients with alopecia areata. This would add another significant opportunity for REZPEG. Now I'd like JZ to walk you through the data in detail. JZ. Thank you, Howard. I'll start with a quick recap of the overall design of the phase IIB study. We enrolled biologic naive patients with active, moderate to severe atopic dermatitis. For the 16-week induction treatment period, patients were randomized 3 to 3 to 3 to 2 to receive subcutaneous treatment across three dose arms of REZPEG: the high dose of 24 micrograms per kilogram, Q2W; the mid dose of 18 micrograms per kilogram, Q2W; and a low dose of 24 micrograms per kilogram, Q4W, or placebo Q2W. In total, 393 patients who received at least one dose of study drug were randomized across the three active dose arms and placebo. The primary endpoint and secondary endpoints were assessed at week 16, at the end of the induction period. Today, we are reporting the results of the completed 16-week induction period. However, the trial has a 52-week design and is still ongoing. In week 16, REZPEG-treated patients who achieved at least a 50% improvement in their disease severity were re-randomized one-to-one to continue at their same dose level on the Q4W or Q12W regimen through week 52 in the ongoing blinded maintenance period. Placebo patients that met this criteria continued on to receive placebo Q4W, and patients that failed to achieve a 50% improvement in EASI at week 16 were given the option to enter the ongoing open-label escape arm with REZPEG high dose administered Q2W. As this is an immune balancing mechanism, and as we observed a remissive effect in phase IB for up to 36 weeks for many atopic dermatitis patients after removing REZPEG treatment, we are eager to see the effect of continuing to treat patients beyond the induction period. The primary endpoint in REZOLVE-AD was the mean change in EASI score following induction treatment at week 16. Key secondary endpoints for disease control being reported today are EASI 50, 75, 90, Itch NRS, vIGA of 0 or 1, and the mean percent reduction in body surface area or BSA. There are additional patient-reported outcome secondary endpoints around quality of life, POEM, sleep disturbance, skin pain, and others that we plan to submit for presentation at a medical meeting later this year. The statistical elements of the study are presented here. In the coming slides, you will see the primary and secondary endpoints reported using primary estimate analysis, which is similar to other contemporary phase IIB and phase III studies. Specifically, patients that discontinued due to disease worsening or take rescue medication outside the protocol-specified period are considered non-responders, and patients that discontinue for other reasons are set to missing. The primary estimate applies to both the continuous and the binary endpoints. We enrolled the typical study population of biologic naive patients with moderate to severe atopic dermatitis. Patients were predominantly from Europe and also included those from North America and Australia. The study was well-balanced among men and women, and the majority of patients were under 65 years old. Mean disease duration was 21 and a half years. The mean baseline EASI score for the overall population was 26.0. About 60% had an EASI of at least 21, and 32% had baseline severe disease as assessed by vIGA score of 4. Mean baseline BSA involvement was 39.5%, and the mean baseline worst daily Itch NRS score was 6.8. The study was well-balanced across arms on these baseline disease severity parameters. Now, let's turn our attention to the clinical efficacy data. As Howard mentioned, the overall study was a success, and the primary endpoint, mean percent change from baseline EASI score, was statistically significant at all doses at week 16, with a p-value of less than 0.001. The REZPEG arms separated from placebo at the earliest two-week post-dose time point and remained separated at all time points measured during the 16-week treatment period. One point worthy of mention is the low placebo response rate of 31% in REZOLVE-AD. As you all know, we implemented a number of proactive measures to address the placebo response rate, and we are very pleased with the outcome. For key EASI responder endpoints at week 16, all REZPEG dose levels and regimens met statistical significance versus placebo for the EASI 50 and EASI 75 endpoints. EASI 75 is a key registrational endpoint in both Q2W arms met with a p-value less than 0.001 and responder rates of 42% and 46% as compared to 17% for placebo. For EASI 90, the high dose arm met significance with a 25% response rate compared to 9% in placebo. Another key registrational endpoint is the vIGA responder analysis. For this endpoint, both Q2 week REZPEG arms were significant, with 20% and 26% response rates as compared to 8% in placebo. The Itch NRS score was notable in the study, with 42% of patients who started with a baseline Itch NRS score of 4 or greater seeing a drop of at least 4 points on Itch NRS. The placebo rate was only 16%. Body surface area mean change and improvement was consistent with what we saw with the EASI mean score reductions, with all three dose arms of REZPEG showing significant separation from placebo. Digging deeper on key responder metrics, as Howard stated earlier, we saw a rapid onset of response for primary endpoints. Shown here are the time course responder plots for EASI 75, EASI 90, vIGA, and Itch NRS. We could see quick separation from placebo beginning within a few weeks of patients starting on REZPEG. This is a key differentiator from some approved biologic agents and other immune modulation approaches, such as OX40 pathway inhibitors, which are currently in phase III. Looking at EASI responder rates by baseline vIGA scores, we see comparable efficacy in more severe patients with vIGA baseline scores of 4, as we do in moderate patients with baseline scores of 3. For example, you can see the clear difference in placebo response rates between the moderate and severe patients when comparing the gray lines on the left hand versus the right hand charts. There is essentially no change for the REZPEG arms. In addition, when we look at EASI 90, one of the deepest efficacy measures we deployed in the study, you can see the notable performance of the high dose arm, especially in the patient population with baseline severe disease. Now, let's look at the initial translational data showing a clear, objective, and meaningful immunological impact of REZPEG on lowering key Th2 inflammatory markers associated with atopic dermatitis. We observed dose-dependent reduction in IL-19, TARC, also known as CCL17, periostin, and MDC, also known as CCL22. Shown here are the absolute mean reductions from baseline to week 16 in patients that had baseline levels of these markers above the upper limit of normal. Consistent with what we reported from the phase I studies of REZPEG in dermatological settings, we saw a dramatic decrease in CCL22. CCL22 is one of the chemokines for the CCR4 receptor. The other chemokine ligand for CCR4 is CCL17. We observed a dose-dependent reduction at week 16 for CCL17. In contrast, placebo patients showed increased levels of CCL17 over the 16-week induction period. Also consistent with our prior reports in our phase I data, we saw dose-dependent decreases in serum IL-19. Another new observation following REZPEG treatment was a dose-dependent reduction in periostin, a key marker present in the lesions of patients with atopic dermatitis. Interestingly, expression