Nektar Therapeutics (NKTR) Earnings Call Transcript & Summary

Ladies and gentlemen, thank you for joining us, and welcome to Nektar Therapeutics EADV Analyst and Investor Event. [Operator Instructions] I will now hand the conference over to Vivian Wu, Investor Relations and Corporate Affairs. Vivian, please go ahead.

Thank you, and good morning, everyone. Thank you for joining us today to discuss new data being presented at the EADV 2026 Congress. On today's call, we expect to make forward-looking statements regarding our business, including statements regarding the potential of and future development plans for rezpegaldesleukin, the timing and plans for future clinical data presentations and other statements regarding the future of our business. Because forward-looking statements relate to the future, they are subject to uncertainties and risks that are difficult to predict, many of which are outside of our control. Our actual results may differ materially from these statements. Important risks and uncertainties are set forth in our most recent annual report and quarterly report on Form 10-Q 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. Today, you will hear from Dr. Jonathan Zalevsky, our Chief Research and Development Officer; and Dr. Mary Tagliaferri, our Chief Medical Officer. We're also joined today by Dr. Benjamin Ungar. Dr. Ungar is an assistant professor of the [ Walden ] Department of [indiscernible] at [indiscernible] Medicine at Mount Sinai and an expert in this field. We are very glad to have him with us here today. With that said, I would like to hand the call over to our Chief Medical Officer, Mary Tagliaferri. Mary?

