Good day, and thank you for standing by. Welcome to the Nektar Therapeutics third quarter 2023 financial results conference call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star one one on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Vivian Wu. Please go ahead. Thank you, Crystal, and good afternoon, everyone. Thank you for joining us today. With us on the call are Howard Robin, our President and CEO, Dr. Jonathan Zalevsky, our Chief of Research and Development, Dr. Mary Tagliaferri, our Chief Medical Officer, and Jennifer Ruddock, our Chief Business Officer. Unfortunately, Sandra Gardiner, our acting Chief Financial Officer, was not able to make it on today's call due to an unexpected family emergency. On today's call, we expect to make forward-looking statements regarding our business, including statements regarding the therapeutic potential of and future development plans for drug candidates in research programs, the timing of the initiation of clinical studies, and the availability of clinical data for our drug candidates, the timing and plans for future clinical data presentations, the formation, future development plans, or success of our collaboration arrangements, the expectations following our corporate restructuring and reorganization, financial guidance, and certain other statements regarding the future of our business. Because forward-looking statements relate to the future, they are subject to uncertainties and risks that are difficult to predict, many of which are outside of our control. Our actual results may differ materially from these statements. Important risks and uncertainties are set forth in our Form 10-Q that was filed on August 9, 2023, which is available at SEC.gov. We undertake no obligation to update any of these forward-looking statements, whether as a result of new information, future developments, or otherwise. A webcast of this call will be available on the IR page of Nektar's website at nektar.com. With that said, I would like to hand the call over to our President and CEO, Howard Robin. Howard? Thank you, Vivian, and thank you all for joining us today. In the third quarter, we made substantial progress in advancing our development programs. First, on REZPEG, we're pleased to say that we began initiating our first clinical sites in October for the phase 2b trial of REZPEG in patients with atopic dermatitis. We expect the first data from this study on the primary endpoint of EASI reduction over the 16-week induction period, sometime in the first half of 2025. The strength of our data from the randomized phase Ib study gives us much optimism that we will be successful in the phase IIb study. These data were recently presented at the 2023 EADV meeting in an oral late-breaking news plenary session, and JZ will summarize some of the new data presented later on in this call. But importantly, we observed a consistent benefit with monotherapy REZPEG across multiple clinical efficacy endpoints and patient-reported outcomes. As Dr. Silverberg mentioned in his plenary talk, the phase Ib trial of REZPEG is the first randomized, placebo-controlled study to offer an exciting proof of concept for the important role of T-regulatory cells in treating autoimmune disease. It was exciting to see that this benefit was maintained for many patients through 36 weeks after treatment ended. This substantial benefit observed with REZPEG could eliminate the need for frequent maintenance dosing for patients with atopic dermatitis, and it positions REZPEG with its novel regulatory cell mechanism as a potential new treatment option, which could be highly disruptive in the biologic treatment landscape for atopic dermatitis. The biologic market for atopic dermatitis is a multibillion-dollar market and growing. This landscape includes many IL-13-based mechanisms which overlap with one another, and REZPEG offers the unique promise of a new mechanism in this landscape and a new treatment paradigm that is well-tolerated. This is why we're so optimistic about REZPEG's potential. Our goal is to ensure enrollment proceeds on track to deliver data from the randomized phase IIb trial on our planned timeline in the first half of 2025. This past quarter, we expanded our plan for a second study in alopecia areata from its original randomized phase IIa study design in approximately 40 patients to a randomized phase IIb study design in approximately 80 patients. This is consistent with standard studies in this area, and the incremental cost of this study is still within our projected budget. Importantly, this study will read out around the same time as the atopic dermatitis study. We believe there's an opportunity for Rezpeg to become a novel biologic mechanism in alopecia, which has no currently approved