levels of periostin are positively correlated with itching intensity. In the future, we will be extending this translational analysis, covering additional proteomic endpoints and aiming to correlate baseline and on-treatment biomarker effects with treatment outcomes. Our PK and PD profile is consistent with prior studies of REZPEG. We saw up to a six-fold increase in Tregs at the high dose of the study, which is very similar to what we observed with the same high dose level and regimen in our phase IB study. Not shown here, all other cellular PD results and flow cytometry analyses were similar to our historical studies and prior publications. REZPEG had no effect on conventional CD4 or CD8 T cells, and the second most expanded cell population after Tregs were the CD56 bright, CD16 dim subset of NK cells. Our PK profile was dose-dependent and produced the expected exposure, which ranked from highest to lowest as 24 Q2W, 18 Q2W, and 24 Q4W. There is a clear dose response observed in this study, and the consistency of this dose response across PK, PD, and efficacy endpoints gives us confidence in these dose ranges for an induction regimen in atopic dermatitis. Moving on to a summary of safety. The safety profile for the 16-week induction period of REZPEG was consistent with previously reported safety results. We saw no increased risk of conjunctivitis, infections such as oral herpes or oral ulcers in the REZPEG arms. There was no difference in all-cause infection risk between placebo and the REZPEG groups, consistent with its immunoregulatory mechanism of action. Serious and severe adverse events were rare at 1.6% and 3.1%, respectively, for REZPEG-exposed patients. Discontinuation rates due to AEs was low at 5.6% for REZPEG-exposed patients and was lower than what we observed in the phase IB, within the ranges seen in contemporary phase IIB studies. The most common treatment-emergent adverse events were local injection site reactions, or ISRs, which were observed in 69.7% of all REZPEG-treated patients, with the largest proportion of these being mild or moderate at 99.6%. All ISRs self-resolved, and less than 1% of patients discontinued because of an ISR. Further, almost all reports of ISRs are mild to moderate, self-resolve, and didn't lead to discontinuation in our study. Nevertheless, we are actively planning an ISR mitigation strategy for commercialization, including a shift to an autoinjector and other mitigation approaches. We have already conducted mechanistic studies that help us understand the underlying cause and inform our mitigation approaches. In the pooled REZPEG arms, TEAEs excluding ISRs were reported in 60.3% of patients and in 57.5% of placebo-treated patients. Other TEAEs more commonly observed at a greater than 5% frequency in the study treatment arms, comparing 320 people exposed to REZPEG versus 73 exposed to placebo, included eosinophilia 7.8% in REZPEG versus 2.7% in placebo, pyrexia 6.3% in REZPEG versus 2.7% in placebo, headache 6.3% for REZPEG versus 4.1% for placebo, upper respiratory tract infection at 5.9% for REZPEG versus 5.5% for placebo, and arthralgia at 5% for REZPEG versus 1.4% for placebo. When looking more closely at ISRs across all REZPEG doses administered in the study over the 16-week induction period, we see that more than half of all dose administrations are not even associated with an ISR. Specifically, 56% of dose administrations were associated with no ISRs. In the remaining reports, 30% were mild and 14% were moderate. Many patients only had one or two reports of ISRs at all over the entire 16-week treatment period. The majority of ISRs are mild and associated with faint erythema and are asymptomatic. In this table, we show key phase IIB studies in atopic dermatitis arranged chronologically with the most recent studies shown on the left. As you can see, we achieved the target range of efficacy for REZPEG that has been observed with other agents in phase III development or approved biologics. I will note, though, that comparison to prior phase IIB studies has some challenges due to differences between the studies, including differences in patient population and statistical methodologies. Yet these benchmarks are still quite important. Since REZPEG is an immune modulator and the REZOLVE-AD study completed enrollment in 2025, it is highly instructive to compare REZOLVE-AD results for REZPEG to the phase IIB studies for the OX40/ OX40 ligand class, since these are also immune modulating mechanisms. The studies were completed in similar time frames, had similar global footprints, and had most similar statistical designs. As you can see, focusing on the primary and secondary endpoints of each study, REZPEG has a compelling 16-week induction profile. Diving deeper into one of the registrational endpoints, EASI 75, you can see the results of EASI 75 response rate over the 16-week endpoint, comparing REZPEG to the OX40 ligand class. We can see how REZPEG compares to the phase III dose levels advanced into registrational studies by those programs. REZPEG begins to separate at week 4, which is earlier in treatment compared to the OX40s. This slide shows a similar time course analysis for the IGA endpoint. Note that the REZPEG and ROCA studies used a validated IGA or vIGA endpoint, while Mlight-Lamab used an IGA endpoint, as did all of the IL-13 development programs. Even with this methodological difference, we see the comparability of the vIGA response rates at week 16 between REZPEG and the OX40 class. REZPEG begins to separate at week 6, which is earlier in treatment as compared to the OX40s. We are pleased to have two of the leading thought leaders and practitioners in the field today with us, Dr. Jonathan Silverberg and Dr. David Rosmarin. I'd now like to ask Dr. Silverberg and Dr. Rosmarin to share their impressions and perspectives on the REZOLVE-AD trial results. Jonathan, may I please turn the floor over to you first? Sure. Good morning. Good morning, everyone. First, congratulations. These are very impressive data. You know, just some free thoughts, if you will. I mean, I think the first thing we see here is we have a drug. That's a very important conclusion to make, I think, looking at the totality of the data. I think there's a lot of, I mean, we obviously showed a ton of data, and there's a lot of key elements, I think, that we can focus on. I mean, first, the dose response, you know, supporting the mechanism, supporting the drug, the overall consistency between the clinical endpoints and the translational markers like TARC and periostin. It's not like, you know, we're going to prescribe a drug purely on TARC and periostin, but having that overall consistency and supportive package from the translational and the clinical really reassures us. I think the kudos on the strategies taken for management of placebo responses, this has been the bane of many trials and been a big discussion in the field. You know, everything we see here makes sense. You know, we see a little bit of a higher placebo response in the moderate patients than in the severe patients. We expect that. That's totally par for the course. Overall, these numbers are quite low, and you've done a great job in this trial landscape in managing that. I would say, you know, what you've done, just keep doing it for phase III. You know, looking at the kinetics of response, I think there's a few key things that I focus on. I think first, you know, is the early onset for some of these endpoints. You know, we see the EASI 