Thank you, Vivian. At Nektar, our strategy has been to advance the first-in-class regulatory T cell or Tregs mechanism to address the underlying biology of autoimmune and inflammatory diseases. Rezpegaldesleukin, also known as REZPEG, is a first-in-class IL-2 pathway agonist designed to selectively expand regulatory T cells. With Tregs, we can address multiple inflammatory pathways at once, including TH1, TH2, TH17, Th22, JAK STAT and others, which drives the efficacy and resolves the symptoms and underlying heterogeneous pathology of the disease. This is in contrast to therapies that only target Th2 disease pathways. Our REZPEG development program is addressing three distinct autoimmune diseases, Atopic Dermatitis, Alopecia Areata and type 1 diabetes, each of which represents a substantial commercial opportunity. Alopecia Areata affects roughly 160 million people worldwide with approximately 30 million new cases diagnosed every year. The only class of systemic medicine approved our oral daily JAK inhibitors, which have significant drawbacks. JAK inhibitors possess box warnings and they are also associated with high relapse rates after patients stop treatment. We believe this provides a significant opportunity for Nektar to advance REZPEG as the first biologic to be approved to treat these patients offering potentially better safety and efficacy, which could improve our time with continued treatment. Additionally, JAK inhibitors are taken orally once daily, which can present challenges for long-term drug adherence. A therapy with less frequent dosing makes long-term treatment more manageable for patients. Beyond adherence, a therapeutic option, which has an extended biologic pharmacodynamic effect can offer durable and stable efficacy even in the setting of imperfect compliance. There also remains an opportunity for a therapy that reduces or eliminates the routine labor and long-term requirements associated with JAK inhibitors. Finally, an option that offers a more straightforward market access with broader eligibility to greatly benefit patients. These parameters, if met, could provide physicians with an alternative to JAK inhibitors and redefine first-line systemic treatment in Alopecia Areata. And we believe that REZPEG novel Tregs mechanism has the potential to address these major unmet needs. Shown here findings presented at the 2026 AAD meeting from external analysis of Symphony claims data, evaluating treatment patterns of patients treated with approved JAK inhibitors. These results demonstrate that most patients are initiated and treated with low-dose [ baricitinib ]. The data also demonstrate poor persistence on therapy with most patients discontinuing treatment within the first 6 months. We designed the treatment period of the Phase IIb REZOLVE-AA study to answer four important development questions for our Phase III study design. First, can a Treg cell directed biologic provide meaningful efficacy with a robust safety profile? And the answer to this first question is yes. REZPEG demonstrated consistent separation from placebo across efficacy measures valuated with the safety profile consistent with prior studies. Second, because we haven't completed any prior trials in AA, we wanted to understand the kinetics of hair regrowth. What the trial showed is the greatest increase in hair regrowth occurred after week 16 and continued beyond the initial 36-week induction period. Third, we asked what dose should be advanced to the registrational trial. And based on the data, the 24-microgram per kilogram Q2 week regimen has been selected for our Phase III clinical trial. Finally, we needed to determine how long the induction period should date. The additional responses observed from week 3 to 6 and to week 52 in the treatment extension cohort support the 52-week Phase III induction period for the evaluation of the SALT score of 20 or less, which is the registrational end point. As a reminder, our Phase III REZOLVE-AA trial enrolled 92 adult patients with severe to very severe Alopecia Areata. The current episode duration was up to 8 years. Patients receive treatment every 2 weeks with subcutaneous REZPEG 24 micrograms per kilogram, 18 micrograms to kilogram or placebo. Unlike a traditional maintenance phase of an atopic dermatitis trial where responders advance to additional weeks of treatment. This study included a blinded 16-week treatment extension for patients who demonstrated hair growth but have not reached SALT 20 or less at week 36. This created a total treatment period of 52 weeks for the extension cohort. We previously announced in April the 52-week treatment data from the study. Today, we are presenting the 6-month off-treatment data. This slide shows the SALT 20 responses over time to REIT 52 for the entire enrolled patient population. Recall [ CLT20 ] corresponds to at least 80% scalp hair coverage and represents a clinically meaningful endpoint. The central observation is that the REZPEG response curve continued to rise through the week 52. It does not plateau. These data support that extended treatment beyond 1 year could result in additional gain in SALT 20 responses. On the right side are the corresponding 52-week time points for low dose [ baricitinib ] from the brave registrational studies. We achieved our goal of a similar response rate compared to low dose [ baricitinib ] at 52 weeks for the key SALT 20 registrational endpoint. With comparable clinical benefit to a low-dose JAK inhibitor, plus twice monthly dosing and a more favorable safety profile, it's easy to see have rested to become the first biologic used as first-line therapy for Alopecia Areata. This previously reported analysis shows patients who completed 52 weeks of treatment, 8 new patients treated with breast peg converted to SALT 20 among the 27 REZPEG treated patients in the 52-week treatment cohort. The new response rates were 29% in the 18 -- microgram group and 31% in the 24-microgram group. No new SALT 20 responses were observed in the four placebo patients. Here, we present for the first time a new analysis from the 52-week treatment cohort. For context, duration of the current Alopecia Areata episode is considered an important prognostic factor with longer continuous episode established as a more difficult-to-treat patient population. In this cohort, REZPEG achieved similar week 52 SALT 20 response rates regardless of current episode duration with comparable outcomes observed in patients with episodes shorter than 4 years, and those with episodes of 4 years or longer. You can see the response rates were 29% and 30%, respectively. Approximately 37% of the REZPEG treated patients had a current continuous episode of at least 4 years. While the subgroup sizes are small, these results suggest that clinically meaningful hair regrowth was not limited to patients with a shorter duration of disease. And looking at current episode duration with low dose [ baricitinib ] you can see a clear difference between the two cohorts. Patients whose current episode is 4 years or longer, achieved a lower SALT 20 response than those who curse current episode is shorter than 4 years. Now let's look at the off-treatment durability. In this trial, we followed all patients for up to 6 months of treatment. We believe this was particularly relevant to evaluate because REZPEG Treg-directed biologic that enhances endogenous immune regulation rather than simply suppressing a downstream inflammatory signal. Shown here is the durability data for both the 4-month and 6-months