Ladies and gentlemen, thank you for joining us, and welcome to the Nektar Therapeutics Analyst and Investor event to discuss REZOLVE-AA 52-week top-line results from the extension treatment period. After today's prepared remarks, we will host a question-and-answer session. If you would like to ask a question, please raise your hand. If you have dialed into today's call, please press star nine to raise your hand and star six to unmute. I will now hand the conference over to Vivian Wu, investor relations and corporate affairs. Vivian, please go ahead. Thank you, and good morning, everyone. Thank you for joining us today. Today, you will hear from Howard Robin, our President and Chief Executive Officer, Dr. Jonathan Zalevsky, our Chief Research and Development Officer, and Dr. Mary Tagliaferri, our Chief Medical Officer. We're also joined today by our panel of experts in dermatology and alopecia areata, who will join us in Q&A, Dr. Jonathan Silverberg, Dr. David Rosmarin, and Dr. Benjamin Ungar. On today's call, we expect to make forward-looking statements regarding our business, including statements regarding the therapeutic potential of, and future development plans for rezpegaldesleukin, the timing and plans for future clinical data presentations, and other statements regarding the future of our business. Because forward-looking statements relate to the future, they are subject to uncertainties and risks that are difficult to predict, many of which are outside of our control. Our actual results may differ materially from these statements. Important risks and uncertainties are set forth in our most recent annual report on a Form 10-K, available at sec.gov. We undertake no obligation to update any of these forward-looking statements, whether as a result of new information, future developments, or otherwise. A webcast of this call will be available on the IR page of Nektar's website at nektar.com. With that said, I would like to hand the call over to our President and CEO, Howard Robin. Howard? Thank you, Vivian. Good morning, everyone. We're very pleased this morning to share the exciting top-line results from the 16-week extension period of our ongoing REZOLVE-AA phase II-B study, which is evaluating rezpegaldesleukin in patients with severe to very severe alopecia areata. At Nektar, our strategy has been to advance a first-in-class regulatory T cell, or Treg mechanism, to address the underlying biology of autoimmune and inflammatory diseases. Rezpegaldesleukin, also known as rezpeg, is a first-in-class IL-2 pathway biologic designed to selectively expand regulatory T cells, also known as Tregs, to address the underlying biology of immune and inflammatory disease. Our phase II program currently spans three indications, each of which could offer significant commercial opportunity for rezpeg: atopic dermatitis, alopecia areata, and type 1 diabetes. With the transformative data today, we have now demonstrated that rezpeg can offer a truly meaningful clinical benefit in two different and distinct immune-mediated diseases. We will be initiating the phase III ZENITH-AD studies in atopic dermatitis around the middle of this year. If we're successful in phase III, we expect to report our first pivotal data in mid-2028 and to submit the first BLA filing for the program by the end of 2029. In February, we announced very strong 52-week data for rezpeg, including 36 weeks of once-a-month and once-quarterly maintenance therapy in patients with moderate to severe atopic dermatitis. Today, we will show the potential for rezpeg in patients with alopecia areata at 52 weeks of twice-monthly dosing. We believe a novel mechanism of action, which is distinct from the existing approved classes of IL-13 and JAK inhibitor medicines, is greatly needed by physicians and patients in both of these disease settings. Importantly, these two global markets alone are expected to reach close to $40 billion over the next five years. Finally, through our collaboration with TrialNet's type 1 diabetes consortium, rezpeg is also being evaluated in new-onset stage 3 type 1 diabetes, further extending the reach of this mechanism into another autoimmune disease setting. The phase II study is sponsored and funded by TrialNet, and we expect initial data from this trial in 2027. The TrialNet study is evaluating rezpeg's ability to preserve beta cell function in patients with stage 3 new-onset type 1 diabetes. Currently, Tzield is the only agent approved to treat new-onset type 1 diabetes, and although it represented a breakthrough for patients at the time of its approval, it carries a risk of cytokine release syndrome and infection and requires daily intravenous administration challenges. We're hopeful that rezpeg could offer a potentially better option for these patients and look forward to seeing the results from this trial. Look, as I said earlier, we have now demonstrated rezpeg has shown meaningful clinical efficacy in atopic dermatitis and alopecia areata, and this sets the stage for the use of this novel Treg mechanism in other immune and inflammatory disease settings. With that, I'm going to turn the call over to JZ. JZ? Thank you, Howard. I'd like to spend a few minutes talking about the opportunity to help patients with alopecia areata and reviewing the mechanism of Treg biology in this disease setting. Alopecia areata affects roughly 160 million people worldwide, with approximately 30 million new cases diagnosed every year. The only class of systemic medicines approved are oral daily JAK inhibitors, and as a result, there remains a major unmet need in this indication for safe and durable therapeutic options. These agents carry multiple box warnings and are also associated with high relapse rates after patients stop treatment. In spite of that, because of the patient need, the sales of JAK inhibitors are expected to grow significantly by 2033. We believe this opens 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 over time with continued treatment. We know many physicians and patients are seeking alternative first-line treatment options for patients with alopecia areata. Here, we present the scientific perspective of how we believe Tregs are addressing the disease pathology behind alopecia areata. In healthy individuals, the hair follicles are in an immune privileged state, meaning that they suppress immune responses, thereby protecting themselves. In alopecia, however, this immune privilege is lost, leading to an immune-mediated attack on the hair follicle, and ultimately resulting in hair loss. Rezpeg targets and proliferates Tregs, which play a central role in maintaining immune tolerance. By enhancing Treg function, rezpeg can help restore the immune balance to once again protect the hair follicle from immune attack, halting hair loss and supporting hair regrowth. This slide shows published results from an anonymous survey of 131 board-certified dermatologists and underscores that the majority of doctors would consider alternative therapies for alopecia areata before initiating a JAK inhibitor. They cited primary factors including boxed warnings, routine safety monitoring, extensive testing, and high rebound rates upon cessation of therapy. Taken together, these findings highlight a clear need for additional therapeutic options, particularly those that can offer differentiated safety profiles and improved durability of response. Shown here are findings presented at AAD from an 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 2 mg baricitinib, and the data also demonstrate poor persistence on therapy, with most patients discontinuing treatment within the first six months. The persistence was even shorter among patients who stayed on baricitinib 2 mg treatment, with median duration of time on therapy approximately 3.7 months. This poor persistence tells us that there remains a significant unmet need for effective treatment options. We believe there are several factors that lead to the challenges with JAK inhibitors being used more widely. We've already mentioned the safety concerns and the box warnings that limit JAK inhibitor use, and additionally, JAK inhibitors are taken orally once daily, which can present challenges for long-term drug adherence. A treatment with less frequent dosing could improve persistence on therapy. 