biologic treatments, and JAK inhibitors are the primary treatment mechanism. We know JAK inhibitors have cardiac safety concerns, and patients experience a rebound after discontinuing therapy, so there's a high unmet medical need for those patients for a new treatment option. With the collective data we've generated to date on Rezpeg in atopic dermatitis and als... In other autoimmune diseases, we believe there's a strong scientific rationale for Rezpeg, with its Treg mechanism in action, to be able to address the underlying pathogenesis of alopecia, and JZ will discuss the scientific rationale for this study in a moment. We plan to submit the IND for this study to the FDA by year-end, and we expect to initiate the study shortly thereafter. We're also continuing to advance our preclinical programs in immunology, including our TNFR2 agonist antibody, that offers a promising mechanism for multiple sclerosis, ulcerative colitis, and other autoimmune indications as well. Our goal is to submit an IND for this antibody program in 2024. Moving on to NKTR-255, we're pleased to have recently announced our new clinical study collaboration with Cellular Biomedicine Group, also known as CBMG, to evaluate NKTR-255 in combination with CBMG's TIL therapy in lung cancer patients that don't respond to anti-PD-1 therapy. CBMG is adding NKTR-255 to its ongoing phase I study being conducted at Duke University Cancer Institute and other investigator sites, in the U.S. We're also continuing our other clinical work with NKTR-255 while we evaluate additional strategic partnership pathways for the program. We ended the quarter in a strong financial position with $373 million in cash, and as I stated earlier, we are well positioned to be able to advance our planned clinical studies while maintaining a cash runway into the middle of 2026. The goal is to reach multiple value-enhancing phase II milestones for REZPEG in the first half of 2025, and we believe we are well positioned to execute on this. Since many of you have been asking about the status of our litigation with Lilly, I'll make a brief comment that we continue to actively pursue the litigation and remain confident in our legal position. With that, I'll hand the call over to JZ for an R&D discussion. JZ? Thank you, Howard. Starting off with our lead immunology program, Rezpeg. As Howard stated earlier, this program is uniquely positioned as the most advanced IL-2 based Treg mechanism in the clinic and has potential in multiple autoimmune diseases, including our current focus areas of atopic dermatitis and alopecia areata. Last month, Dr. Jonathan Silverberg presented compelling data for Rezpeg from the phase Ib trial in atopic dermatitis during a late-breaking abstract session at the 2023 EADV Congress. This presentation of the final study results for that trial highlighted the potential of Rezpeg for the treatment of atopic dermatitis. Through the 12-week induction period, Rezpeg demonstrated dose-dependent efficacy across both physician-assessed and patient-reported efficacy measurements, reaching statistical significance across many of these measures. Importantly, we are encouraged by the extended durability seen for Rezpeg long after the completion of the 12-week induction period. Many patients maintained durable disease control for an additional 36 weeks after the end of dosing, and this type of extended disease control after the end of dosing is not observed for dupilumab or for JAK inhibitors. Time to response was rapid, with over 40% of atopic dermatitis patients achieving EASI 75 by week 3, after only 2 doses of Rezpeg at the highest dose level. Rezpeg's rapid onset of action rivals that of JAK inhibitors, which have outperformed dupilumab in head-to-head studies to date in this regard. Durability of the EASI 75 response was also observed, with approximately 70% of EASI 75 responders maintaining their response for 36 weeks after the end of the 12-week induction period. This is a very exciting result and suggests that Rezpeg has the potential to be the first remittive therapy for atopic dermatitis. Additionally, REZPEG was well tolerated, and treatment with REZPEG did not induce anti-drug antibodies in patients, which has been reported with some examples in the IL-2 mutein class. Compared with placebo, there were sustained increases in absolute numbers of circulating total and CD25 bright Tregs in the REZPEG treatment arms. The peak increase in CD25 bright Treg number was tenfold above baseline at the highest REZPEG dose group. Despite a shorter than typical induction period of 12 weeks, as compared with a 16-24-week induction period for most other biologics, there were clear improvements for all efficacy endpoints, including EASI scores, the IGA, BSA, itch NRS, DLQI, and