75 responses look like maybe they jump a little faster than, let's say, the NRS4 responses, which would support sort of more of an indirect effect of the mechanism on itch. We're seeing really a very nice efficacy overall for itch. Actually, relatively early responses. As you optimize the dose, I think we'll get even better. You know, I think some folks might take that for granted, but I think in the current trial landscape, we shouldn't. You know, when we look at some of the readouts from phase II and some of the phase III readouts for the OX40/OX40 ligand class, itch kind of did weird things. There were unexpected things. And so, you know, and we've seen some drugs that work better on itch than they do on lesions, sometimes better on lesions than itch. Here to see that consistency between lesional efficacy and the itch is nice. It shows, you know, because obviously for this disease, you need a drug that works on itch as well. I think also importantly, no plateau, you know, for a number of the endpoints. You're already seeing good efficacy at the primary efficacy time point, but a suggestion that would continue dosing beyond, you know, week 16, that you would get even more efficacy. I think the last thing is just to note that, you know, here, we're not even fully potentially optimized on dose in the sense that, you know, we haven't seen the, you know, the loading dose put into play. I think we've seen for every drug out there that when you put that loading dose into play, you get even faster responses and potentially even deeper responses in that induction period. To me, I look forward to seeing what, you know, a loading dose would bring because my expectation is that it'll increase the efficacy and speed up the responses even more than the great data you've shown so far. Those are just some of my high-level thoughts. I'm happy if David wants to chime in. Yes. Thank you, Jonathan. I want to echo what you said. You made many excellent points. The first one that I want to start with is that the study is very well designed. Equally important, it was really well executed. The results are quite consistent. You see this nice dose response. It's great to see that low placebo, which has been a problem for other studies. We now have some great itch data as well. It's nice to see it perform similarly well in both the severe and moderate patients. I think one of the big news from the data here is that patients were not dropping out due to the injection site reactions, which I think is really an important point. Personally, I'm a fan of this mechanism. The idea of agonizing the brakes on the immune system is very appealing to some of my patients, that kind of concept. I'm also optimistic, as Jonathan stated, about potential for not only sustained response, but a deepening of that response. He mentioned that there was no plateau yet. I think that that's something that we can be optimistic about, given both the mechanism as well as the phase IB data. Jonathan also commented on the faster speed of onset, which is certainly a plus and potentially a differentiator from the OX40s. There's opportunity for infrequent dosing and maintenance, which is, again, quite appealing. Overall, given everything we're seeing, I think I personally have high confidence that a phase III program will be successful and the medicine will have a place in our armamentarium. I also wanted to comment that there's quite a bit of potential for alopecia areata as well as other dermatologic diseases, for example, lupus, GVHD, etc. In terms of the alopecia areata, it's really a disease where we have tremendous need, need in terms of efficacy, safety, and a drug for a sustained response. Given the mechanism of REZPEG, it really makes sense that this is being studied for this condition. With the capacity for rapid onset, sustained response, and the safety thus far, again, I'm very optimistic and looking forward to those results in quarter four. Overall, just to echo what Jonathan said, congratulations. It's a great result, and you have a drug. Excellent. Thank you so much, Jonathan and David, for your comments. To summarize, we are exceptionally pleased with the results for the 16-week induction period that we reported today. Nektar has established a novel Treg MOA and a whole new biology, which differentiates from existing and in development biologics. Furthermore, REZPEG is the only T regulatory mechanism and the only IL-2 based therapy to show significant and compelling efficacy data across all endpoints in a large phase IIB study. We know this MOA translates. We saw a Treg fold increase up to sixfold and a clear reduction across key pro-inflammatory markers of atopic dermatitis. On the efficacy profile, the highest dose arm was significant on the primary and all key secondary endpoints. Importantly, we observed a rapid onset of clinical benefit observed within the first few weeks of starting therapy. We saw a clear dose-dependent efficacy across multiple dose arms, and we had no drop-off in treatment effect in the patients that had baseline severe disease. The safety profile of REZPEG is consistent with previously reported safety results. Most notably, we saw no increased risk of conjunctivitis or oral herpes or oral ulcers as found with other biologics and JAK inhibitors. We know from our phase IB results that REZPEG has potential for a long-standing clinical benefit, potentially even remission. With REZOLVE-AD, we have now firmly established the induction period. Moreover, we are eager to see the results from the maintenance and escape arms in REZOLVE-AD, where we aim to show a sustained and even potentially a deepening of response with infrequent dosing in patients with atopic dermatitis. For next steps, we plan to schedule an end of phase II meeting with the FDA to review the results of this study and the phase III development plan. We intend to submit these data for presentation at a future medical meeting where we will present the results in greater detail as well as additional endpoints from the 16-week induction period, including a number of the patient-reported outcome endpoints. As we mentioned earlier, we plan to present the top-line results from the phase IIB REZOLVE-AA or alopecia study in December of this year. This study enrolled approximately 90 patients with severe to very severe alopecia areata. Now that we have strong phase II results in the dermatological setting of atopic dermatitis, we're incredibly optimistic about the second phase II study. From this REZOLVE-AD study in atopic dermatitis, we also plan to present 52-week maintenance and escape arm data in early 2026. This will allow us to evaluate that continued dosing of REZPEG beyond the 16-week induction period. We will be looking at the potential of sustained and possibly deepened responses from that part of the study. In dermatology and immunology, we see great potential for REZPEG across multiple blockbuster indications. In dermatology, of course, atopic dermatitis and alopecia areata, two immune-driven skin conditions, and we're running those studies. Beyond that, we believe the Treg mechanism could translate to vitiligo and other skin conditions. In immunology, our partner TrialNet will initiate the phase II study in type 1 diabetes in the second half of this year. The study, which is funded and sponsored by TrialNet, will evaluate REZPEG in new-onset stage 3 type 1 diabetes patients. We also believe REZPEG has potential in lupus. Although our study conducted by Lilly did not meet its endpoints, we