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 routine laboratory monitoring that comes with prescribing JAK inhibitors. Finally, an option that offers a more straightforward market access with broader eligibility can 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. We believe that rezpeg novel Treg mechanism has the potential to address these major unmet needs. With that, I'll now turn the call over to Mary to discuss our findings from the phase II-B REZOLVE-AA 16-week treatment extension. Mary? Thank you, JZ. Before we dive into the findings, I'd like to briefly review the clinical trial design. As a reminder, our phase II-B REZOLVE-AA trial enrolled 92 adult patients with severe to very severe alopecia areata. Patients received treatment every two weeks with subcutaneous rezpeg 24 mcg/kg, 18 mcg/kg, or placebo. The primary and key secondary endpoints shown here were assessed at the end of the 36-week induction period. We reported on these data in December of last year. Now, let me explain the purpose of the blinded 16-week treatment extension. Unlike a traditional maintenance phase of an atopic dermatitis trial where responders advance to additional weeks of treatment, the alopecia areata study selected for the non-responders to continue treatment. The sole purpose of the extension was to determine if continued treatment with rezpeg beyond 36 weeks could yield a higher proportion of patients achieving a SALT 20, which is the FDA registrational endpoint. This was an important question to ask to determine if our phase III trial should have a 36-week or 52-week treatment interval. To this end, patients with a SALT score greater than 20 at week 36 of treatment, who also demonstrated hair growth, had the opportunity to enter the blinded 16-week treatment extension. All non-responding patients who crossed over to the extension period continued on their original dose assigned at randomization. Patients who achieved a SALT score 20 or better in the first 36 weeks of treatment were not eligible for treatment extension, and therefore completed dosing at week 36. Grasping this design element is essential to understanding why the trial is focused on the SALT 20 endpoint. From a statistical standpoint, when we're looking at week 52 endpoints today, we are carrying forward the patient data from the 36 weeks of induction for the patients who did not enter the extension. One last comment on this slide, later this year, we will have the blinded data for all patients observed for an additional 24 weeks off treatment, a period of time which will help us understand the maintenance dosing regimen for rezpeg beyond 52 weeks. As shown here, a total of 31 patients with a SALT score greater than 20 at week 36 entered into the blinded treatment extension period to receive 16 weeks of twice monthly dosing of rezpeg. Today's presentation will review data from these patients who completed the full 52-week treatment regimen and then analyzed the entire 52-week patient population. Again, the exploratory treatment extension was specifically designed to assess whether additional dosing beyond 36 weeks would enable more non-responding patients to achieve a SALT score of 20 or less. Remember, a patient with a SALT score of less than or equal to 20 has 80% or more hair coverage on their scalp. This is an important measurement because this is the registrational endpoint used in the U.S. for phase III approvals in alopecia areata. Now recall, as I just mentioned, we did not permit the best responders at week 36, those who achieved a SALT 20 or better, to continue on treatment. That said, there was one placebo patient with a SALT 20 who advanced to the extension because the investigator asked for special dispensation. When the decision was made, everyone was blinded to the patient's treatment arm. One other important point, given that SALT 20 responders did not continue on treatment, this study was not designed to evaluate deepening of responses as we did in our maintenance phase of the atopic dermatitis phase II-B study that we presented earlier this year. Ultimately, the extension period allowed us to confidently select the optimal dosing interval, 36 weeks or 52 weeks, for the phase III, as well as evaluate the safety for twice monthly dosing over 52 weeks. Now, drilling down into the extension phase of REZOLVE-AA, 13 patients continued on the 24 mcg/kg dose every two weeks, 14 patients continued on 18 mcg/kg dose, and four patients continued on placebo. Consistent with our primary goal for the extension period, we are presenting SALT score 20 results, as well as other dichotomous endpoints. Because not all patients who completed dosing at week 36 continued treatment, we are not presenting the continuous endpoint of mean percent change. With that introduction, the exploratory endpoints at week 52 that will be presented today include new SALT score 20 responders between weeks 36 and 52 for only those patients who entered extension. For the complete patient population presented in December, we will also report the overall SALT score of 20 or less at week 52 and the overall SALT score of 30 or less at week 52, which correlates to 70% or more hair coverage on a patient's scalp. In addition, we will look at the overall SALT 30 at week 52, which is a 30% improvement from a patient's baseline SALT, and overall SALT 50 at week 52, which is a 50% improvement in the baseline SALT score. Now moving to our findings. Let me first start by showing a waterfall plot that illustrates the overall deepening of response from all 31 patients who entered the blinded 16-week treatment extension period. On the left is the best SALT percent reduction for the 36-week treatment period, and on the right is the improvement seen for these same patients during the treatment extension out to 52 weeks of total treatment. These data unequivocally show that rezpeg-treated patients in the extension period achieved deepening of responses. At the end of 36 weeks of treatment, 4% of responders achieved a 75% or greater reduction in their baseline SALT score. After 52 weeks of treatment, 26% of patients achieved a 75% or greater reduction in their baseline SALT score. It's important to note that 94% of the patients who entered the blinded 16-week extension period completed treatment to week 52. This demonstrates that when patients understand the promise of rezpeg to grow hair, they will continue on twice-monthly treatment. Now looking at new SALT 20 responses in the 16-week extension, we're excited to share a total of eight new SALT 20 responses were seen in the 27 patients on the rezpeg arms, four in each treatment group. The low dose of 18 mcg/kg had 29% of the patients in that arm achieve a new SALT 20 response, and in the high dose of 24 mcg/kg, 31% of patients achieved SALT 20 responses. There were no new SALT 20 responses in the placebo arm. Now let's see how these 16-week results look across the entire study population. Shown here on the left are the data reported in December at 36 weeks of treatment, and shown on the right are the 52-week data. When we compare the SALT 20 response rates at week 36 and week 52, you can see that the percentage of responders increases from 15.6%- 27.6% with the additional 16 weeks of treatment. This rate for the high dose of rezpeg compared to placebo reaches statistical significance with a p-value of 0.049. Also note, no patient who achieved a SALT 20 score or better in the 36-week induction period relapsed while on treatment. You can see the slope of the curve has an upward trajectory without a plateau, so it is plausible that rezpeg-treated patients will continue to achieve