POEM. These improvements begin as early as weeks 2-4 and continue through week 12 of treatment. To give you some perspective, with historical studies in atopic dermatitis at the lower dose level of REZPEG, the improvements we saw were similar to those observed for biologic therapies, and at the higher dose level, REZPEG demonstrated a comparable activity to those reported with JAK inhibitors. The 83% improvement in EASI score from baseline observed at only 12 weeks of induction with REZPEG, was superior to what was seen in the dupilumab studies after 16 weeks. These promising data have us and KOLs very enthusiastic about the potential for long-lasting responses and a frequent maintenance dosing with REZPEG in the setting of atopic dermatitis. The results we have obtained so far with REZPEG are significant for a number of reasons. Firstly, before this work was conducted...... Relatively little was known about the ability to restore Treg function to reverse immunological pathogenesis and improve the severity of dermal or cutaneous diseases. Now, with REZPEG and its Treg mechanism, we have demonstrated clinical efficacy against the cutaneous manifestations of lupus, psoriasis, and atopic dermatitis. These results begin to validate the Treg mechanism for the treatment of multiple pathologies of the skin. REZPEG's attractive mechanism employs the body's own immune system to restore tolerance by inducing the Treg pathway and presents a novel approach, differing from the available broad or targeted strategies to block inflammatory pathways in dermal diseases such as atopic dermatitis. Secondly, our hypothesis is that administration of the agonist drug REZPEG induces Treg expansion and engages multiple immunoregulatory mechanisms to facilitate immune tolerance and regulation by attenuating TH1, TH2, and TH17 effector T cells, suppressing antigen-presenting cell activity, and fostering tolerogenic dendritic cells. We believe this science translates to the durability of response we observed in the atopic dermatitis trial and is the differentiating element that allows us to pursue an every three-month dosing regimen in our ongoing Phase IIb atopic dermatitis study. Biologically speaking, REZPEG, through its central pathway of Treg rescue, is uniquely poised to address a diversity of immune pathologies, giving it broad potential for targeting multiple dermal diseases, including atopic dermatitis, alopecia areata, and others. In October, we initiated the Phase IIb study of REZPEG in biologic-naive atopic dermatitis patients. Our goal is to enroll roughly 400 patients with three different regimens of REZPEG versus placebo, evaluated over a 16-week induction period. After the induction period, patients that meet a threshold to advance from induction to maintenance will be re-randomized into one of two maintenance regimens at different dosages at either once a month or once every three-month dosing schedule that will continue for another 28 weeks. We expect the study will take approximately 54 weeks to conduct, and we expect data in the first half of 2025. We also plan to initiate a phase IIb study of REZPEG in alopecia areata later in early next year. Alopecia areata is an indication with a high clinical unmet need for a biologic, as the only approved agents are JAK inhibitors, which come with a black box warning and lack durability after cessation of dosing. For these reasons, we believe there's an opportunity for REZPEG to become a novel biologic therapy in alopecia areata. As I just mentioned, we believe that REZPEG and its Treg mechanism of action has great potential for addressing this indication, which is essentially a dermal disease of the scalp. Across all of our studies, with nearly 600 people treated, REZPEG demonstrates a consistent and highly predictable Treg cell pharmacodynamic profile in different autoimmune disease pathologies and even in healthy volunteers. Taken together, we believe there's strong rationale for REZPEG for the treatment of alopecia. The phase IIb study plans to recruit roughly 80 patients with moderate to severe alopecia that will be randomized to REZPEG or placebo. As Howard mentioned, while it was previously our plan to run a phase IIa trial with roughly 40 patients, after reviewing historical trials in this indication, we decided to increase the size of our study to achieve a phase IIb design at minimal incremental cost. Patients will be treated for a period of 36 weeks and observed up to 48 weeks in total. Our primary endpoint for this study is mean% improvement in SALT, or the Severity of Alopecia Tool, at week 36, which is very standard in the field. We will also be looking at a number of other secondary endpoints, including proportion of patients who saw a reduction in SALT. Now