This Phase 2 study is a 2-arm, multi-center, double-masked, placebo-controlled, 2:1 randomized sequential trial design in new onset T1D participants (within 100 days of diagnosis). Participants will be administered rezpegaldesleukin/placebo once every 14 days over 26 weeks with an additional 6-month follow-up period.

开始日期2025-11-13

申办/合作机构

National Institute of Diabetes & Digestive & Kidney Diseases

NCT06340360

/ Active, not recruiting临床2期

A Phase 2b, Randomized, Double-Blind, Parallel Group, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Rezpegaldesleukin in the Treatment of Severe to Very Severe Alopecia Areata in Adult Patients (Rezolve AA)

This is an interventional, randomized, double blind, parallel group, placebo-controlled, Phase 2b, 3-arm study to assess the effect of pegylated-recombinant-human interleukin-2 (rezpegaldesleukin) in adult participants with severe to very severe alopecia areata.
The estimated duration includes a screening period of up to 35 days, a 36-week treatment period, an optional 16-week treatment extension period, and a 24-week follow-up period. The maximum study duration is approximately 81 weeks for all participants.

开始日期2024-04-02

申办/合作机构

Nektar Therapeutics

NCT06136741

/ Active, not recruiting临床2期

A Phase 2b, Randomized, Double-Blind, Parallel-Group, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Rezpegaldesleukin in the Treatment of Adult Patients With Moderate-to-Severe Atopic Dermatitis (REZOLVE-AD)

This is an interventional, randomized, parallel group, treatment, Phase IIb, double blind, 4-arm study to assess the effect of pegylated-recombinant-human interleukin-2 (rezpegaldesleukin) in adult participants with moderate to severe atopic dermatitis.
The estimated duration is 15-35 days for screening, an Induction Period of 16 weeks, a Maintenance Period from Week 16-Week 52, and a Posttreatment Follow-Up Period for an additional year up to approximately Week 104 for all patients. Patients with a response at Week 16 (end of induction therapy) will be re-randomized for the maintenance therapy period.

开始日期2023-11-15

申办/合作机构

Nektar Therapeutics

100 项与 Rezpegaldesleukin 相关的临床结果

登录后查看更多信息

100 项与 Rezpegaldesleukin 相关的转化医学

登录后查看更多信息

100 项与 Rezpegaldesleukin 相关的专利（医药）

登录后查看更多信息

项与 Rezpegaldesleukin 相关的文献（医药）

2025-04-18·Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences

[Biological activity and antitumor effect of long-acting recombinant human interleukin-2 drug].

Article

作者: Zhang, Fengxia ; Zhu, Jingjing ; Jin, Ting ; Liang, Xuejun

OBJECTIVE:

To investigate the biological activity and antitumor effect of pegylated recombinant human interleukin 2 (PEG-rhIL-2) obtained by site-specific conjugation of polyethylene glycol (PEG) with non-natural amino acids, and to explore its antitumor mechanism.

METHODS:

The binding activities of PEG-rhIL-2 at three different sites (T41, Y45, and V91) to human interleukin 2 receptors α (IL-2R_α) and β (IL-2R_β) and were detected by surface plasmon resonance (SPR) technology. Western blot was used to detect the levels of the Janus kinase-signal transducer and activator of transcription 5 (JAK-STAT5) signaling pathway activated by different doses of rhIL-2 and PEG-rhIL-2 in CTTL-2 and YT cells. Blood was collected after a single administration in mice to detect the drug concentration at different time points and evaluate the pharmacokinetic parameters of Y45-PEG-rhIL-2. Mouse hepatoma cell line Hepa1-6, pancreatic cancer cell line Pan-02, and colon cancer cell line MC-38 were selected. Tumor models were constructed in C57BL/6 mice. Different doses of Y45-PEG-rhIL-2 and excipient control were administrated respectively to evaluate the tumor suppression effect of the drug. In the MC-38 colon cancer model, the tumor suppression effect of Y45-PEG-rhIL-2 combined with anti-programmed death-1 (PD-1) monoclonal antibody was evaluated. Hepa1-6 mouse tumor models were constructed and rhIL-2, Y45-rhIL-2 and Y45-PEG-rhIL-2 were administrated respectively. The proportion of tumor-infiltrating lymphocytes was analyzed by flow cytometry.