off-treatment period for patients who received 52 weeks of treatment in a stent. For 4-months or 6-months off-treatment, you can see highly durable efficacy with REZPEG, with 75% of patients maintaining a SALT 20 response at 4 months and 63% maintaining the SALT 20 responsive 6 months. For context, we have shown here the historical data for low dose [ baricitinib ] also at 4 months and 6 months of treatment. These patients in the [ baricitinib ] studies also received 52 weeks of treatment prior to being followed off treatment. You can see that only 30% of and 20% of patients on low-dose [ baricitinib ] maintain SALT 20 at 4 months and 6 months, respectively. This notable sustained salt response of treatment is consistent with our findings in atopic dermatitis. These data support less frequent monthly and quarterly dosing as for 52 weeks of rested induction treatment in Alopecia Areata, and this will be incorporated into our Phase III long-term extension study. The proceeding analysis used the stringent SALT 20 or less threshold shown here is an analysis that asks a broader question. Do patients preserve the debrief par growth they had achieved by week 52, when evaluated 6 months after withdrawing from risk had treatment. Among the 21 patients who completed 52 weeks of treatment, and had observed data at the end of the 6-month follow-up. Nearly half of the patients maintained or grew additional hair 6 months off treatment. These findings, coupled with the SALT responses, suggests that treatment with REZPEG leads the restoration of immune tolerance and subsequently durable immune responses. Now this waterfall plot provides a patient-level view of hair regrowth of patients in the 52-week treatment cohort. During the 6-month off-treatment follow-up 41% of patients achieved a deeper best response than they had achieved during active treatment and 22% maintain care growth. Taken together, 63% of patients experienced either additional hair growth or maintenance of their prior best response during follow-up. The important takeaway here is twofold. First, response to REZPEG did not simply erode across the entire patient population when treatment was stopped. And second, many people continue to regrow hair in the off-treatment period. Now shown here is what happens when we look at deeper responses such as Salt 10, which represents near complete scalp hair regrowth. On the left side, at week 52, 7% of the 27 extension patients had achieved SALT 10 or less. 6 months after treatment ended, that portion almost tripled to 19%. Three patients with SALT 20 score at week 52, converted to SALT 10 for during follow-up, demonstrating a deepening of clinical responses after treatment discontinuation and suggesting durable biological activity. Now on the right side of the slide, we are presenting historical [ baricitinib ] provide context for these results for REZPEG. Among [ baricitinib ] treated patients who achieved a SALT 20 after 1 year on treatment, only 10% had a salt 10 at 6 months after treatment discontinuation. To contrast that, among REZPEG-treated patients who achieved the salts for 20 at week 52, 63% had a SALT 10 at 6 months after treatment discontinuation. From a safety perspective, the 52-week safety findings remained consistent with the previously reported breast safety profile. Importantly, no increased risk or safety signal was observed for oral herpes, [ congenicabitis ], facial slowing [indiscernible], aptos ulcers, myocardial infarction, pulmonary embolism, deep vein thrombosis or malignancy. No adverse events were observed that will require routine laboratory testing and monitoring. This favorable safety and monitoring profile is particularly relevant for our chronic dermatologic disease and may represent an important point of differentiation from oral JAK inhibitors. Now the photograph shown here are from a 40-year-old man whose response continued to improve with extended treatment beyond the original 36-week induction period. We previously presented this case in April when he had already demonstrated meaningful hair regrowth. Following an additional 16 weeks of treatment, the patient experienced a further 63% improvement in SALT score by week 52. Importantly, the clinical benefit did not plateau when treatment stopped. During the 6-month off-treatment follow-up, the response continued to deepen, improving from a SALT 20 at the end of 1-year treatment to a SALT 10. This case illustrates that continued treatment and further enhance clinical responses and that those gains may not only be maintained but can continue to improve even after REZPEG is discontinued. This second case highlights a similar pattern of continued improvement in durable efficacy in a patient with a much longer history of disease. The patient had been living with Alopecia Areata for 13 years prior to treatment and received REZPEG 24 micrograms per kilogram for 52 weeks. At week 36, the patient's SALT score remain 24 including that assault in response had not yet been achieved by the end of the original induction period. However, with an additional 16 weeks of treatment, the response improved substantially by week 52 and then continue to deepen during the 6-month off-treatment follow-up period ultimately [indiscernible]. This case is particularly noteworthy given the patient's age, at age 64, she represents a population where JAK inhibitors are less desirable because of age-related comorbidities including hypertension, [ hyperlithidemia ], obesity and diabetes. Despite a long-standing disease history, the patient achieved a durable SALT response with near complete scalp pay regrowth that was maintained and further improved 6 months after discontinuing reset. Importantly, this case underscores the potential for REZPEG to provide meaningful, durable clinical benefit in patients with limited treatment options. Now closing for clinical data, let's review the highlights from the study. First, REZPEG demonstrated consistent efficacy through 52 weeks and the response curve continued to rise beyond week 36. Second, efficacy of patients treated for a year was similar for individuals with a current episode shorter than 4 years or longer than 4 years with SALT 20 response rates of 29% and 30%, respectively. Third, as just mentioned, the safety profile remains assisted with prior studies with no new findings during the 16-week extension and a low adverse event discontinuation rate. Fourth, longer treatment was associated with greater off-treatment durability. 6 months after the last dose, 63% of week 52 SALT 20 are less responders maintain that response. Fifth, responses did not nearly persist. Some continue to deepen after treatment ended with SALT 10 or less increasing from 7% at 52 to 19% 6 months later. Finally, these fine teams support the planned Phase III strategy of advancing REZPEG, 24 micrograms per kilogram every 2 weeks for an induction period of 52 weeks as well as evaluation of a less frequent monthly or quarterly maintenance dosing and responders. The Phase III [ ZENICH-AA ] trial is planned to enroll approximately 850 patients and initiated in early 2027. Collectively, these data support REZPEG as a potentially differentiated first-in-class Treg-directed biologic for severe to very severe Alopecia Areata combining meaningful clinical activity, durability after withal and a favorable safety profile. With that, I'll hand the call over to JZ to discuss the biomarker findings from the Phase III REZOLVE-AD study in patients with moderate to severe Atopic Dermatitis. JZ?