turning to our lead immunology research program, a TNFR2 agonist antibody program. TNFR2 is highly expressed on Tregs, neuronal cells, and others, and TNFR2 agonism has been shown to potentiate the suppressive effect and overall functional properties of Tregs. If TNFR2 is absent, it is associated with autoimmunity and other genetic conditions resembling FoxP3 loss of function. In contrast, its presence has been associated with immunoregulatory function and protective effects for multiple cell populations and tissues in the body. Building upon what we know of the potential of regulatory T cell mechanisms, this makes this program incredibly exciting to us. Nektar has identified two lead antibodies that we have now validated for selective TNFR2 binding, cell type specificity, and TNFR2 agonism in primary human cell-based assays. We believe that a selective TNFR2 agonist holds great promise for the treatment of multiple autoimmune diseases and are aggressively pursuing this program and on track to submit our IND in 2024. And now I'd like to turn the call over to Mary to provide a brief update on our NKTR-255 program in oncology and our recent collaboration with CBMG. Mary? Thank you, JZ. Moving to NKTR-255, we are continuing our work with NKTR-255 while we evaluate strategic partnering pathways. We believe there is a potential broad application for NKTR-255 to enhance the efficacy of cellular therapies. And to that end, as Howard mentioned earlier, we are pleased to have recently announced our new clinical study collaboration with a leading cell therapy company, Cellular Biomedicine Group, to evaluate NKTR-255 in combination with their TIL therapy known as C-TIL051. The study, which is being conducted by and fully funded by CBMG, is in advanced non-small cell lung cancer patients who do not respond to anti-PD-1 therapy. With few treatment options for these individuals, we are excited about the potential for this regimen to help patients. Preclinical and early clinical data suggest that IL-15 can improve proliferation and persistence of cellular therapies, such as TIL, to increase specific antitumor activity. The first investigator site is at Duke University with a leader in the lung cancer research field, Dr. Scott Antonia. Positive data from this study could lead to exploration of a pathway for accelerated approval by our partner, CBMG. Our other studies are continuing in cell therapy, and we expect that we could see data reported next year from these trials, including the phase II JAVELIN Bladder Medley study, which is being conducted and funded by our partner, Merck KGaA. Because of its unique potential as a combination agent with cell therapies and other mechanisms, we are exploring the best partnering and development path for continued development of NKTR-255. And with that, I will turn the call over to Jennifer for a review of our financial guidance. Jennifer? Thank you, Mary, and good afternoon, everyone. We ended the third quarter with $373 million in cash and investments, with no debt on our balance sheet. We now expect to end this year with at least $320 million in cash and investments, slightly higher than our prior projection of $315 million. As we had previously announced earlier this year, we reduced our San Francisco-based workforce by approximately 60%, and this personnel reduction represents approximately a $30 million a year in operating expense reduction. The costs related to the restructuring were substantially paid in June. We will fully realize annual savings in 2024 as a result of this restructuring, and our financial position remains strong, with a cash runway that extends into the middle of 2026. Importantly, this runway will take us through several key value-generating milestones for our pipeline. In Q3, we recorded a $10 million non-cash impairment charge for real estate leased assets in San Francisco, which contributed $0.05 to our net loss per share in the quarter. As a result, for the full year, we now expect to recognize restructuring, impairment, and costs of terminated programs of approximately $50 million-$55 million, which includes $37 million of non-cash impairment charges recognized through the first nine months of 2023. There is more detail on this in our Form 10-Q, which is being filed this afternoon. We now expect G&A operating expense for the full year of 2023 to be between $80 million and $85 million, which includes approximately $15 million-$20 million of non-cash depreciation and stock comp expense. Our GAAP revenue for full year 2023 is still expected to be between $80 million and $90 million. This revenue includes $65 million-$70 million in non-cash royalties and $15 million-$20 million in product sales. We anticipate full-year GAAP R&D operating expenses will range between $105 million and $115 million, which includes approximately $15 million-$20 million of non-cash depreciation and stock comp expense. Our full-year non-cash interest expense is expected to be between $20 million and $25 million. As I stated earlier, we expect to end this year with at least $320 million in cash and investments. And with that, we will now open the call for questions. Crystal? Thank you. As a reminder to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. Our first question will come from Jay Olson from Oppenheimer. Your line is open. Oh, hey, congrats on the progress, and thanks for providing this update. Can you talk about the phase IIb trial in atopic dermatitis? Congrats on the initiation of that study. Can you just talk about the feedback you're hearing from investigators? When do you expect to provide some guidance on enrollment rates, and when do you expect to complete recruiting for that study? Yeah, thanks. Thanks, Jay. I'm gonna ask Mary, as she's been meeting with a lot of these investigators over the past couple of months, to comment on that. Mary? ... Thank you, Jennifer, and thank you, Jay, for asking the question. We recently attended EADV in Berlin, and we were able to meet with 30 different investigators, mostly from Europe. And we're going to recruit this trial at 100 different clinical sites in the United States, Canada, Europe and Australia. And I can tell you that the investigators are very excited about REZPEG, the mechanism of action, and its application in atopic dermatitis. The presentation that Dr. Jonathan Silverberg made was very well attended and very well received. And Jonathan Silverberg, you know, mentioned that for many years we've known the importance of T regulatory cells, but we had never seen any data from a drug that actually expands T regulatory cells to improve dermal indications such as atopic dermatitis. And with an 83% reduction in the mean EASI score from baseline, this was what he calls best in industry. So there is a widespread enthusiasm from the investigators. I will tell you that a couple other things that are very compelling about our clinical trial are the following: Number one, we have a very good safety profile. Our drug is highly tolerable, and we've now shown that in roughly 600 patients. Number two, they really like the idea in the maintenance setting that we're gonna evaluate a monthly and a three-monthly maintenance regimen. And number three, the fact that their patients are going to be able to continue to receive REZPEG beyond the induction period of 16 weeks is very attractive to their patients and to the investigators as well. We feel that we will absolutely be able to deliver this trial on track and on time, with data, top-line data available in the first half of 2025. Hope that answers your question. Yeah, that's super helpful. Thank you so much for the details, and we'll look forward to future updates. On the phase IIb study of REZPEG and alopecia areata, can you just talk about how you're thinking about dosing? And then what's the bar there to initiate a phase III study? And how will you compare the performance of REZPEG with recently approved oral drugs in alopecia? Mary or JZ, would you like to take that? Sure. I'm happy to address that. So, you know, the JAK inhibitors, as you know, are efficacious. We see an effect after roughly 36 weeks of treatment. There are, as you know, many problems with JAK inhibitors. One, when you stop taking the JAK inhibitors, patients very rapidly lose their hair. And of course, you're well aware that there are black box warnings with the JAK inhibitors. You know, we've very closely looked at the baricitinib data, and we believe if we have efficacy similar to baricitinib, but don't accompany two things: One, a rapid loss of hair after cessation of treatment, or the ability to have, again, just like we're looking at in atopic dermatitis, a maintenance regimen that is far more convenient and favorable for the patient. We believe that a biologic would have, you know, great appeal in the area of alopecia areata. We are gonna look at 2 different doses versus placebo, and we will evaluate this at 36 weeks. Again, I think analogous or better efficacy than has been seen with the JAK inhibitors, with an improved safety profile, tolerability profile, and without accompanying black box warnings would make REZPEG highly competitive in this space. Great. Thank you for the super comprehensive responses, and congrats again on all the progress. Thank you very much, Jay. Thank you. As a reminder to ask a question, please press star 1 1. Our next question will come from Chris Shibutani from Goldman Sachs. Your line is open. Hi, everyone. This is Charlie on for Chris. Thanks so much for taking our questions, and