benefit after a year of dosing. These data strongly support a 52-week induction interval for phase III and suggest that patients who stay on treatment can continue to do better and better over time. Now shown here are the 52-week time points for rezpeg and the results for low-dose Olumiant from the BRAVE registrational studies. Our goal was to achieve a similar response rate compared to Olumiant 2 mg at 52 weeks for the key SALT 20 registrational endpoint. These data show that rezpeg met the target product profile that we pre-specified at the outset of the study. With comparable clinical benefit to a low-dose JAK inhibitor, plus twice monthly dosing and a more favorable safety profile, it is easy to see how rezpeg could become the first biologic used as first-line therapy for alopecia areata. Now moving on to review a few additional exploratory endpoints. Here we present the proportion of patients achieving a SALT score of 30 or less, which represents 70% or more hair coverage on the scalp, as I mentioned earlier. On the left are the SALT 30 response rates from week 36, and on the right, you can see the improvement at week 52 across both cohorts. The high-dose 24 mcg/kg cohort saw response rates increase from 29% at week 36 to 35% at week 52, and this was statistically significant compared to placebo. Now shown here are the 52-week observations for SALT score 30 seen with Dupixent on the right, which is from a single-site, investigator-sponsored study with a similar number of patients enrolled as in REZOLVE-AA. As you can see, Dupixent has shown some promise in alopecia areata and even has a new Delphi consensus guideline recommendation to be used in patients with a history of atopic dermatitis and alopecia areata. Not surprising, in contrast to the SALT 20 graph, where the slope of the curve continues in an upward trajectory, you can see on this slide, with a lower threshold of efficacy, there is a plateau in the curve that begins around week 36. It is possible that with greater retention in the phase III trial, even this endpoint can reach a higher proportion of patients attaining at least a 30% reduction in their baseline SALT score. All in all, as clearly demonstrated, rezpeg has a very attractive profile. Here we are showing patients with a 50% reduction in SALT score from their baseline value compared to the same data for Dupixent. The comparison highlights the promise of rezpeg as a potential first-line biologic for alopecia areata. In summary, given the major unmet need for a safe biologic as an alternative treatment to JAK inhibitors, the totality of the data presented today support that rezpeg could be a real breakthrough therapy for patients with AA. Now moving to safety. Overall, the safety profile observed in REZOLVE-AA is consistent with previously reported studies. Patients in this study received every two-week treatment, with a proportion of them receiving treatment out to 52 weeks. This represents the longest twice-monthly dosing duration studied in the rezpeg program, and we are pleased to say that the safety profile remains very favorable, and there were no new safety findings. No patients discontinued treatment during the 16-week extension due to an adverse event, and nearly all AEs were mild to moderate in severity and self-resolve. The placebo-adjusted ISR rate was consistent with prior studies, and no patient discontinued due to an ISR after 52 weeks of treatment. There was also a lower frequency of ISRs observed over the longer dosing duration in the extension period, similar to what we saw in the atopic dermatitis 52-week treatment data. Importantly, the median time to ISR resolution was five days. Now, as a point of differentiation, there were no indications of increased risks associated with oral herpes, conjunctivitis, facial swelling or erythema, oral ulcers, myocardial infarction, pulmonary embolism, deep vein thrombosis, or malignancy. Importantly, the known AE profile of rezpeg should not require the extensive laboratory testing or monitoring typically associated with JAK inhibitors. Now I'd like to move on to case studies so you can see the significant hair growth patients experienced during the trial. Here we have a 40-year-old man who experienced improved efficacy with extended treatment. This was a case we presented in December, and a patient who entered into the extension period and achieved a SALT score of 20 at week 40. At the top of the photos, you can see this patient had a shaved head, and he went on to benefit from a 63% improvement in SALT score over the 16-week extension period. Cases like this further support the importance of a 52-week induction period for the phase III program. Here's another case of a 20-year-old female who entered into our treatment extension on the 24 mcg/kg dose. She demonstrated consistent hair growth and achieved a SALT score of 20 by week 48. This patient also achieved substantial improvement over the 16 weeks of additional dosing. It's really not hard to imagine how a young woman's self-esteem, confidence, and quality of life would be dramatically improved when you go from an appearance shown in the photos on the top of the slide to the ones on the bottom. Here's a new patient case of a 64-year-old white female who entered into extension on 24 mcg/kg dose. This patient demonstrated consistent hair growth and achieved a SALT score of 20 by week 52. It is important to note that patients in their 60s may be poor candidates for initiating a JAK inhibitor due to comorbidities that increase cardiac risks, such as high cholesterol, hypertension, obesity, and/or diabetes. Here's a 50-year-old woman who entered into the extension on 18 mcg/kg dose. You can see that her SALT score improved rapidly after roughly 20 weeks of treatment, and ultimately, she achieved a SALT score of 20 by week 48. This case and the next one highlight the need to set clear expectations with patients that visible hair growth may take six to nine months on treatment. Finally, we have a 64-year-old white female. This patient's SALT score improved tremendously after the 36-week treatment period, and she achieved a staggering 82% reduction over the 16-week treatment extension. Now with all that, let me summarize the key takeaways from the REZOLVE-AA study. Most importantly, the study results demonstrate proof of concept for rezpeg as a first-in-class biologic for the treatment of alopecia areata. We are very pleased that rezpeg achieved our target product profile for favorable clinical efficacy and tolerability, along with a differentiated safety profile. Our target product profile was designed to meet the significant unmet need for a safe alternative to low-dose JAK inhibitor class for alopecia areata. The results reported today from the 16-week extension period support the decision to advance a 52-week treatment interval into our phase III program. Now turning to our next steps for the rezpeg program. In the second quarter, we plan to conduct an end-of-phase II meeting with the FDA to align on the phase III registrational strategy. In Q4, we will report the blinded 24-week off-treatment data from REZOLVE-AA. These results will include data from patients who achieved a SALT score 20 by 36 weeks and how they performed off therapy. Importantly, these off-treatment data will help inform the design of the phase III program, including elements of a long-term extension and the appropriate dosing frequency to administer in that trial. Turning to atopic dermatitis, I am proud to announce that we have alignment with the FDA on our phase III program, and we plan to share the full design of our pivotal studies over the coming months. We plan to initiate the ZENITH-AD phase III program in June or July of this year. In the first quarter of next year, we also plan to report additional data from the 52-week off-treatment data from the phase II-B REZOLVE-AD study. In type 1 diabetes, we expect to share initial data together with our partner, TrialNet, in 