Thank you, Mary. Switching gears, I'll be talking about the biomarker sub study we conducted in the Phase IIb REZOLVE-AD study in patients with moderate to severe Atopic Dermatitis. Now let's first look at the initial translational data we presented a year ago. Here, we show a clear objective and meaningful neurological impact of REZPEG on lowering key TH2 inflammatory markers associated with Atopic Dermatitis. We observed dose-dependent reduction in IL-19 TARC, which is also known as CCL17 and Perry Austin in MDC, which is also known as CCL22. These are the absolute mean reduction from baseline to week 16 in patients that had baseline levels of these markers above the upper limit of normal. And as you can see, we saw a dramatic decrease in CCL22, one of the key products for the CCR4 receptor and dose-dependent reduction at week 16 for CCL17 the other [ chemokine ] ligand. In contrast, placebo patients showed increased levels of CCL17 over a 16-week induction period. And consistent with our profile, we saw dose-dependent decreases in serum IL-9 in [ periostin ] a key marker present in the lesions of patients with Atopic Dermatitis. Our PK and PD profile is consistent with prior studies of REZPEG. We saw up to a sixfold increase in Tregs at the high dose of that study which is very similar to what we observed with the same high dose level in regimen in our Phase Ib study. Now I'd like to briefly discuss some of the highlights from yesterday's late-breaking presentation from Dr. Emma Guttman-Yassky lab is Mount Sinai. Emma's Lab conducted [ transcriptomic ] and [ proteomic ] analysis of skin tape strips and matching blood samples. So let's turn to that talk and briefly profile the disease. Atopic Dermatitis is a chronic inflammatory skin disease characterized by T cell-mediated immune disregulation, highly impacting patients' quality of blood. Although current biologics effectively target Type 2 inflammation, more than 50% of adults report inadequately controlled disease despite treatment, underscoring the complexity of treating this heterogenous disease and leaving a major unmet need for a novel approach to immune modulation. As you know, REZPEG targets the IL-2 receptor complex to preferentially stimulate the proliferation of Tregs, thus working as a master immune modulator upstream of the pro-inflammatory cytokine pathways and other currently available therapies. The Phase IIb REZOLVE-AD study enrolled 393 biologic-naive patients with active moderate-to-severe Atopic Dermatitis. For the 16-week induction treatment period, patients were randomized to receive 1 of 3 dose arms of REZPEG or placebo. The primary endpoint and secondary endpoints were assessed at week 16 at the end of the induction period and these results were recently published in the [ Lancet ]. Emma's Lab conducted a biomarker substudy analyzing samples taken from the induction portion of the study from patients in the high 24-microgram per kilogram Q2 week dose that we're taking into the Phase III as well as their comparison to samples from the placebo group. Tape strips were collected from lesional skin and blood samples of 100 patients, 59 in the high dose and 41 in the placebo. And shown here are the study methods and objectives. Samples were collected at baseline and at weeks 2 and 4, while clinical assessments were conducted at baseline in every 2 weeks through week 16. The analysis was designed to profile gene protein expression in the same serum during the first weeks of treatment and to assess whether early molecular signals were associated with later clinical outcomes, further allowing us to identify correlations between REZPEG dosing, pharmacodynamic changes seen in blood and tissue and the correlation of those to each other as well as their correlation to the clinical efficacy of REZPEG in this indication. Patients in the REZPEG and placebo arms were well balanced throughout demographics and baseline design characteristics. The mean reduction from baseline in EASI in week 16 was 64% in the biomarker substudy population. Consistent with the 61% reduction observed in the overall 24-microgram per kilogram Q2 week cohort in the entire study population. These results from the biomarker substudy showed a broad [ transcriptomic ] response in skin as early as week 2. REZPEG induced rapid Tregs associated molecular changes including significant upregulation of FOX P3 and IL-2 receptor alpha genes as early as week 2 of treatment as compared to baseline and as compared to placebo. We also saw concurrent modulation of multiple immune pathways, which are dysregulated in Atopic Dermatitis and a notable magnitude of difference between REZPEG and placebo by week 4. These results are very consistent with REZPEG's agonistic mechanism of action. [ Transcriptomic ] and proteomic analysis demonstrated significant systemic and cutaneous normalization across multiple immune pathways, including TH1, TH2, Th17, Th22 and the JAK-STAT signaling pathways. And these normalization responses across multiple immune pathways were also seen in the proteomic networks as early as week 2 of treatment as compared to baseline. Importantly, these changes included early modulation of key disease-associated T helper inflammatory pathways, including fibrosis and tissue remodeling biomarkers that further deepened by week 4. Proteomic analysis also demonstrated significant improvements in cardiovascular atherosclerotic and alopecia area of signatures as compared to baseline or placebo. And these results are consistent with REZPEG's broad Treg targeted agonist profile. Finally, we looked at correlations between these early biomarker signals and subsequent clinical responses at the end of induction. And we see that early serum biomarker changes at week 2, including increases in IL-10 and TGF-1 expression and reduction in CCL17 park expression were associated with subsequent easy improvement at week 16, linking early molecular effects with later clinical responses. Correlations between early biomarker changes and week 16 easy improvements were statistically significant in the REZPEG treated patients, but not in the placebo-treated patients. In conclusion, REZPEG induced rapid Tregs associated molecular changes with concurrent modulation of the complex immune disregulation underline atopic dermatitis. These changes demonstrate the breadth of REZPEG effect on different inflammatory pathways, which span both direct immune targeting and disease resolving mechanisms. So taking a step up to 10,000 feet, these translational data provide to us a scientific framework for how the REZPEG mechanism of action addresses disease pathology through causal biology, and how it can result in deep and durable responses that persist for months after dosing is completed. With today's data, we now have multiple examples of off-drug durability in two different diseases. Our 9-month off-drug results in our Phase Ib study in patients with Atopic Dermatitis that will be published in 2024. And now today, the 6-month off-drug durability we reported in patients with Alopecia Areata. This highlights the unique and what we believe to be transformational properties of REZPEG. On this theme, we look forward to the 52-week AC treatment data from our Phase IIb Atopic Dermatitis study that we will report in the first quarter 2027. And with that, I'd like to turn the call over to Dr. Ungar to share his perspective on both the REZOLVE-AA 6-month off treatment durability data and the biomarker findings from the REZOLVE-AD induction period. And Dr. Ungar, we would welcome your insights on the clinical significance of these results. And what they may tell us about the potential of REZPEG in restoring immune balance and delivering durable patient benefit. Benjie?

