Nektar Therapeutics Study update

Vivian, please go ahead. Thank you, and good morning, everyone.

Thank you for joining us today to discuss new data being presented at the EADV 2026 Congress. On today's call, we expect to make forward-looking statements regarding our business, including statements regarding the potential of and future development plans for rezpegaldesleukin, the timing and plan for future clinical data presentations, and other statements regarding the future of our business. Because forward-looking statements relate to the future, they are subject to uncertainties and risks that are difficult to predict, many of which are outside of our control. Our actual results may differ materially from these statements. Important risks and uncertainties are set forth in our most recent annual report and quarterly report on Form 10-Q, available at sec.gov. We undertake no obligation to update any of these forward-looking statements, whether as a result of new information, future developments, or otherwise.

A webcast of this call will be available on the IR page of Nektar's website at nektar.com. Today, you will hear from Dr. Jonathan Zalevsky, our Chief Research and Development Officer, and Dr. Mary Tagliaferri, our Chief Medical Officer. We are also joined today by Dr. Benjamin Ungar. Dr. Ungar is an Assistant Professor of The Kimberly and Eric J. Waldman Department of Dermatology at the Icahn School of Medicine at Mount Sinai and an expert in this field. We are very glad to have him with us here today. With that said, I would like to hand the call over to our Chief Medical Officer, Mary Tagliaferri.

Mary? Thank you, Vivian. At Nektar, our strategy has been to advance 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 agonist designed to selectively expand regulatory T cells. With Tregs, we can address multiple inflammatory pathways at once, including Th1, Th2, Th17, Th22, JAK/STAT, and others, which drives the efficacy and resolves the symptoms and underlying heterogeneous pathology of the disease. This is in contrast to therapies that only target Th2 disease pathways. Our REZPEG development program is addressing three distinct autoimmune diseases: atopic dermatitis, alopecia areata, and type 1 diabetes, each of which represents a substantial commercial opportunity. Alopecia areata affects roughly 160 million people worldwide, with approximately 30 million new cases diagnosed every year.

The only class of systemic medicines approved are oral daily JAK inhibitors, which have significant drawbacks. JAK inhibitors possess box warnings, and they are also associated with high relapse rates after patients stop treatment. We believe this provides a significant opportunity for Nektar to advance REZPEG as the first biologic to be approved to treat these patients, offering potentially better safety and efficacy, which could improve over time with continued treatment. Additionally, JAK inhibitors are taken orally once daily, which can present challenges for long-term drug adherence. A therapy with less frequent dosing makes long-term treatment more manageable for patients. Beyond adherence, a therapeutic option which has an extended biologic pharmacodynamic effect can offer durable and stable efficacy even in the setting of imperfect compliance. There also remains an opportunity for a therapy that reduces or eliminates the routine laboratory monitoring requirements associated with 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's novel Treg mechanism has the potential to address these major unmet needs. Shown here are findings presented at the 2026 AAD meeting 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 baricitinib. The data also demonstrate poor persistence on therapy, with most patients discontinuing treatment within the first six months. We designed the treatment period of the phase IIb REZOLVE-AA study to answer four important development questions for our phase III study design.

First, can a Treg cell-directed biologic provide meaningful efficacy with a robust safety profile? The answer to this first question is yes. REZPEG demonstrated consistent separation from placebo across efficacy measures evaluated, with the safety profile consistent with prior studies. Second, because we hadn't completed any prior trials in AA, we wanted to understand the kinetics of hair regrowth. What the trial showed is the greatest increase in hair regrowth occurred after week 16 and continued beyond the initial 36-week induction period. Third, we asked what dose should be advanced to the registrational trial, and based on the data, the 24 microgram per kilogram Q2W regimen has been selected for our phase III clinical trial. Finally, we needed to determine how long the induction period should be.

The additional responses observed from week 36 to week 52 in the treatment extension cohort support a 52-week phase III induction period for the evaluation of the SALT score of 20 or less, which is the registrational endpoint. As a reminder, our phase IIb REZOLVE-AA trial enrolled 92 adult patients with severe to very severe alopecia areata. The current episode duration was up to eight years. Patients received treatment every two weeks with subcutaneous REZPEG 24 micrograms per kilogram, 18 micrograms per kilogram or placebo. Unlike a traditional maintenance phase of an atopic dermatitis trial where responders advance to additional weeks of treatment, this study included a blinded 16-week treatment extension for patients who demonstrated hair growth but had not reached SALT 20 or less at week 36. This created a total treatment period of 52 weeks for the extension cohort.

We previously announced in April the 52-week treatment data from the study. Today, we are presenting the six-month off-treatment data. This slide shows the SALT 20 responses over time to week 52 for the entire enrolled patient population. Recall, SALT 20 corresponds to at least 80% scalp hair coverage and represents a clinically meaningful endpoint. The central observation is that the REZPEG response curve continued to rise through to week 52. It does not plateau. These data support that extended treatment beyond one year could result in additional gain in SALT 20 responses. On the right side are the corresponding 52-week time points for low-dose baricitinib from the BRAVE registrational studies. We achieved our goal of a similar response rate compared to low-dose baricitinib at 52 weeks for the key SALT 20 registrational endpoint.

With comparable clinical benefit to a low-dose JAK inhibitor, plus twice monthly dosing and a more favorable safety profile, it is easy to see how REZPEG could become the first biologic used as first-line therapy for alopecia areata. This previously reported analysis shows patients who completed 52 weeks of treatment. Eight new patients treated with REZPEG converted to SALT 20 among the 27 REZPEG-treated patients in the 52-week treatment cohort. The new response rates were 29% in the 18 microgram group and 31% in the 24 microgram group. No new SALT 20 responses were observed in the four placebo patients. Here we present, for the first time, a new analysis from the 52-week treatment cohort. For context, duration of the current alopecia areata episode is considered an important prognostic factor, with longer continuous episodes established as a more difficult to treat patient population.

In this cohort, REZPEG achieved similar week 52 SALT 20 response rates regardless of current episode duration, with comparable outcomes observed in patients with episodes shorter than four years and those with episodes of four years or longer. You can see the response rates were 29% and 30% respectively. Approximately 37% of the REZPEG-treated patients had a current continuous episode of at least four years. While the subgroup sizes are small, these results suggest that clinically meaningful hair regrowth was not limited to patients with a shorter duration of disease. Looking at current episode duration with low-dose baricitinib, you can see a clear difference between the two cohorts. Patients whose current episode is four years or longer achieved a lower SALT 20 response than those whose current episode is shorter than four years. Now let's look at the off-treatment durability.

In this trial, we followed all patients for up to six months off treatment. We believe this was particularly relevant to evaluate because REZPEG is a Treg-directed biologic that enhances endogenous immune regulation rather than simply suppressing a downstream inflammatory signal. Shown here is the durability data for both the four-month and six-month off-treatment periods for patients who received 52 weeks of treatment in the study. For four months or six months off treatment, you can see highly durable efficacy with REZPEG, with 75% of patients maintaining the SALT 20 response at four months and 63% maintaining the SALT 20 response at six months. For context, we have shown here the historical data for low-dose baricitinib, also at four months and six months off treatment. These patients in the baricitinib studies also received 52 weeks of treatment prior to being followed off treatment.