2027. Finally, as mentioned at the beginning of this call, we are actively exploring other indications for rezpeg and expect to initiate a proof of concept study for a potential new indication in the second half of this year. I'll briefly mention the possibilities. Given rezpeg's mechanism of action, we believe it could have potential across a number of other autoimmune disease settings. Rezpeg acts upstream of multiple inflammatory pathways through Treg biology, and this could be applicable across a broad range of autoimmune and inflammatory diseases where immune dysregulation is a key driver. Many of these indications represent large markets with a significant unmet need, particularly for therapies like rezpeg with a novel mechanism of action that can provide durable disease control with a favorable safety profile. We are actively evaluating opportunities for rezpeg across these indications, and our goal is to target the start of a small proof of concept study in a potential new indication later this year to generate data in 2027. To that end, we've already initiated a phase II study in new onset stage 3 type 1 diabetes, a trial sponsored and funded by TrialNet, a consortium of type 1 diabetes doctors in the United States. One of the indications we are exploring is an area where we know rezpeg has already demonstrated some promise. Shown here are the data from a phase I multiple ascending dose study that Nektar ran in patients with mild systemic lupus. 22 patients in the study were enrolled who had cutaneous symptoms with CLASI-A scores of four or higher at baseline. These patients received three doses in the study at day one, day 15, and finally at day 29. A clear dose-dependent effect was observed in reduction of CLASI-A scores in this 22-patient subset. We have already seen good results now in two other inflammatory skin disease settings, and cutaneous lupus will be an area where we potentially can move quickly to understand whether rezpeg can help patients battling this disorder. With that summary, I will introduce you to our KOL panel and renowned experts in both dermatology and alopecia areata, Dr. Jonathan Silverberg, Dr. David Rosmarin, and Dr. Benjamin Ungar. Before we take questions, we would like to ask each of our KOLs to provide their assessment of the data. Dr. Silverberg, can you please go first? Then we'll ask Dr. Rosmarin and Dr. Ungar to comment. After that, we will open the Q&A to our KOL panel as well. Dr. Silverberg, floor is yours. Thank you very much, Mary. Good morning. Good afternoon, everyone. I'm excited. I've been excited about this for a while. I think we've had some conversations over the past year, looking initially at the 36-week data and, of course, at the atopic dermatitis data. I think these data really just reinforce the efficacy. I think the potential commercial competitiveness. I think it's particularly impressive that even at week 52, where we're seeing nice demonstrable efficacy and competitive efficacy, that there is no clear indication of plateau, suggesting that there's even more efficacy to be gained over time. I think that's a big deal. I've long said, I'm not here to knock JAK inhibitors or anything else, but I think all the market research is clear from both a patient perspective, from a provider perspective, that in a scenario where one has a clean biologic to choose from, the vast majority of the time, that will become the first-line approach. I think rezpeg really has that potential as a clean and effective biologic in alopecia areata to become that preferred first-line approach. I think there still will be a role for the JAK inhibitors, but I suspect that they will end up getting shifted markedly towards second- or third-line use in alopecia areata once rezpeg's on the market. Thanks, Jonathan. David, can you go next, please? I agree with my colleague, with Jonathan. Also, congratulations on this data. I think it's convincing that rezpeg does work for alopecia areata, and I have very high confidence that a phase II program is going to be successful. Like Jonathan said, dermatologists like myself, when I speak to other colleagues, we would love to have a targeted medication that has a more favorable safety profile. That is the greatest need in alopecia areata right now. There are many people who have alopecia areata who are not being treated with JAK inhibitors that I think would be willing to go on to rezpeg. Further, it expands the market for patients who have more moderate disease as well. I think a strategy, as Jonathan said, is that the vast majority of patients will go on rezpeg first, and I think many will respond, but if there are those that don't, then they can always go on to a JAK inhibitor like upadacitinib subsequently. I think that this is a big deal that will change the way we treat the disease. Thanks, David. And Benji? Good morning, everyone. Yeah. I completely agree with what both Jonathan and David said, so I'm not going to necessarily repeat that part of things. When we saw the 36-week data, I think many of us who understand the mechanism, the kind of kinetics of alopecia areata treatment responses, there was maybe a hypothesis or expectation that we would see continued improvement beyond that time point, just because of the nature of the disease. Really, I think this trajectory exactly matched my most optimistic hopes for how this would continue to improve. That's sort of what I maybe in a sense expected, but actually seeing the data are quite convincing. I think it's just worthwhile noting, thinking about a phase III program, that this disease is not really associated with those kinds of placebo responses. Seeing that tremendous separation really gives me a ton of confidence. David said this, but I'll just echo this, that this will show success in a phase III program. As both my colleagues have said, there is very much an appetite for additional MOAs to help treat patients with alopecia areata, and that's a conversation that we could go on at length about. There's a huge need still for alternative approaches, and the fact that we're seeing these results in a small study is incredibly encouraging for what a large study can show us. Thanks, Benji. Now we'll open to questions. We will now begin the question-and-answer session. Please limit yourself to one question. If you would like to ask a question, please raise your hand now. If you've dialed into today's call, please press star nine to raise your hand and star six to unmute. Please stand by while we compile the Q&A roster. Your first question comes from the line of Julian Harrison with BTIG. Your line is open. Please go ahead. Hi. Congrats on this data update, and thank you for taking the questions. First, for the dermatologists on the call, if these results were replicated in phase III, I'm wondering what percentage of your alopecia areata patients you would envision ultimately utilizing rezpeg, assuming the choice continues to be just rezpeg versus JAK inhibitors. For management, I'm wondering if you could talk more about your confidence around SALT 20 responders by week 36, likely maintaining response through 52 weeks if they continue to be followed. Sure. Julian, thank you for the questions. I can take your second part first. We do know that all patients that achieved a SALT 20 prior to week 36 maintained their SALT 20 through to treatment. We are going to follow those patients now off treatment. It's a blinded 24-week period, and we will have the data for the durability of those SALT 20 responses in the fourth quarter of this year. With respect to your first question, what proportion of patients would use rezpeg? I'd like to turn it over to Jonathan first. Maybe, in addition, the three of you can address how many of your colleagues are willing even to prescribe a JAK inhibitor today. Jonathan, if you can go first. Sure. The latter question, we have clear data. The vast, actually, majority of dermatologists will not touch a JAK inhibitor with a 10-foot