Hi everyone, absolutely. So I'll get started with the REZOLVE-AA [indiscernible] -- excuse me, durability data. So just as a reminder to everyone who's listening about the disease of Alopecia Areata. It is -- and I think any conversation about drugs to treat Alopecia Areata really need to keep this in mind. Alopecia Areata is a hugely monumental condition for patients suffering from it and treating it is very, very crucial, and patients are very, very motivated. The impact of the disease on patients who suffer permit can be negatively transformative and successful treatments conversely could really influence our lives in a dramatic ways. . One of the challenges with Alopecia Areata is that clinical responses improve how people feel. But for many cases, there is still this kind of fear that hangs over patients' minds that they will lose response whether that be because a drug stops working, whether that be because they lose access to the medication, if there are life circumstances that lead to delays in having the treatment or they have to be off of it for some reason, and that can have a huge impact. And when patients subsequently lose hair, it really sets things back by months or even years because it takes time for the hair to regrow. Because of that, one of the key factors that I and many of my colleagues look for in terms of treatment and thinking about treating patients long term is if responses are durable and if there is some level of confidence that if we continue treatment and stay on track that they'll maintain responses. Because of all of what I just said, the idea that we have responses that are maintained or in some cases, even improve off of treatment for the -- over the course of months, in this case, 6-months follow-up is very encouraging. And I think in general, as we collect more data on exactly this question, the more confidence that we have that there is the ability to maintain responses. If life gets in the way and people are not strict in terms of dosing for reasons they may be out of their control. I think that would be very, very encouraging for patients and just treating them. My initial response to the REZOLVE-AD biomarker data is also encouraging as well. So one of the things that we have seen very consistently in inflammatory skin diseases and probably even more so specific to Atopic Dermatitis is that biomarker changes with treatments are much more strongly predictive of clinical responses than other clinical responses in many ways. The sensitivity of biomarker assays is much greater than the clinical responses and changes occur earlier and more clearly definable. And so from my perspective, whenever I see a new treatment or a treatment used in a new area, the question that I want to see is are we seeing molecular changes that are consistent with what we would expect clinical responses to look like? And in short, we are seeing that here with REZPEG and that provides to me a lot of confidence that the drug is addressing the underlying biology. And in general, once we see changes in underlying biology that we are looking for to normalize disease pathology then we have a lot more confidence that the clinical responses are going to be extrapolated in a much more significant way. So again, the biomarkers are something that I'm always looking for actually for drugs and seeing the changes gives me a lot of confidence that we're going to see continued clinical responses that again extrapolate from what we've seen so far.