RESULTS:

The SPR detection results showed that the binding activities of PEG-rhIL-2 to IL-2R_α/IL-2R_β were both reduced. The affinity of Y45-PEG-rhIL-2 to IL-2R_α was reduced to approximately 1/250, and its affinity to IL-2R_β was reduced to 1/3. Western blot results showed that the activity of Y45-PEG-rhIL-2 in stimulating JAK-STAT5 signaling in CTLL-2 cells expressing heterotrimeric IL-2 receptor complex IL-2R_αβγwas reduced to approximately 1/300, while its activity in YT cells expressing heterodimeric IL-2 receptor complex IL-2R_βγwas reduced to approximately 1/3. The pharmacokinetic evaluation after a single dose in the mice showed that the elimination half-life of Y45-PEG-rhIL-2 was 17.7 h. Y45-PEG-rhIL-2 has pharmacokinetic characteristics superior to those of rhIL-2. Y45-PEG-rhIL-2 showed dose-dependent tumor suppression activity, and the combination of Y45-PEG-rhIL-2 and anti-PD-1 antibody had a better tumor-inhibiting effect than the single use of Y45-PEG-rhIL-2 or anti-PD-1 antibody. Flow cytometry analysis demonstrated that 72 h after the administration of Y45-PEG-rhIL-2, the proportion of tumor-infiltrating cytotoxic T lymphocytes (CD8⁺T cells) increased by 86.84%. At 120 h after administration, the ratio of CD8⁺T cells to regulatory T cells (Treg) increased by 75.10%.

CONCLUSION:

Y45-PEG-rhIL-2 obtained by site-specific conjugation via non-natural amino acids changed its receptor binding activity and inhibited tumor growth in dose-dependent manner in multiple tumor models by regulating CD8⁺T cells.

2022-01-01·Journal of translational autoimmunity

Selective expansion of regulatory T cells by NKTR-358 in healthy volunteers and patients with systemic lupus erythematosus

Article

作者: Levin, Robert ; Furie, Richard ; Diab, Isam ; Fanton, Christie ; Hanan, Nathan ; Chindalore, Vishala ; Zalevsky, Jonathan ; Dixit, Neha ; Dickerson, Daniel ; Haglund, Cat ; Kotzin, Brian L ; Gibbons, Jacqueline

Objective:

To evaluate NKTR-358, a polyethylene glycol-interleukin-2 conjugate composition designed to selectively induce regulatory T cells (Tregs), in first-in-human studies.

Methods:

Healthy volunteers and patients with systemic lupus erythematosus (SLE) received single- or multiple-dose (biweekly) NKTR-358 or placebo in two sequential, randomized, phase 1 studies (single ascending dose [SAD; NCT04133116] and multiple ascending dose [MAD; NCT03556007]). Primary objectives were safety and tolerability; secondary objectives included pharmacokinetics (PK) and immune effects of NKTR-358; exploratory objectives included effects on SLE disease activity.

Results:

There were eight ascending dose cohorts in the SAD study (0.3-28.0 μg/kg: n = 76; placebo: n = 24) and four in the MAD study (3-24.0 μg/kg: n = 36; placebo: n = 12). Most adverse events (AEs) were grade 1-2 injection-site reactions, with no treatment-related serious or severe AEs, or deaths. PK data showed dose proportionality and prolonged exposure (mean half-life: 7.4-12.9 days). Dose-dependent, selective, and sustained increases in percentages and absolute numbers of total CD4⁺ Tregs and CD25^bright Tregs were observed, with no significant changes in conventional CD4⁺ and CD8⁺ T cells, and low-level increases in natural killer cells. At the highest doses tested, administration of NKTR-358 resulted in a 12-17-fold increase in CD25^bright Tregs over baseline that was sustained for 20-30 days.