pole, and certainly not on label when there are clean biologics to choose from. In other words, there'll be docs who might turn to a JAK inhibitor that's approved in atopic dermatitis, but they won't use it in atopic dermatitis. They'll turn to it off-label out of desperation because there's nothing else to use in some other indication. And I think that just illustrates the point why here I have such a high degree of confidence that it will get taken up first-line. For my own personal practice, I'm sure there's going to be a handful of patients here or there who are truly needle-phobic. Putting aside a teeny minority, I would assume, realistically, 90% or more of my patients. I'm just being conservative because it might be 100% of my patients that I'm going to be encouraging to use this first-line before going to that JAK inhibitor. Again, I think there's going to be a role for the JAK inhibitors, but I really do think there's going to be a paradigm shift in the same way that the FDA has positioned the JAK inhibitors as second-line options in the world of atopic dermatitis and rheumatoid arthritis. I think once you've got a clean biologic, I don't see them necessarily rewriting the label of the JAK inhibitors. But I think that conceptually, there will be that frame shift, where providers will turn to the clean biologic first. Certainly in my practice, that is what I expect. If I have a patient who's grandfathered in and doing fantastic on a JAK inhibitor, will I necessarily take them off and fight with them and change it? No. For any of the new starts, I would expect almost certainly they would be rezpeg patients. For so many patients who are on JAK inhibitors now, where they may be doing okay, but what else do we have to offer them? I think there will be a lot of switching and openness to trying rezpeg in those situations as well. I think both first and second-line, there's going to be a very high rate of use. Thanks, Jonathan. David, can you go next? Yeah. I agree. Actually, the number that I was going to give as well was 90% of my patients. I would put on rezpeg first for new starts. If I have a patient who has alopecia totalis, who is getting married in six months, that might be an exception for me to use a JAK inhibitor. The vast majority of patients, I plan to give rezpeg first. I think in terms of my colleagues, more than half of them will not prescribe oral JAK inhibitors. I think it will be closer to 100% of their prescriptions. Again, I think it's pretty clear that this will be a paradigm shift, as Jonathan said, and will be used first. We are hungry for a medication that doesn't have these boxed warnings. Thank you, David. Benjamin? Yeah. I'm going to start with the second part, which is my colleagues. I couldn't agree more. We know through a tremendous amount of data that people are not prescribing it. Even in alopecia areata, where there are no approved alternatives or really demonstrated great other options for many people, they're just not getting treated. There's a huge population of untreated patients that I believe would now be treated with a drug that has this profile. I myself am not representative of most of my colleagues because I do use JAK inhibitors, and I use them frequently because patients are coming in wanting to get treated. Very often, that's after seeing someone who has not treated them. These are very motivated people trying to get treated. I think if we were to fast-forward, yes, a very high proportion of my patients would be started on this treatment. I think that one of the very interesting potential aspects about this mechanism that is going to be elucidated with longer-term trials is what the maintenance of response and dosing interval and all that means. I think we have reason for optimism based on the biology, that this drug potentially has a unique characteristic of perhaps producing long, sustained responses. I'll just give one example of how that really impacts things. Very often, there are women who are considering becoming pregnant, and because of that, are not really great candidates for JAK inhibitors, because we know if you stop treatment, there's a high likelihood of loss of response. Because it takes time to work, if they're planning pregnancy in the next year, it just may not be an option. Now, envision a treatment where we can induce regrowth and then potentially stop for an extended period, can become pregnant, deliver. This is potentially a very big shift in the way we think about treating things. Can I build on that point just briefly? Because I think I hear almost, I don't want to say an irrational conversation, but sort of an incomplete conversation around the value of orals. Because when you do this market research, patients always like, conceptually, it sounds great, they want an oral over injection, until they do it. Patients who have had even miraculous responses with JAK inhibitors, let's say in atopic dermatitis, whatever it might be, that same patient comes back to me six months later complaining. They hate the drug. I'm like, "What do you mean you hate the drug? It stopped working?" "No, it didn't stop working, but if I miss one day, or I miss a few days, I'm right back to where I was. I start feeling the itch again." In the case of alopecia areata, when they start losing hair again because they missed a few doses, oh boy, are they not happy. I think this is a real issue. We need more forgiving medications on dosing. Ones that we understand patients are human, and they miss a day or two. You can't just blame the patient that they're supposed to take once daily for the rest of their life. That's what we're asking them with these pills. That is a very, pun intended, tough pill to swallow for patients. I think that from an adherence perspective, and from a patient friendliness perspective, from a simplicity perspective of not having to think about their disease every day, it is a big deal to have this kind of shift in dosing. Thanks. Great points. Next question, Nicole. Your next question comes from the line of Samantha Semenkow with Citi. Your line is open. Please go ahead. Hi. Good morning. Thanks so much for taking my question. Apologies for the background. I am on a flight. Just one for the physicians. I've got a couple questions in about this data maybe not reaching the upper bar, what JAKs can do, call it north of 50%. Just want to give your perspective on if that's relevant at all given the data that we've seen today. Just for the company, a clarifying question. Are you able to share whether we have any patients, whether in the 36 weeks or post into the extension, that regressed in their hair growth? Thanks very much for taking the question. Yep. Great. I'll just start with your second one, Sam. In terms of the off-treatment, right now, that's a blinded period. We have not looked at any of the data off treatment. Again, as I just mentioned to Julian, on treatment, we know that no patient relapsed who achieved a SALT 20. We will have those data in the fourth quarter of this year. Then we'll start in the other order. Benji, if you could address the first question about the upper value of SALT 20 for higher doses of JAK inhibitors. Absolutely. Happy to. I think the first point that I think is really important, I believe it was Jonathan who brought this up earlier, is we actually don't know yet what the maximal efficacy is. I think there's a reason to believe, based on the trajectory, that people continue to improve beyond 52 weeks, which on the one hand, may seem like it's a long period, but given that they are improving before then, patients, I think, have the willingness to wait if they're seeing regrowth. Even if the maximal effect is several weeks after that, even months, they'll be very happy with this. I think that there are two points I want to add. Number one is, I mentioned this, but I'll keep saying this. There's a huge pool of untreated patients, and one big reason for that is that dermatologists and