Great. Thank you so much, Dr. Ungar for your thoughts. And operator, we can now open the presentation for questions.

[Operator Instructions] Your first question comes on the line of Yasmeen Rahimi from Piper Sandler. Please go ahead. A reminder to unmute yourself locally. If you are wanting to ask your question. We will move on to our next question. Your next question comes from the line of Julian Harrison from BTIG.

Congratulations on all the updates here. limit itself to one question. And what I'd love to get your perspective on more is any read-through to REZPEG remitted potential in Atopic Dermatitis. I understand you have Phase Ib results already providing some evidence of a [ remit ] of effect in atopic derm. But what would maybe be a win in your mind in terms of duration of responses off drug in the data you plan to share next year? .

Julian, it's Mary. Thank you for the question. I think right now, the way we look at it is we have three different studies now that show strong durability of effect. When you go back to our Phase Ib data and the nature of communications paper, we dosed patients for 12 weeks. And then in atopic dermatitis, patients who have very severe -- moderate to severe disease. And when you remember, we then followed them for 9 consecutive months of treatment. And those patients who had a [ EC75 ] response, 71% maintain their [ EC75 ] 9 months off treatment and 80% maintain their [ VIGA ] off-treatment. And then we did our large Phase IIb study. And in that study, when we looked at the maintenance cohort after 16 weeks of induction and then follow those patients for through to 52 weeks, even on the Q12 week dosing where patients only had 3 doses, we had 83% of patients maintain their [ EC75 ]. And now the Alopecia Areata study, we have a third trial to show this durability of effect. So I think when we unblind the data from the Phase II, we're going to want to see that those patients with the EC75 in particular, the primary efficacy endpoint for registration that they -- with a high proportion can maintain that EC75. And I think we go into those data optimistic with these three different distinct clinical trials showing this level of durability after cessation of treatment with restage. So thanks for the question, Julian. And we look forward to sharing the data with you.

Your next question comes from the line of Yasmeen Rahimi from Piper Sandler. Your line is open. Please go ahead. .

Team, can you hear me?

Yes.

I am so sorry for the technical difficulties in creating -- to my colleagues you guys. Team, obviously, this data is absolutely outstanding. How has it changed your view in terms of the inclusion, exclusion of the patients that you'll be enrolling and I know it seems like from the prepared remarks that maybe there's not a modification to the Phase III but I would love to give this new data onset, especially when it comes to the continued response you're seeing, if you expect that? And then a second quick question that we've been getting from clients is like -- have you seen a deepening of response depending on whether it's on SALT 10 or SALT 20 based on time of diagnosis. Thank you again, and sorry for my technical interruptions.