congrats on the progress as well. Just a couple quick ones from us. First, on the 255 plans for strategic partnership, wondering if there's any update on the expected timeline for that partnership. I know year-end 2023 was the previous target. Wondering if that was still the case or if we had a new timeline in mind at this point. And then on the subsequent pipeline with the TNFR2, IND coming next year. Wondering if there's any update on the PEG CSF1R program and whether we should expect an IND from that program more on the 2025 sort of scale. Thank you. So I'm gonna have Howard take the first part of that question on 255, and then JZ, will you take the question on the preclinical program? So, yeah, sure. Good question. Look, NKTR-255 is a potentially very exciting program. We're talking to a number of companies. You see that we just completed a collaboration with CBMG in combination with TIL therapy. We have a collaboration with Merck KGaA in bladder cancer. So there's a lot going on with 255. We also have our own study running at the Fred Hutchinson Cancer Center in cell therapy. So there are companies that are interested. I think as a str... We would like to complete a strategic collaboration for NKTR-255. Our focus as a company is in immunology now, although I think this is a very exciting asset, and I can't give you specifics as to, as to, you know, when and how a collaboration will get done, but we're making great progress there. And as you can see by the, with the CBMG collaboration, we've just added, you know, another exciting potential application for NKTR-255. So we'll keep you posted. I don't know that it's gonna be, you know, end of this year, next year. Can't, can't say for sure, but clearly we're focused on that, and I do think it'll get done. JZ, would you handle the, the PEG CSF-1 question? ...Certainly. Yeah, thanks for the question. So at this time, we've really prioritized our efforts on the TNFR2 program, and that's really for a couple of reasons. The first is that TNFR2 builds on a complementary pathway around Treg targeting that's distinct from the IL-2 pathway that Respeg engages. So for example, you know that TNFR2 is a TNF superfamily member, is really one of the strongest signals that induces NF-kappa B in cells like Tregs. And it's also one of the strongest signals for controlling FoxP3 expression, which is a critical enzyme for both suppressive and differentiated and strong Treg responses, right? You know that loss of FoxP3 causes dedifferentiation of Tregs. So it's really a target that's very, very hot, you know, at this time. It's really built off of what we know and have learned through our deep experience with Rezpeg in the Treg field. And it also lets us, you know, leverage all that knowledge and advance our prioritized efforts into TNFR2. And so that's where we're really focused at this time. The PEG-CSF program, we will work on in the future, but it's really TNFR2 where we're focused on right now. I'll also say that as we've had the opportunity to discuss that program with some other outside entities, we have received a lot of interest around the program. We're finding many companies, like pharmas and large biotechs and others, that have really allocated time for TNFR2 into their strategy. So much is known around TNF inhibition, you know, with drugs like Humira, you know, Golimumab, Infliximab, Enbrel, and so on, that have had such a profound effect on rheumatology. Through that period of time, we've understood about the TNFR1, TNFR2 receptor axis, and what's missing, would you just block all TNF-alpha signaling, which includes also blocking the TNFR2 pathway. So this is something that we're very excited about. We like all of the interest and where we're really prioritizing our energy. We're very excited that we're on track. You know, we're moving into our cell line stage, you know, aiming into the manufacturing setting, and we're on track to be submitting our IND next year in 2024 for that program. Great. That's helpful. Thank you all so much. Thank you. I am showing no further questions from our phone lines, and I'd like to turn the conference back over to Howard Robin for any closing remarks. Well, thank you everyone for joining us today, and we remain focused on executing on the development of REZPEG and our immunology-focused research programs. And I think we have a clearly defined path forward. I'd like to thank all of our employees for their efforts and their hard work, and I want to thank our shareholders for their continued support. So we look forward to providing you with updates on our progress. Stay tuned, and thanks for joining us today. This concludes today's conference call. Thank you for your participation. You may now disconnect. Everyone, have a wonderful day.