providers are not even offering JAK inhibitor treatments. You can imagine now coming in with a safe treatment that's easy to use, that's going to be much more effective than no treatment at all. I think it's important to keep in mind what we're comparing this treatment to. Then the last point I'll just make is, we have an analogy that I think we all raised before, but it's really worth highlighting again. Which is in the psoriasis landscape that is populated by very safe, extremely effective, and frankly, quote unquote, "easy to use" treatments. Otezla remains a very commonly used drug. The reason is not because it is extremely efficacious in terms of PASI scores. The primary reason is that it's safe and easy to use. People feel comfortable getting someone started on a treatment for their psoriasis, and it's not the most effective. This, again, is in a very saturated market of alternative treatments. Now, you can imagine a drug like rezpeg that actually has good efficacy, that we expect to continue working. It has potential, all sorts of other benefits that we've talked about, dosing intervals, and things like that. This efficacy, in my mind, clearly exceeds the bar that will make people interested. I'll pause there and Those are my thoughts. Yeah. Thanks, Benji. Yeah, David, it'd be great if you could address this question too. To me, safety trumps efficacy, and that is not only my own sentiment, it is the general feeling within dermatology that we care about safety first, do no harm. That is even more true in a disease like alopecia areata, which doesn't have physical symptoms to it. I would easily try a medicine that may have slightly lower efficacy or takes a little bit longer to work before one that has more risk, especially when we're going to commit somebody to decades and decades of treatment. To me, I think it's not even a question. I think it's very clear. I'm very confident that people will choose the safer option almost every time. Further, in terms of the efficacy, so baricitinib 2 mg is the dominant dose of Olumiant. This efficacy is comparable to that, as I would say, within that timeframe. What may happen is, over time, rezpegaldesleukin may actually have superior efficacy to Olumiant, and I think that that really may be the case. Plus, I think you would find in a phase III study that not only would the data be replicated from the phase II data that was just presented, but I'm actually optimistic we could even see a boost in efficacy for multiple reasons. One is, ideally, adolescents would be included, and they are more responsive. Two, I expect fewer dropouts in the study as well because now we know it's proven to work. And two, there will hopefully be a crossover as well, so patients are motivated to stay in, knowing that they'll get medicine after the induction phase for a year. There's many reasons to be very optimistic in the data. Thanks, David. Jonathan, we'll save you for the next question in the queue. Sure. Your next question comes from the line of Yasmeen Rahimi with Piper Sandler. Your line is open. Please go ahead. Good morning, team. Thank you so much for the excellent presentation and the KOL's thoughtful commentary. Question to our three experts. The Nektar team did a very nice job on the phase II-B design. Maybe now that the data is on hand, what would your recommendation be on patient selection for phase III that they could further optimize? Are there certain patients that you think could benefit more from rezpeg that we could enroll in the study? And then also would love to get your thoughts on, we're very much looking forward to see the off-treatment data from rezpeg. Any color on what that data and how important that response could be for you in the utility of rezpeg in AA? And thank you for allowing me to ask my questions. Thanks, Yasmeen. Jonathan, can you take this question? Sure. I guess I can start with the second one first, because to me, I think that's easy. It's always the more data, the better, and I think it would potentially build a very interesting story around concepts of remission, disease modification. In truth, I don't think it's going to change anything in terms of my prescribing habits, in the sense that what I said earlier about 90% or more of my patients going on rezpeg as new starts would be true with or without any kind of off-drug effects. Because what I need is clean drugs with clean safety profiles while they're on it. Knowing full well that probably the majority of patients, or at least a large subset, are going to need to be on drug for a really long period of time. I need to know they're going to be on safe drugs. I think that's always been the biggest issue that we've had with the JAK inhibitors. It's not like if you treat with a JAK inhibitor, we expect them to be cured. We know that's not the case. They can never get off it, and now you've got potentially cumulative exposures over time and cumulative risk that comes. For me, even if patients need to be on drug, as long as the safety looks as good as it does, to David's point earlier, to Benji's point earlier, this is going to still be that first approach. Sorry, I lost track of what the first question was. The eligibility criteria for the phase III. Oh, I think the reality in the world of the real world for alopecia areata is, I think this is going to be used across probably all subsets of patients. Clinicians will figure out how to optimize in different subsets. I think right now, we've learned a lot of lessons, and I would say that stable patient has worked well in terms of balancing placebo responses, et cetera. I think I would actually try to recapitulate with almost identical inclusion criteria in the future studies. I think they did a great job on the operations of that and just in terms of that placebo-adjusted deltas. Thank you so much. We'll go to the next question, but one more comment. As David said, we will include, as long as we have buy-in with the FDA, the adolescent patient population. I n the phase III, and that population, we believe, will respond even better than the adult population. That's an exciting change, Yasmeen, that we foresee in our phase III trial. Nicole, next question. Your next question comes from the line of Jay Olson with OpCo. Your line is open. Please go ahead. Oh, hey. Congrats on these impressive results, and thank you for hosting this event. First, we have a question for the KOLs. What are the baseline characteristics of the AA patient population in your clinical practice who may benefit most from rezpeg treatment? Related to that, are you currently using Dupixent off-label for AA, and would you consider switching those patients to rezpeg? If I could please sneak in another question for the Nektar team. For your phase III program, will you include both JAK-naïve and JAK-experienced patients? Do you think that one phase III study may be sufficient for regulatory filing? Thank you. Thanks, Jay. I'll take the second question, then Benji, you can answer the first. With respect to the phase III program, we are going to speak to the FDA later this quarter to have a discussion about the phase III program. We do believe there's precedent for one phase III trial in the area of alopecia areata. Pfizer was able to advance Litfulo, their JAK inhibitor, in one phase III trial and achieve approval. We will have that discussion with the agency. We are working on the ideal patient population with respect to patients who have either had JAK inhibitors previously or a naïve population. The second question, Benji, if I can turn that over to you, as the expert in the use of Dupixent for alopecia areata on a panel. Yeah, absolutely. Yes, I have many patients that I used Dupixent off-label for alopecia areata. Again, I think that's an illustration of there being an appetite for alternatives. I have many patients on JAK inhibitors too, but that's not always going to be the best fit for patients. I do have many patients. We're actively involved in