Conclusion:

NKTR-358 was well tolerated, had a suitable PK profile for biweekly dosing, and led to marked and selective dose-dependent increases in CD25^bright Tregs, with no significant changes in conventional T cells. These results provide strong support for further testing in SLE and other inflammatory diseases.

2021-01-01·Journal of translational autoimmunity

NKTR-358: A novel regulatory T-cell stimulator that selectively stimulates expansion and suppressive function of regulatory T cells for the treatment of autoimmune and inflammatory diseases

Article

作者: Zhang, Ping ; Dixit, Neha ; Kuo, Peiwen ; Lee, Myong ; Fanton, Christie ; Doberstein, Stephen K ; Cetz, Janet ; Sweeney, Theresa D ; VanderVeen, Laurie A ; Kamihara, Yusuke ; Chang, Thomas ; Dixit, Vidula ; Rubas, Werner ; Langowski, John L ; Kirksey, Yolanda ; Ritz, Jerome ; Tang, Yinyan ; Zalevsky, Jonathan ; Maiti, Mekhala ; Ji, Chunmei ; Kim, Grace ; Kirk, Peter

Impaired interleukin-2 (IL-2) production and regulatory T-cell dysfunction have been implicated as immunological mechanisms central to the pathogenesis of multiple autoimmune and inflammatory diseases. NKTR-358, a novel regulatory T-cell stimulator, is an investigational therapeutic that selectively restores regulatory T-cell homeostasis in these diseases. We investigated NKTR-358's selectivity for regulatory T-cells, receptor-binding properties, ex vivo and in vivo pharmacodynamics, ability to suppress conventional T-cell proliferation in mice and non-human primates, and functional activity in a murine model of systemic lupus erythematosus. In vitro, NKTR-358 demonstrated decreased affinity for IL-2Rα, IL-2Rβ, and IL-2Rαβ compared with recombinant human IL-2 (rhIL-2). A single dose of NKTR-358 in cynomolgus monkeys produced a greater than 15-fold increase in regulatory T-cells, and the increase lasted until day 14, while daily rhIL-2 administration for 5 days only elicited a 3-fold increase, which lasted until day 7. Repeated dosing of NKTR-358 over 6 months in cynomolgus monkeys elicited cyclical, robust increases in regulatory T-cells with no loss in drug activity over the course of treatment. Regulatory T-cells isolated from NKTR-358-treated mice displayed a sustained, higher suppression of conventional T-cell proliferation than regulatory T-cells isolated from vehicle-treated mice. NKTR-358 treatment in a mouse model (MRL/MpJ-Fas^lpr) of systemic lupus erythematosus for 12 weeks maintained elevated regulatory T-cells for the treatment duration and ameliorated disease progression. Together, these results suggest that NKTR-358 has the ability to elicit sustained and preferential proliferation and activation of regulatory T-cells without corresponding effects on conventional T-cells, with improved pharmacokinetics compared with rhIL-2.