Yes. Great. Thank you so much for asking the question. So what we're excited about in our 850 patient Phase III study is we will be enrolling patients who are JAK inhibitor naive and patients who have previously experienced been on a JAK inhibitor as well as adolescents. So when we think about the label, it's a broader label. And then with respect to some people have run clinical trials where they only look at patients that have an episode of their Alopecia Areata that's less than 4 years. And our data now provides the confidence that we can, again, address a patient population up to 8 years of a current episode. So that was very exciting for us as well. And then in terms of the time of diagnosis, you just saw that we shared with you this man aged 64 who had a diagnosis of 13 years, and she did quite well. So we do believe that we will be able to address patients both who have had a longer history of Alopecia Areata as well shorter. And then again, in our trial, we did enroll patients that were both severe as well as very severe. And so we're feeling very optimistic going into the Phase III, one, that we can treat a broad patient population with REZPEG, and two, that we really have identified the proper schedule on the proper dosing and proper induction period to have a very competitive first line treatment for the disease. So thanks a lot, yes, for the question.

Your next question comes from the line of Samantha Semenkow from Citi.

Congratulations on this great data update. My question is just about the greater response durability you seem to see with the patients that were treated through week 52. I'm wondering, just broadly, when you look on a patient level, is there a correlation between the amount of time a patient spends a SALT 20 responder or in any response for that matter and the magnitude of the durability benefit that they received off treatment? .

Yes, it's a great question. We have saved data to share in a publication, Sam. And I think you're touching on a really great point that if a patient reaches a stable SALT 20, meaning that in the 52-week time frame, they had achieved to SALT 20 or more than one time point. while they were in the 52-week period. And we did find that those patients have greater durability. And so when we do look at our open-label extension, we can really hone in on those patients with a stable SALT 20 and really look at this longer maintenance still seeing look at 12 weeks as opposed to just even a monthly, so we're really excited about that. I will say in terms of magnitude of benefit, we're seeing a diverse group of patients achieving a deep magnitude of benefit. And so I think when we have data from 850 patients, we'll be able to look further in these subgroups, and you have a good sense. But I think going into the trial, what we're excited about is both if you had a current episode of less than 4 years is greater than equal to 4 years we see analogous efficacy, which you don't see with the [ analogous baricitinib ] and that gives us a lot of confidence, too, about being able to treat both patients with a poor prognostic factor as well as those patients who have been easy to treat. And again, you brought it up, too, we really firmly believe the 52 weeks leads to improved immune tolerance and is the right time frame for our induction period in the Phase III program. So thanks for the great question.

Your next question comes from the line of Jialiang Liang from Jefferies.

Thank you for hosting this call and congrats on all the updates at EADV. There were quite a lot. It's great to see you guys. I have a question for Dr. Ungar, if he's still on. Just based on this new data, based on the totality of data for the alopecia program. Can you tell us more about the specific types of patients that you see REZPEG being a natural fit for in your practice?

I'm sure. I'm happy to in on that. So when I'm thinking about treating patients, it's a conversation and an evaluation that's holistic that has to factor in their comorbidities, their risk factors, the impact of their hair, their goals, and importantly, thinking about this as a chronic condition that requires ongoing treatment certainly in the current paradigm that we have. Patients are very motivated to have their hair regrown and to maintain it, and they, therefore, are really looking for treatment very, very commonly and really willing to go ahead with that. Now with that said, there is also a balance of safety considerations and risks involved that factor into really any treatment, let systemic treatment. And that's part of the conversation that we have. Based on the data that we see so far in the Phase II in terms of the magnitude of clinical responses, in combination with the safety profile that we're seeing and now adding to the mix, this potential for kind of sustained responses even with gaps in treatment. I guess the answer is it's hard to see I mean who wouldn't be a candidate for this kind of approach is a short answer. I don't know that I see any patient for whom this wouldn't be a strong consideration.

Your next question comes from the line of Tara Bancroft from TD Cowen. Please go ahead. . And just a reminder to unmute yourself locally, if you are wanting to ask a question. We will move on to the next question that comes from Arthur [ Hee ] from H.C. Wainwright.