researching Dupixent as an approach to treating this for exactly that reason. I do think that if someone's doing well, and Jonathan, I believe, mentioned this earlier, if someone's doing well on a treatment, it's more challenging to switch. There are people coming in every day where we're having a conversation of what the treatment approaches are, and if there's a drug that has the profile that we've talked about with rezpeg that's approved and available on label, it kind of makes it a very easy approach to take. Now, in terms of what patients, which I think you started off, would be most, kind of best candidates for rezpeg. The answer is, in principle, everyone. In fact, I think that one of the biggest challenges we have is that there are limitations with treatments, whether it's the severity scores. Is it worth putting someone who's a little more mild on a treatment, and take potential safety risks? If you have a safe, effective treatment, the answer is really for everyone. I'll just add, and this goes back to the previous point also about the trial design. The MOA, without going too much of the immunology, really does not suggest limitations on subsets of populations. In principle, this could be effective, really for everyone. Now, obviously, not 100% of people are going to respond, but there's no reason to believe that there are specific subsets that are going to be more or less aligned with that. The short answer is everyone, I think, may benefit from this. Thanks, Benji. Nicole, can we have the next question? Your next question comes from the line of Roger Song with Jefferies. Your line is open. Please go ahead. Great. Congrats for the data, and thanks for putting together this presentation. Very informative. Then just quick ones from us. Firstly is, I think, as the KOL just mentioned, the MOA should work across different subgroups. Just curious about in the phase II, how do you think about those a little bit more severe patients responding to rezpeg? Because when we look at the baseline, the SALT score a little bit lower than the Olumiant or the JAK inhibitor. How should we think about in the broader population? Also, we notice in the induction period, you have about 20 patients discontinue, due to patient decision, likely driven by the efficacy, we don't know. Do we know the SALT score for those patients? How likely those patients could improve if they stay on the treatment for a bit longer? Thank you. Thank you, Roger. I can take the first part, and David, if you could take the second, and David, also talk about the moderate patient population as a possibility. Roger, you bring up a great question. As you mentioned, in the 36-week treatment period, we did see 20 patients go off due to patient decision. That was the reason they left the study. That being said, we then went and looked at the SALT scores you're mentioning of those 20 patients, and 15 out of the 20% or 75% had not reached the SALT 30% reduction from baseline. We do believe, as we've shown you here, there's some patients who aren't going to start to grow hair until six and even nine months out. When we start our phase III trial, in the informed consent, we're going to advise patients that it may take a long time for hair to regrow. We're also going to ask the principal investigators to, again, as they are consenting patients, to advise that this is a treatment that may take a long period of time to grow hair and that participants need to understand the kinetics of hair regrowth that we've seen with this agent. David, if I can turn it over to you. Yeah. The first comment is that it does work in the most severe patients. We've seen patients who have alopecia totalis respond. The other supporting data is that we see that eyebrows and eyelashes are regrowing as well. Those often correlate, eyebrow and eyelash regrowth, with SALT 20 score. It's much harder to regrow eyebrows and eyelashes than just for patch alopecia, and we're seeing that happen here. There is confidence that it works even in the most severe patients, although we know we have better responses in patch alopecia, just like in JAK inhibitors. Now, in terms of the population in the study, and this is true across different disease states, not just alopecia areata, AD, HS, that after the first studies for approval, the patient populations often moderate in nature. If you look at this patient population in the study, it's not that different from AbbVie's latest phase III study for upadacitinib. I strongly suspect the phase III will be more moderate as well in nature, and it'll be similar to AbbVie's study because that's just the trend that happens. As we have other treatments available, it's not just the most severe patients going into the study. Plus, I think there are many patients who have more moderate disease that may be unwilling to go on JAK inhibitors that will now be captured by this treatment. Again, I think this is a good thing. Yeah. Thank you, David. We appreciate it. Nicole, could we have the next question, please? Your next question comes from the line of Mayank Mamtani with B. Riley Securities. Your line is open. Please go ahead. Yes. Good morning, team. Thanks for taking our questions, and congrats on the totality of the very positive data set. I would love to also hear your expectation for the SALT 10 endpoint and if there's similar kinetics observation that you had in SALT 20. Obviously, SALT 30, you see the plateauing because a lot of patients get over that mark. I was just curious if SALT 10 curve would look very similar to the SALT 20 in terms of the climb you see. Just a final point on the off-therapy durability data. What sort of data do you expect to see there to make a decision on, a less frequent regimen, like a once monthly versus maybe once quarterly, if you could maybe speak to that. Yep. Yeah. Thanks, Mayank. First, with respect to the off-treatment data, we need to look at that closely to see, does it make more sense to, have a monthly, as you mentioned, or continue even with twice monthly, or can you go out longer? We will size up how many of those SALT 20 patients were able to achieve durability of response in that entire treatment period. We will definitely make a data-driven decision. With respect to SALT 10, we believe that the trajectory of that curve, when we are able to follow patients for 52 weeks, will probably look very similar to what we've seen with the SALT 20. After 52 weeks, the curve and the slope is still upward, which would mean that we believe that patients will derive benefit in the second year as well as the first year. We look forward to analyzing the SALT 10 in a large phase III study to best understand how deepening of response happens over time, especially into the second year of treatment. With that, if, Nicole, we can take the next question. Your next question comes from the line of Marc Frahm with TD Cowen. As a reminder, please press star six to unmute. Thanks for taking my questions and congrats on the data. I recognize some of this will get informed by seeing some of that off-treatment data, but just, for the company, can you walk through your current assumptions on how you would approach maintenance dosing? For the physician, similarly, how are you expecting to use this in the real world? Would you try to maybe a treat and extend type of model once a response is induced, or would you just keep the Q2 weekly dosing indefinitely? Maybe also for the physicians, just, I completely appreciate that there's this large population of dermatologists who just aren't even willing to touch or discuss a JAK inhibitor with their patients. In your practices where you are using JAK inhibitors, can you maybe speak to what percent of patients with alopecia areata, either you yourself are unwilling to discuss it because you look at them and say the risk factors are just too much to justify a JAK inhibitor. Or once you do discuss it with them, they ultimately decide not to pursue a JAK inhibitor because of