believe this is because the fixed dose arms were not chosen properly. With the experience of our weight-based dosing in the REZOLVE-AD study, we believe there is a real opportunity to translate this dosing into a potential opportunity in lupus. Finally, with this validation of a Treg mechanism, I'd like to also mention our antibody program in preclinical development. Our lead antibody, a TNF-R2 agonist, which is planned for an IND at the end of this year, is a unique Treg stimulator. Because of its monomeric activity, we are building a large bispecific program based upon this mechanism combined with other validated targets in immunology. We believe this mechanism has potential in multiple indications, including Crohn's, ulcerative colitis, multiple sclerosis, and others. With that, I will now open the call for questions. Operator. Great. Thank you, Jonathan. Yes. At this time, we will be conducting a question-and-answer session with our speakers. As a reminder to our analysts that are joining us live, please use the raise hand feature to indicate you have a question. Please hold for a brief moment while we pull for questions. Our first question comes from Yasmeen Rahimi at Piper Sandler. Please go ahead, Yas. Good morning, team. Tara, can you hear me? Yes, we can. Okay, perfect. Congrats, team, to the fantastic data and really an incredible execution. Very proud to see the top-line data. I guess the first question is for the Nektar management team. I think, Jay-Z, the expectation was static across one dose, which would have made our life easy to figure out what is the dose moving forward. I guess help us understand how you're thinking about dosing strategies in phase III. For our KOLs, I think you alluded to in your prepared commentary around translation from phase II to phase III. Obviously, you know, given the same execution, what would your prediction be in terms of a larger phase III study, even though this was quite one of the most robust phase IIBs we have ever seen? Then the second question for the KOLs is, if they could just comment on what you would predict REZPEG's effectiveness to be in a study where we would include biologically experienced patients. Again, congrats, and I'll jump back in the queue. Okay. Thanks, Yasmeen. I'll start off with the first question. The first key thing is in this phase IIB study, as you saw, we studied a dose range. That dose range was clearly resolvable, meaning not only could we separate the PK and PD, but we could also separate the efficacy where we looked across the study. We also saw that in the Q2 week regimen, we actually hit the majority of the endpoints. At the highest dose, the 24 microgram per kilogram Q2 week, we hit on all of the secondary endpoints as well, including EZ90. In fact, that was the only dose that hit on the EASI90 endpoint. In kind of, you know, processing all of this data and thinking forward to phase III, there's still a little bit more that we are aiming to get out of this study. For example, we discussed the endpoint at week 16. As we've discussed in this call, like we're not flattening out yet. We still keep going. One of the things that we'll be looking into is the overall totality of the dose level, the dose regimen, and the duration of dosing, all that come together into optimizing, you know, the key phase III dose level range regimen and duration that we'll put forward into the design of the phase III. I'm very happy to say that this study really gives us everything that we need to design the phase III regimen. Some of the things that we're doing to prepare for the end of phase II meeting, which address the kind of questions that the health authorities ask as you prepare for phase III, is all of the PK data from the study is modeled into a population PK model. Then exposure response modeling is done with that data as well. That is always used to support, you know, all of the phase III dose decisions. We're in great shape. I'm also very confident we're in great shape to have just one dose level and regimen for the phase III as well. I think the next question was about the translatability of phase IIB to phase III results. Maybe I can ask Jonathan to comment on that. David, if you could comment on a bio-experienced combination, you know, both naive and experienced patients. Jonathan, would you like to go first? Sure. Okay, I think it's obviously a very important question. You know, my take on this is there is a very, and I think, you know, David actually mentioned this in passing before, I think there is a very, very high probability of success in terms of achieving statistical significance in phase III. I don't see any holes in the data. What I mean by that is, you know, sometimes you look at the data and you're seeing wonky signals or, you know, you're only getting efficacy in some endpoints, but not in other endpoints. You're really seeing consistency across everything in terms of whether it's the moderate endpoints, the robust endpoints, the itch, the lesions, it's all behaving the way it should. You've got predictable time course in terms of the kinetics and the curves. You're not seeing this sort of fluctuation, you know, these are bouncing up and down that you'll see with smaller trials, which may suggest, you know, it's just a few patients skewing things here or there. I mean, you're really seeing a consistent package here. The biomarkers are just icing on the cake to reaffirm that you're, you know, you're really having a consistent biologic activity. On top of that, I would argue that, you know, the opportunity for loading dose only gives you more potential for efficacy, faster responses, getting you there quicker to make you even more competitive. I think the probability of stats, you know, in phase III is extremely high. I look, you know, the other thing you need to think about is what about, you know, would safety or would ISRs or other things be an issue? That's always something that you just, you don't know safety until you study it long enough, but we haven't seen anything that has been an issue. I think based on the mechanism, we're very optimistic overall. The ISRs was the one thing that we were keeping an eye on. I mean, it's come out beautifully so far. I don't think that that's going to be a major rate limiter in any way in phase III. You know, when you think about how safety can sometimes impact an NRI analysis, you know, type of thing, we're not seeing massive dropout. We're not seeing those issues come up. My expectation is that this is manageable safety and something that can deal with in phase III should not be an obstacle. I think these results do translate into phase III well. You know, I'm really trying to think about this critically. I mean, I just don't see anything here that would get me nervous in this sense other than you've got to roll the dice and run the trial. Yeah, I completely agree with what Jonathan was saying. I would be surprised if the phase III weren't successful based on what we're seeing. In terms of biologically experienced patients, that, you know, you truly don't know until you test it. However, I'm optimistic they're going to have a similar response to the biologically naive because this is really an alternative mechanism to those patients. If patients fail via the IL-4 blockade, that is, we are treating them with a completely different mechanism. I think that for those reasons, I do not see that those patients necessarily will have a poor response to REZPEG. I also think what is helpful is seeing