172

项与 Rezpegaldesleukin 相关的新闻（医药）

2026-02-25

·医学新视点

有望接受每季度一次维持治疗！潜在“first-in-class”免疫疗法试验结果积极

Nektar Therapeutics近期宣布，其用于治疗中重度特应性皮炎（AD）患者的创新调节性T细胞（Treg）靶向生物制品rezpegaldesleukin，在REZOLVE-AD研究中为期36周的盲法维持治疗阶段取得积极结果。分析显示，在每月和每季度24 µg/kg给药方案下，分别有71%和83%的患者维持了湿疹面积和严重程度指数（EASI）评分较基线降低至少75%（EASI-75）应答，同时分别有85%和63%的患者维持了经验证特应性皮炎研究者总体评估（vIGA-AD）皮损清除（0）或几乎清除（1）应答。 REZOLVE-AD是一项全球性2b期研究，共入组393例中重度特应性皮炎患者。患者按3：3：3：2的比例随机分配，在16周诱导期内接受三种不同剂量的rezpegaldesleukin或安慰剂皮下注射治疗。完成16周诱导期后，接受rezpegaldesleukin治疗且达成EASI-50的患者，再次按1：1比例随机分配，在随后的36周盲法维持期内，以与诱导期相同剂量按每4周一次（Q4W）或每12周一次（Q12W）给药，直至第52周。 Rezpegaldesleukin在维持期内显示出长期疗效持久性，并持续改善AD疾病症状。疗效持久性方面，Q4W和Q12W给药方案在EASI-75、EASI-90、vIGA-AD应答以及瘙痒数字评分量表（NRS）应答方面均实现了持续的疾病控制，其中24 µg/kg的Q4W和Q12W方案在第52周表现出最高的疗效维持水平。随着治疗时间延长，部分患者在第52周新获得或进一步加深了EASI-75、EASI-90、瘙痒NRS评分及vIGA-AD 0/1应答，支持在更长疗程及更低给药频率下实现更强的疾病控制。 ▲试验疗效结果摘要（图片来源：参考资料[1]）在达到EASI-100方面，维持治疗阶段中，24 µg/kg的Q4W和Q12W方案下，实现EASI-100的患者比例较基线提高了2至5倍。在所有从第16周至第52周重新随机分配的患者中，Q4W维持给药使EASI-100应答率从4%提升至22%，Q12W给药则从9%提升至18%。在维持期基线时已达到EASI-75或vIGA-AD应答的重新随机患者中，Q4W给药使EASI-100应答率从6%提高至30%，Q12W给药则从14%提高至27%。在维持期内，rezpegaldesleukin的安全性特征与诱导期观察结果一致，未发现新的安全性问题，整体耐受性良好。在所有患者中，因不良事件导致的停药率为3.5%。治疗伴发不良事件（TEAE）总发生率为：重新随机并接受rezpegaldesleukin治疗的患者为72%，维持期安慰剂患者为65%。最常见的TEAE为注射部位反应，几乎均为轻度（77%），其发生率和频次均低于研究初始诱导期，因注射部位反应导致的停药率为0.7%。图片来源：123RF 自身免疫性和炎症性疾病会导致免疫系统错误攻击并损伤机体自身的健康细胞，其根本原因在于机体免疫自我耐受机制失效，从而促成致病性T淋巴细胞的形成并介导攻击。Rezpegaldesleukin是一种潜在“first-in-class”疗法，旨在解决患者免疫系统的失衡。它通过作用于体内白细胞介素-2受体复合物，刺激具强效免疫抑制性的调节性T细胞的增殖。通过激活这些细胞，rezpegaldesleukin有望帮助免疫系统恢复平衡。2025年2月，美国FDA授予rezpegaldesleukin快速通道资格，用于治疗12岁及以上、对外用处方疗法应答不佳或不适合使用该类疗法的中重度特应性皮炎成人及儿童患者。2025年7月，FDA再次授予rezpegaldesleukin快速通道资格，用于治疗体重至少40 kg、年龄在12岁及以上的成人及儿童重度斑秃（AA）患者。参考资料： [1] New REZOLVE-AD Maintenance Data in Atopic Dermatitis Demonstrate Rezpegaldesleukin Resulted in Durable and New Responses Across Key Disease Measurements with Both Monthly and Quarterly Dosing. Retrieved February 10, 2026 from https://ir.nektar.com/news-releases/news-release-details/new-rezolve-ad-maintenance-data-atopic-dermatitis-demonstrate 免责声明：本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，传递医学新知