the safety issues? Thanks, Marc. I'll take the first question. Interesting, in atopic dermatitis, we had a phase I-B study that helped guide us on the type of durability we could see after dosing. In the atopic dermatitis study, we selected Q monthly and every three-monthly dosing. We were very fortunate to see the ability to maintain the durability as well as deepen responses, was successful with both those doses. In fact, we'll take both into the phase III. I think the same is true, we can look at this phase II-B study as really the guiding light for what our maintenance doses should be. I think the full range goes from an additional Q2-week all the way to Q12-week. I think, as the saying goes, pornography's difficult to define, but you know it when you see it. I think many of us who've been running clinical trials for decades understand the same principle applies to clinical data, and we will have a good sense of where we want to land in terms of a maintenance dose. It may be that we evaluate more than one in that second year of dosing. With respect to discussions with patients, patient's decision, let me turn it over to Jonathan to summarize his experience. Sure. I think there's a lot of different subsets of patients where we would take real pause with JAK inhibitors, really that 60-year-old and older, 65 and older, just because we know that there's an age-related big increase in adverse events with the JAKs. Even among younger, healthier patients, particularly parents of children, adolescents, there's a lot of hesitation in my practice around the use of JAK inhibitors, even though officially on paper, the safety profile can look cleaner there. There's just general hesitancy. I will say there are differences in terms of the threshold, and how we would apply it between indications. Because in alopecia areata, to date, we've kind of reached even to patients that we really aren't comfortable with because we didn't have anything else. Boy, oh boy, if I had a clean option, I wouldn't have gone there. In AD, I don't. Because I've got now multiple biologics to choose from, I'm going to go biologic, and I'll cycle through biologic before I want to go to a JAK inhibitor. Again, I think it just gets back to that point that there will be a paradigm shift here. Certainly, in that older patient population, the patients who've got those risk factors for any of the JAK side effects, any of the patients who are risk averse, which is a whole lot of them. I find, David mentioned this earlier, it's not just his experience, it's my experience, it's all my patients' experience. Safety first in almost everyone. The threshold will change, I think, drastically in alopecia areata, where people will realign the way they're going to think about risk tolerance. Thanks. Thanks, Jonathan. Nicole, is that the end of our questions? We do have a couple more questions. Your next question comes from the line of Arthur He with H.C. Wainwright. Your line is open. Please go ahead. Hey, guys. Congrats. I just had a quick question for the management and a couple of questions for the physicians. Maybe for the physician first. When we look at this data, how should we think about the rezpeg efficacy in the alopecia patient with a SALT score less than 50? And, if we want to explore that efficacy in the pivotal trial, how should we think about the design for the pivotal trial? For the management, I think just quickly want to see, could you give us more color on the two discontinuations during the extension period? Great. I can take the second question, Arthur. Neither patient reached a SALT 20, and quite frankly, they were far away from that. That endpoint was, they did discontinue due to patient decision. But they were not deriving benefit when they did leave the study. David, you've talked a lot about moderate patients with us, if you could address that topic. Okay. First, for moderate patients, we know that as patients' disease is less severe, it is more likely to respond. I think that I wouldn't expect rezpeg to be an exception to the rule. We would expect even greater efficacy the more moderate the patient. Now, in terms of for a regulatory trial design for a SALT <50, well, I would not recommend including patients with SALT <50 with patients of severe or very severe, because you can increase the placebo rates as well. However, if you were to design a separate study for moderate patients, which is defined by SALT 20 to SALT 50, perhaps the primary endpoint for that type of study could be a SALT 10 or less. There would need to be discussions with the FDA. I absolutely think that a label expansion for this population would be a very positive and doable thing for rezpeg. Much more challenging for the JAK inhibitors. Thanks. Thanks, David. Thanks, Arthur. Nicole, next question, please. Your next question comes from the line of Andy Hsieh with William Blair. Your line is open. Please go ahead. Andy, a reminder to please press star six to unmute. Nicole, are there any other questions? Moving on to our next question from Martin Fan with Wedbush. Your line is open. Please go ahead. Hi, good morning, everybody. Congrats on the data. I have a question for the experts. Could you comment, not in terms of first line, but in second line, patients who are already on Olumiant or other JAK inhibitors. Assuming that Rinvoq is eventually approved, how many you anticipate to switch to Rinvoq as opposed to rezpegal for patients who are already on a previous JAK inhibitor? And then if you could also comment on your experience with getting payer approval for JAK inhibitors in the context of alopecia. Hey, Benji, can we have you answer this question, please? Yeah. I think that the major factor, to answer your question, is how they're doing on the current JAK inhibitor. If someone has regrown all their hair, then they're not going to be switched to a different JAK inhibitor like Rinvoq. They're going to either maintain that, or there's a conversation about switching to a different kind of treatment like rezpeg. I think there's initially the bifurcation of how well they're doing, and then there's a question of where we go from that. There are some clinical questions that remain outstanding in terms of what it would be like to switch someone from a JAK inhibitor doing well to rezpeg. I think that there is a large population of patients who are currently doing well on JAK inhibitors that would love to switch to a treatment like rezpeg. Hard to quantify exactly, but a very non-negligible proportion. I think that's very much. There was a second part to the question. Reimbursement, Benji. Oh, reimbursement. Yeah. There's definitely been a shift towards payers recognizing that this is something that really deserves and requires treatment. It's not a cosmetic condition. It's still a work in progress. I think that part of this has to do with the holistic understanding of what the costs are, potential adverse events, things like that. Since the approval of Olumiant to now, what is it, four years ago, there has been a shift, and I think there's positive momentum towards increased support on the payer side. It's still a work in progress, but we have good momentum, and I would say a fair proportion of patients are getting covered. Thanks, Benji. Nicole, is that our final question? There are no further questions at this time. I will now turn the call back to Howard Robin for closing remarks. Okay, thank you. Thank you for everyone for joining us today. We greatly appreciate your continued support. It's not often that a company has the opportunity to develop an important new mechanism that can greatly benefit patients. I want to thank all the patients who participated in the trials, and I want to thank all of our employees for their hard work and diligence. Again, thank you for joining us today, and we look forward to presenting additional data in the future. Please stay tuned. This concludes today's call. Thank you for attending. You may now disconnect.