that the more severe patients behave similarly well to the moderate patients, which also gives me a little bit more confidence in that speculation as well. The truth is you just have to run the study to truly know. Again, I am optimistic that those biologically experienced patients will also respond. Great. Thanks for the questions, Yas. Our next question comes from Arthur Heat at H.C. Wainwright. Please go ahead, Arthur. Hey, guys. I want to extend my congratulations to achieving this milestone. I had a couple of questions. For Jay-Z, could you give us a little bit more color on the patients who have been eroding to the escape arm so far? For Jay-Z and the doctors, I just want to see, besides the auto injector, what kind of strategy could further mitigate the ISR in the phase III study? Thank you. Sure. Thank you, Arthur. Let me begin. You asked a question about the patients that moved into the escape arm. Just to kind of briefly remind the way the study was designed, right? Patients were treated for 16 weeks in completely blinded fashion, of course. For patients that did not achieve an EASI50 response, they had the opportunity to move into an open label escape arm. In the escape arm, they would receive the high dose of REZPEG, which was 24 micrograms per kilogram on the Q2 week regimen. We did an interesting analysis to look at the people that escaped at the end of week 16. What we found is that actually 65% of patients in the placebo group that completed 16 weeks did not have sufficient efficacy. Those were the people that transitioned into the escape arm. As you'd expect, you know, about two-thirds or, you know, a large majority of the people in the escape arm moved into, the people in the placebo and during the induction period moved into the escape arm. In contrast, for people that were on the REZPEG arms, again, all blinded, nobody knew what they were on. There you saw a very low frequency, less than 25% move into the escape period. That did give us a great sense of reassurance, right, of what you're seeing. You'd expect the majority of placebo-treated patients to not achieve sufficient efficacy and move into the escape arm. That was one piece of information. I think related to that is that, you know, this is just, you know, a portion of the study that's ongoing. All of the people that are in that arm have the opportunity for 36 weeks of additional treatment until they reach week 52. As mentioned earlier, our goal in the early part of next year, once we complete that 36-week extension part of the study, is to report the results of all of the people that were treated in the study for a year. That would include the people in the escape arm. It would also include all the people that are in the ongoing maintenance arms as well. I think your other question, Arthur, was about some of the ISR mitigation strategies. Maybe I'll start off and then I'll ask maybe some of our doctors to comment. The first thing is that we definitely have started to do mechanistic studies. One of the things that we've begun to do is to do skin organoid cultures where we can actually study the biology, you know, it's happening. In these studies, we actually are able to collect skin samples from tummy tuck surgeries. That's great because it's abdominal skin, which matches the abdominal site of administration of the drug. You can culture the skin in an air-liquid interface, maintaining the barrier at the top layer of the skin and maintaining all the layers of the skin down to the subcutaneous tissue. You can actually study, you know, the biology that's going on. We've been able to assess gene expression changes using skin organoids following REZPEG injection into that organoid culture. That's been a huge breakthrough for us because we're starting to see the genetic pathways that are induced. Specifically to your question, that leads us to targeting mitigation approaches, right? When we know the kinds of pathways and signaling that's happening and, say, the cell types that are firing, then we can isolate, you know, on mitigation strategy. That's one set of activities that we're doing. Others are, of course, switching to really a more typical presentation of the drug, right? Our intention at commercial launch is that this is a self-administered product. The patient would have an auto injector device and they would self-administer REZPEG as we do typically for just about all, you know, injectable biologics. Maybe just to discuss the significance of ISRs because we can go into so many different levels of them, but maybe I would ask David and Jonathan to comment on, you know, just sort of, you know, your interpretation of that as really the most frequently observed adverse event. I'm happy to take a crack at this. I mean, I think obviously there's all different types of ISRs, but when you're dealing typically with just localized, you know, reactions, you know, and cutaneous reactions that may be more persistent. I mean, there's all different scenarios, but if you're dealing with things that resemble more of a sort of dermatitis scenario, typically they're not a big issue in the real world. There's a number of different strategies that can be employed. It's something we encounter with all kinds of drugs and not even just dermatologic drugs. It comes up in Parkinson's disease and all kinds of other disorders where we deal with ISR. This is something that derms are quite comfortable and I think familiar with already. You know, certainly if you think about potential for even just maintenance dosing and spreading out the interval of dosing in the long run for patients who would like to be on drug real world, that might be an opportunity even just to spread it out a little. Even just from the, you know, day-to-day, we've used things, simple conservative strategies like cold compresses. Sometimes actually it's warm compresses that do better than cold compresses, right? Sometimes it's just a gentle little massaging that can help for patients. It doesn't always even require treatment, honestly. In the real world, you know, you have to figure out how you do this in a trial, but in the real world, most of the time it's simple. We just give them a topical steroid or a calcineurin inhibitor or some other non-steroidal. That's it. It's stuff that they'd be using anyway for their atopic dermatitis. I don't think it's anything that worries us. There's a bunch of different things we can do. I will say even we've seen with certain drugs, even just injection site matters, meaning sometimes patients who inject in the abdomen just get fewer injection site reactions than those who inject, let's say, in the thighs, right? It's something that I think we'll learn with continued use, but it's not something that I think is going to really be a rate limiter in any way. Yeah, I agree with Jonathan. I think the key for a successful trial is education. If you discuss the ISR side effect with patients in advance, that is extremely important at retaining those patients in the study. I think what's also helpful, again, is looking at what is the discontinuation rate or the dropout rate while patients are forgetting these ISRs. The fact that it's very low is really what I was looking at. I think that is the key point. I also agree with Jonathan as well that I find ice can be quite helpful if patients are experiencing it. However, I suspect that most patients won't even bother. Thank you very much and congratulations again. Great. Thank you for the questions, Arthur. Our next question comes from