2026-02-24

·PRNewswire

Nektar Therapeutics to Participate in Two Investor Conferences in March

SAN FRANCISCO, Feb. 24, 2026 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) today announced that company management will be participating in the TD Cowen 46th Annual Health Care Conference taking place March 2-4, 2026 in Boston and the 2026 Jefferies Biotech on the Beach Summit taking place March 9-11, 2026 in Miami. TD Cowen 46th Annual Health Care Conference in Boston on Wednesday, March 4, 2026 – webcast of the presentation to be available at 9:10 a.m. Eastern Time / 6:10 a.m. Pacific Time – link here 2026 Jefferies Biotech on the Beach Summit in Miami – March 9-11, 2026 – company management to be available for one-on-one meetings The presentation will be accessible via the webcast link above as well as on the Investor Events section of the Nektar website: . A replay of the presentation will be available for 30 days. If you would like to request a one-on-one meeting with company management during the conferences, please reach out to your respective representative. About Nektar Therapeutics Nektar Therapeutics is a clinical-stage biotechnology company focused on developing treatments that address the underlying immunological dysfunction in autoimmune and chronic inflammatory diseases. Nektar's lead product candidate, rezpegaldesleukin (REZPEG, or NKTR-358), is a novel, first-in-class regulatory T cell stimulator being evaluated in one Phase 2b clinical trial in atopic dermatitis, one Phase 2b clinical trial in alopecia areata, and one Phase 2 clinical trial in Type 1 diabetes mellitus. Nektar's pipeline also includes a preclinical bivalent tumor necrosis factor receptor type II (TNFR2) antibody and bispecific programs, NKTR-0165 and NKTR-0166, and a modified hematopoietic colony stimulating factor (CSF) protein, NKTR-422. Nektar, together with various partners, is also evaluating NKTR-255, an investigational IL-15 receptor agonist designed to boost the immune system's natural ability to fight cancer, in several ongoing clinical trials. Nektar is headquartered in San Francisco, California. For further information, visit and follow us on LinkedIn. For Investors: Vivian Wu 628-895-0661 [email protected] Corey Davis, Ph.D. LifeSci Advisors, LLC [email protected] 212-915-2577 For Media: Jonathan Pappas LifeSci Communications 857-205-4403 [email protected] SOURCE Nektar Therapeutics 21% more press release views with Request a Demo

临床2期

2026-02-17

·PRNewswire

Nektar Therapeutics Announces Research Collaboration with UCSF and Dr. Stephen Hauser for NKTR-0165, a Tumor Necrosis Factor Receptor 2 (TNFR2) Antibody, in Multiple Sclerosis