Cha Cha Yang at Jefferies. Please go ahead, Cha Cha. Hi, this is Cha Cha on for Roger. Congrats on the data and thanks for this call this morning. We had a question about your expectation for your phase three and also for your maintenance data. We're really excited to see it in 2026. If you could give any color on the maintenance data, that'd be great. Our second question has to do with timing. For end of phase two meeting or potential initiation for phase three, if you have any sort of guidance that you can give us for that. Thank you. Sure. Maybe I'll start off. The first question was about some of the things that we'll monitor in maintenance. In maintenance, we're really going to be focused on the deepest responses. Remember, we had EASI 50 as a threshold for moving into maintenance, but we really are interested in IGA, EASI 90 as key markers to look at in maintenance. We will obviously follow EASI 75 as well as that is registrational, but we are really looking at how many people that had a response sustain it and then how many people that, say, came in between 50 and 75 made it up to 90, right? Those are the kinds of levels and analyses that we will be looking for. It is really that propagation and stability. We will be looking for improvement, you know, along the way as well. To help make sure that is done well, patients are randomized to two different regimens. We also stratify by depth of response at week 16. For example, we balance EASI 90s between the re-randomization and so on so that you can do a well-addressed analysis. In terms of timing, maybe, Howard, I will turn that question over to you for phase three. Before commenting on phase three, I'll just say that our goal for our end of phase two meeting is we're already on a Gantt chart for that. That's been always a, you know, a heavy part of our plan. We plan to execute an end of phase two meeting before the end of the year. Maybe, Howard, you'd like to comment on phase three timing? Sorry, Howard, you're on mute. Sorry about that. We're looking at a, look, we're looking at a number of different possibilities in terms of moving forward with phase three. We want to certainly move forward as quickly as we can. Our goal would be to, you know, initiate phase three in 2026 and spend the next six months or so, you know, doing all the necessary CMC work and assay work that's required. We're also talking to a number of potential partners and collaborators to help us with that. Stay tuned for that and we'll keep you informed. I certainly think we want to move as quickly as we can. Awesome. Thanks so much for that. Thanks for the questions, Cha Cha. Our next question comes from Julian Harrison at BTIG. Please go ahead, Julian. Thanks for the questions, Cha Cha. Our next question comes from Julian Harrison at BTIG. Please go ahead, Julian. Thanks for the questions, Cha Cha. Our next question comes from Julian Harrison at BTIG. Please go ahead, Julian. Hi, good morning and congratulations on these data. It's great to see a novel mechanism in atopic dermatitis with such a large effect size. A few questions for Howard and Jay-Z. First, I'm wondering if these results change your approach at all to the ongoing litigation versus Eli Lilly. How should we be thinking about Lilly's potential liability here? Second, do you plan to continue weight-based dosing in phase three? If not, are any bridging studies needed before you proceed to phase three? Then third, just revisit a topic raised by another analyst. I'm wondering if you could talk more about how you're thinking about post-IL4R and post-IL13 atopic derm. Do you stay laser-focused on frontline positioning or could there maybe be a worthwhile opportunity to explore later line use maybe in a standalone phase two study? Thank you very much. Okay, I'll take the first part of it. Look, a good question. Certainly, I'm not in a position to comment. Certainly don't want to comment on the progress of our legal action against Lilly. All I would say is that clearly REZPEG performed very well. I think we're going to pursue this legal action vigorously. I'll let Jay-Z handle the rest. Thanks, Howard. Yeah, Julian, your other question was about the way we will approach dosing in phase three. What I'll start with is that in this study, we used weight-based dosing. In the phase one B, we used weight-based dosing. You know, that's really important, you know, to dose with precision. What we learned from, I touched on this earlier in our script, what we learned from the lupus study was that study used a completely flat dosing approach. We conducted a post-hoc analysis by actually focusing on body weight range. We saw that there was a profound impact, you know, what we saw. That actually was one of the things that crystallized in our mind that the dosing precision is important. It shouldn't be a surprise. This is an agonist drug, right? So, you know, agonist, you need to be certain, right, about how you're administering the drug. It's quite different than an antagonist drug. Our plan is to use weight-based dosing for phase three. I mean, we're building on really strong results here. We want to continue that. What we know we can do and are doing for commercial is we're understanding the weight bands. This comes out of our population PK and other studies where we know that there are likely going to be different bands for patients' body weights that will lead to their administration devices. In a sense, you will be basically creating narrower kind of flat dose ranges to accommodate different people's body weights, which give you the same effect as a weight-based dosing. That will be the objective of the commercial launch for the product. That answers your second question. Your third question was about the sort of the patient population post-IL413 and some of the positioning for REZPEG. I will start off by saying that we've conducted a phase I B and a phase II B in biologic naive patients. We're seeing really, you know, strong effects here in this patient population. That definitely will be a key component of our phase III program. We are also interested in adding biologic experienced patients and especially seeking the broadest label, right, which allows use in multiple settings in early and the late line. Dr. Rosemarie and Jonathan already kind of commented on that there's really, even though we haven't done a study yet in bio experience, there's no first principle or scientific reason why we would think a person that either stopped responding or never responded to an IL-4/13 class wouldn't respond to REZPEG. In fact, the more kind of mixed presentation the disease is, probably the more a Treg approach, which can skew to different TH polarities, can be helpful. Excellent. That makes a lot of sense. Thank you and congrats again. Thanks for the questions, Julian. Our next question comes from Mayank Mamtani at B. Riley. Please go ahead, Mayank. Yes, good morning, team. Thanks for taking our questions and congrats on a very impressive data set here. Maybe just a couple of quick follow-ups, just the shape of EASI, vIGA, and NRS curves. You know, how should we think of peak efficacy response rate as you continue dosing up to this 52-week maintenance portion? As was commented, you know, the OX40 takes a bit longer to get to that peak induction efficacy. I also wonder how much of accumulative drug exposure plays a role for you to, you know, go to this infrequent maintenance dose. You're obviously, you know, extending out frequency here. How do you balance getting to peak efficacy versus sort of drug exposure? The second question I had was on the geographical sub-analysis if that was conducted at all yet. I would be curious to learn how, you know, your placebo-adjusted EASI responder analysis looked like in US versus ex-US. Obviously, it was good to see your placebo here go down from phase I B to phase II. An apples-to-apples phase I B versus phase II would be looking at, say, the U.S. population directly. Thanks for taking our questions. Sure. For your first question, it was about the shape of the secondary endpoint curves and their projection to future continued dosing. Jonathan, maybe can I ask you to comment on that? Then I can comment on some of your questions about drug exposure versus peak response as well as the geography. Sure. I mean, just to clarify, we're thinking really, you know, let's just talk at a high level around dose. Just contrasting in your question, thinking about the OX40s and 40 ligands as sort of a comparator, that was a complicated class, remains a complicated class to identify dose because there never was a clear dose response. You looked at their phase IIb data and you're like, what is the optimal dose? And that was very tricky. And that's something that seems to be class-wide. We don't have that problem here, right? We see very clear dose response and consistency, right? In the subset populations, moderate, severe, et cetera. And so I think, you know, it automatically sort of distances itself from that sort of concern that comes up from the OX40 ligand class. I don't know if that fully answers the question, but that's sort of how I'm thinking about this. I, you know, I don't, my first glance at the OX40 is like, okay, well, what is that dose? I don't think we have that concern here. I think we have consistency. I think, you know, and so from my perspective, I'm not worried about that at all. Yeah, thank you. Thank you, Jonathan. Your next question was about sort of the relationship between drug exposure and peak response. It is a very interesting question because as you remember in our phase I B study, we dosed for 12 weeks, withdrew the drug cold turkey, but many of the patients continued to improve, you know, even through the seven-week period up to week 19 and then beyond. There is also this kind of component, which is there is a duration of dosing. We believe a Q2 week is important for this induction because we really saw that dose level separate on the induction. You have kind of a startup of effect on an induction regimen. You have the opportunity to see the impact of that with time. For example, some of the more recent phase three studies have started to move to a week 24 endpoint, which is really designed partly for the OX40 class, as Jonathan mentioned, but it's really designed to allow more time for the efficacy to develop. We'll be considering things like that, which is, I think, squarely into your question in the relationship to the dosing regimen and frequency and then the duration, right, until you read out the primary endpoint. The good thing is that this study is just really well designed to answer those kinds of questions for us. I'll just briefly touch on your question about geography. What I will say is that, you know, when you do look at the different regions, you can see some different trends. In the study, 16% of the patients were enrolled from the U.S., which is about 68 people or so. The placebo rate in the U.S. was quite a bit higher, which is, I guess, not a big surprise, right, to our doctors sitting around the table. That is why for us, it was such a key mitigation for us to really control the U.S. footprint and the U.S. patient population relative to the total, you know, worldwide geographical footprint of the study. I guess as we report more results and, you know, publish these results in the future, we can get into more of these regional breakouts of the data and different patient subsets from different regions. Understood. Look forward to that data set. Thank you. Congrats again. Thanks for the questions, Mayank. Our next question comes from Jay Olson at Oppenheimer. Please go ahead, Jay. Hey, everyone. Congrats on these impressive landmark results with this novel mechanism in atopic dermatitis. Thank you for providing the update. Can you talk about what% of patients have transitioned to maintenance therapy? Since the potential for remission or disease modification was previously observed in the phase I B study, is that something we should expect to see in the maintenance phase of this study? As a follow-up question, since Dr. Silverberg commented on the appealing nature of this immune balancing mechanism to both clinicians and patients for atopic derm, would that same rationale apply to alopecia areata? What sort of read across do you see from these positive AD results to AA or even other areas like vitiligo? Thank you. Sure. Let me start off with your first question. The number of patients that moved into the maintenance arms overall in the study was about actually 48%, about 190 people have moved into the maintenance arms. The way that that broke out was it was about 31% of the placebo patients. For the REZPEG patients, it ranged from 56%-49% across the different dose arms. That is for all of the people throughout the study. As I mentioned, for the people that completed at week 16, it was over 75% on the REZPEG arms that moved into the maintenance period. Your next question was about the remission that we observed. In the phase I B, it was really designed in a kind of a remissive, you know, protocol because you dose for 12 weeks and withdrew. In this study, we are continuing to dose after the induction through the maintenance. We're looking at sort of durability and deepening with ongoing treatment up to 52 weeks. The second year of the study kicks in. In the second year, we're actually observing patients for 52 weeks off drug. That'll really answer, Jay, deeply the remission kind of question. We expect that that for us would be something that we'd report on in the early part of 2027. We're really asking a pretty sophisticated question. We treat for a year, we go off for a year, right? What is the stability or the remissive potential after a year of dosing? That's a future effect. I think your next last question was about the read-through to alopecia. Maybe I'll ask David to comment on that. Jonathan, please feel free to ask. Yeah. First, why am I optimistic about alopecia areata? First, the fact that we know that this medicine, at least it does what it's supposed to do in terms of the Tregs. We know that for sure. We can expect that same result in alopecia areata. There is some data that theory passed around, for example, tried just plain IL-2, aldosulacan, even though it was very imperfectly dosed for a very short period of time, even though we know you really have to treat alopecia for quite a while to see a response. Even with that imperfect medicine and imperfect dosing, there were some patients who responded with hair growth. We know that alopecia areata, there's a dominant form of the TH1 arm of the immune system, but there seems to be some other arms potentially involved as well. There is a break of immune privilege within the hair follicle. Restoring that immune privilege by putting the brakes on the immune system and being able to downregulate these multiple pathways, I think again, all makes us optimistic. Plus, when we actually have clinical data for those imperfect studies by Thierry, who's a friend in France, I