SAN FRANCISCO, Feb. 17, 2026 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) today announced an academic research collaboration with the University of California, San Francisco (UCSF) and Stephen L. Hauser, M.D., Robert A. Fishman Distinguished Professor of Neurology and Director of the UCSF Weill Institute for Neurosciences. Dr. Hauser is a neuroimmunologist whose research work has played a pivotal role in transforming the treatment landscape for patients with multiple sclerosis (MS). NKTR-0165 is a novel, first-in-class tumor necrosis factor receptor 2 (TNFR2) agonist antibody. TNFR2 signaling is an important gatekeeper of inflammation and its absence or deficit is associated with a broad range of autoimmune diseases. TNFR2 is highly expressed on regulatory T cells (Tregs), endothelial cells, and neuronal cells, many of which are involved in the pathogenesis of MS.1 "We are privileged to partner with Dr. Hauser on this important research initiative to explore the role of TNFR2 agonism in several models of MS," said Jonathan Zalevsky, Ph.D., Chief Research and Development Officer of Nektar. "Dr. Hauser is a renowned and pioneering researcher in the field and his work has led to therapeutic approaches from cytokines to B-cell depleting agents that have transformed MS treatment." The collaboration with UCSF will explore the potential role of TNFR2 agonism in the reduction of neurodegeneration and promotion of neuroprotection and cell repair when neurons are exposed to patient-derived B cells. Led by Dr. Hauser and his postdoctoral researcher Dr. Chaitrali Saha, the team at UCSF will conduct and fund all research efforts. Nektar will supply NKTR-0165 and will retain all rights to its programs under the collaboration. "We know that TNFR2 is expressed on specific immune and CNS cells," said Dr. Hauser. "With this important research initiative, we hope to evaluate the potential neuroprotective effect associated with the agonism of this receptor for treating both MS and other neurological conditions." In 2025, Stephen L. Hauser, M.D. won the Breakthrough Prize in Life Sciences for his work in identifying the direct cause of multiple sclerosis, which led to multiple new FDA approved therapies. As Director of the UCSF Weill Institute for Neurosciences, he leads research initiatives that link clinical and basic neurosciences at UCSF to accelerate research against neurologic diseases. His work led to the development of B cell therapies for MS patients, representing a powerful new approach for treating all forms of the disease and the first therapy of proven value for progressive MS. About NKTR-0165 and TNFR2 Bispecific Programs NKTR-0165 is a unique antibody agonist of the tumor necrosis factor receptor 2 (TNFR2). This investigational therapy is currently in IND-enabling studies and is being developed to address a number of autoimmune and CNS disorders, such as multiple sclerosis, vitiligo and ulcerative colitis. Leveraging learnings from the development of NKTR-0165, the company is also developing a pipeline of TNFR2 containing bispecific molecules that pair TNFR-2 agonism with other specificities. Our lead bispecific program, known as NKTR-0166, is a unique bivalent antibody incorporating a TNFR2 agonist epitope and an antagonist epitope validated in the treatment of rheumatology diseases. As a dual agonist:antagonist of known pathways associated with key pathways linked to disease pathogenesis, this investigational antibody is being developed to address a number of rheumatic disorders. About Multiple Sclerosis Multiple sclerosis (MS) is a chronic, unpredictable, and often disabling disease of the central nervous system (CNS) that disrupts the flow of information within the brain and between the brain and body. It is an autoimmune disease in which the immune system's B cells attack the myelin sheath, a protective coating on nerve fibers. Affecting the brain, spinal cord and optic nerve, MS causes nerve signals to slow or stop, resulting in muscle weakness, vision loss, chronic fatigue and cognitive decline in memory, attention or processing speed. According to the National Multiple Sclerosis Society, approximately 2.9 million people globally and 1 million people in the U.S. currently have MS.2 About Nektar Therapeutics Nektar Therapeutics is a clinical-stage biotechnology company focused on developing treatments that address the underlying immunological dysfunction in autoimmune and chronic inflammatory diseases. Nektar's lead product candidate, rezpegaldesleukin (REZPEG, or NKTR-358), is a novel, first-in-class regulatory T cell stimulator being evaluated in two Phase 2b clinical trials, one in atopic dermatitis, one in alopecia areata, and in one Phase 2 clinical trial in Type 1 diabetes mellitus. Nektar's pipeline also includes a preclinical bivalent tumor necrosis factor receptor type II (TNFR2) antibody and bispecific programs, NKTR-0165 and NKTR-0166, and a modified hematopoietic colony stimulating factor (CSF) protein, NKTR-422. Nektar, together with various partners, is also evaluating NKTR-255, an investigational IL-15 receptor agonist designed to boost