mean, that gives me a lot of optimism that we're going to see a response in the phase II proof of concept study. I think a big question is, more likely than will it work, how well will it work is my big question. I would echo that. I think the, you know, we know that alopecia areata is a, you know, a T-cell driven disorder, right? So, and it's something that there is, you know, potentially mixed polarities there. Just logically on the mechanism, it makes total sense, right? You have to obviously have to study and see how well it works, but it, you know, from a mechanistic perspective, you know, the rationale is clearly there. Congrats again. Thanks for taking the questions. Thanks for the questions, Jay. Our next question comes from Andy Hseih at William Blair. Please go ahead, Andy. Thanks for taking our questions and really congratulations on the robust data. I have a question for Dr. Rosmarin and Dr. Silverberg. Really wanting to understand how you think about therapy selection and things and differentiations that you're looking for as you put, you know, patients on different, various different therapies. I'm curious, maybe in a hypothetical situation where you have all three modalities available, right? IL-2, OX40, and then Dupi on the market. How do you think about, you know, patient selection based on the data that you have seen today? Second question I have is really on the higher risk, basically more severe baseline patients, you know, very, very intriguing data there. Maybe for the Nektar team, is there any sort of regulatory or commercial strategy that you can really amplify that differentiation there? Maybe third, on a more kind of biological perspective, you see maybe like a peaking of efficacy for OX40 and for maybe week 30-36. I'm curious in terms of any biological rationale that you might see kind of a more linear and longer, you know, benefit, you know, with REZPEG. Thank you for taking our questions. Yeah, I think the first question was for Dr. Rosmarin and Silverberg was about sort of treatment decisions if you're in a hypothetical situation where you have multiple classes of agents available, IL-13, OX40, and Treg. Dave, you mentioned your name first, but I'm happy to go. Look, this is obviously a billion-dollar question. I mean, I think it's a super important one. I mean, for me, my overall gestalt answer for almost any question would have been shared decision-making, and it is here as well. I think it's going to be part of really understanding the nuances in efficacy, safety, tolerability, dosing. It's really a, it's the whole right package, so to speak, for any drug. You know, the current tools that we have are solid drugs, but they, you know, there's definitely still a lot of unmet needs. I would think of this very high-level first line versus second line and beyond. From a first-line perspective, you know, we still have a lot to learn. It may be that the best is yet to come in terms of some of the potential for remissive effects and longer-term benefits in terms of the persistent Treg populations, et cetera. It is going to come down to, you know, certainly efficacy, you know, at modest endpoints, deeper endpoints, that stability of control, dosing, dosing really in the longer term. The induction period, we are less concerned about, but really in the longer term, what that kind of maintenance dosing would look like versus potential for eventually discontinuing drug. I think there is a lot there. In terms of safety and tolerability, you know, let's say, for example, the type two blockers, you know, overall well tolerated, but there have been adverse events that have been reported. There are issues that come up with conjunctivitis, et cetera. Having a drug that doesn't have or doesn't at least seem to have any of those type two class-wide side effects becomes important both as a first-line consideration when discussing shared decision-making, but also as a second-line consideration because, you know, would I want to go from one type two blocker to another type two blocker down the road if I've got a novel MOA that shouldn't give me any of those type two side effects? If I had a patient already experience them with one, likely not, right? It gives me an opportunity to switch to a novel class. I think there's, you know, there's so much more to discuss about this, but at a high level, I think when you've got a good balance of efficacy, safety, dosing, potential remissive effects, that's giving you a lot to discuss with patients in that shared decision-making conversation. Yeah. Thank you for taking that one first, Jonathan. That's a very, very expansive question to answer. In two minutes, how do you prescribe all the treatments? You know, I think you can look at for some analogies in psoriasis that many of us will use all of the different treatments first line. I think that's probably going to be true with the AD treatments where all of them will be used in some capacity first line. Dupilumab is not going away. You know, that is still a well-beloved drug in dermatology. I think that there is value in looking at the medicine for both first and second-line use. It is going to be about shared decision-making. What does the patient value? If it pans out that this has, you can use infrequent dosing, well, that's going to be very advantageous to a group of patients. If there's deeper responses, again, that is also important. I think we want to learn more about the medicine, especially from the phase three to really decide where it's placed. However, Jonathan's absolutely right. It's shared decision-making is the right answer. Thank you. I think your next question, Andy, was about the approach now that we've observed that there was no softening of efficacy in the patients with baseline severe disease. That's something that we're definitely going to explore. I mean, we know that, for example, even for Dupixent, the dose that's used actually has less activity in patients with baseline severe disease. That's the approved, you know, approved dose that's on the label. We know that there is an unmet need and that there's a different, you know, different level of quality of care in patients that are baseline severe. That is something that we will be looking to really understand in our future regulatory and other positioning and market access approaches. Your last question was about a peak of efficacy. I think for us, like, you know, we are really collecting data, right? I mean, what we are really excited about was between what we learned in this study over the induction and what we learned in the phase one study from the off drug maintenance is that, I mean, we could really get patients to a pretty deep state of efficacy when they are treated in this kind of an induction regimen that the Q2 week has shown. I think this is one of the still stay tuned kind of parts of this story, as the doctors have mentioned. We are very, very eager to look at the results of the maintenance in the early part of next year. Great. Thanks for the questions, Andy. This concludes today's Q&A session. I will now turn it back to Howard for closing remarks. Thank you, everyone, for joining us this morning. I am very proud of the Nektar team and their hard work in developing a new and important mechanistic approach. I also want to thank our shareholders for their continued support. Of course, I want to thank Dr. Silverberg and Dr. Rosmarin for all their great help and advice. Stay tuned for alopecia areata results later this year. Thank you very much.