the immune system's natural ability to fight cancer, in several ongoing clinical trials. Nektar is headquartered in San Francisco, California. For further information, visit and follow us on LinkedIn. Cautionary Note Regarding Forward-Looking Statements This press release contains forward-looking statements which can be identified by words such as: "will," "develop," "potential," "evaluate," "explore," "address," "may" and similar references to future periods. Examples of forward-looking statements include, among others, statements regarding the therapeutic potential of, and future development plans for, rezpegaldesleukin, NKTR-0165, NKTR-0166, NKTR-422, and NKTR-255. Forward-looking statements are neither historical facts nor assurances of future performance. Instead, they are based only on our current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, anticipated events and trends, the economy and other future conditions. Because forward-looking statements relate to the future, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. Our actual results may differ materially from those indicated in the forward-looking statements. Therefore, you should not rely on any of these forward-looking statements. Important factors that could cause our actual results to differ materially from those indicated in the forward-looking statements include, among others: (i) our statements regarding the therapeutic potential of rezpegaldesleukin, NKTR-0165, NKTR-0166, NKTR-422 and NKTR-255 are based on preclinical and clinical findings and observations and are subject to change as research and development continue; (ii) rezpegaldesleukin, NKTR-0165, NKTR-0166, NKTR-422 and NKTR-255 are investigational agents and continued research and development for these drug candidates is subject to substantial risks, including negative safety and efficacy findings in future clinical studies (notwithstanding positive findings in earlier preclinical and clinical studies); (iii) rezpegaldesleukin, NKTR-0165, NKTR-0166, NKTR-422 and NKTR-255 are in clinical development and the risk of failure is high and can unexpectedly occur at any stage prior to regulatory approval; (iv) data reported from ongoing clinical trials are necessarily interim data only and the final results will change based on continuing observations; (v) the timing of the commencement or end of clinical trials and the availability of clinical data may be delayed or unsuccessful due to regulatory delays, slower than anticipated patient enrollment, manufacturing challenges, changing standards of care, evolving regulatory requirements, clinical trial design, clinical outcomes, competitive factors, or delay or failure in ultimately obtaining regulatory approval in one or more important markets; (vi) a Fast Track designation does not increase the likelihood that rezpegaldesleukin will receive marketing approval in the United States; (vii) patents may not issue from our patent applications for our drug candidates, patents that have issued may not be enforceable, or additional intellectual property licenses from third parties may be required; and (viii) certain other important risks and uncertainties set forth in our Quarterly Report on Form 10-Q filed with the Securities and Exchange Commission on November 7, 2025. Any forward-looking statement made by us in this press release is based only on information currently available to us and speaks only as of the date on which it is made. We undertake no obligation to update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise. University of California Disclaimer This press release was prepared by Nektar Therapeutics and reflects solely the opinion of the company. Nothing in this statement shall be construed to imply any support or endorsement of Nektar Therapeutics, or any of its products or services, by the Regents of the University of California, its officers, agents and employees. Contacts: For Investors: Vivian Wu [email protected] Corey Davis, Ph.D. LifeSci Advisors, LLC [email protected] 212-915-2577 Ahu Demir, Ph.D. LifeSci Advisors, LLC [email protected] 212-915-3820 For Media: Jonathan Pappas LifeSci Communications 857-205-4403 [email protected] Faustman DL, Davis M, Kuhtreiber WM. TNFR2 Agonism: Basic Science and Promising Treatment for Multiple Sclerosis and Related Diseases. Int J Mol Sci. 2025 Aug 14;26(16):7839. doi: 10.3390/ijms26167839. PMID: 40869160; PMCID: PMC12386426. SOURCE Nektar Therapeutics 21% more press release views with Request a Demo

临床2期快速通道

100 项与 Rezpegaldesleukin 相关的药物交易

登录后查看更多信息

研发状态

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
斑秃	临床2期	美国	Nektar Therapeutics	2024-04-02
斑秃	临床2期	加拿大	Nektar Therapeutics	2024-04-02
斑秃	临床2期	波兰	Nektar Therapeutics	2024-04-02
中度特应性皮炎	临床2期	美国	Nektar Therapeutics	2023-11-15
中度特应性皮炎	临床2期	澳大利亚	Nektar Therapeutics	2023-11-15
中度特应性皮炎	临床2期	保加利亚	Nektar Therapeutics	2023-11-15
中度特应性皮炎	临床2期	加拿大	Nektar Therapeutics	2023-11-15
中度特应性皮炎	临床2期	克罗地亚	Nektar Therapeutics	2023-11-15
中度特应性皮炎	临床2期	捷克	Nektar Therapeutics	2023-11-15
中度特应性皮炎	临床2期	德国	Nektar Therapeutics	2023-11-15

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT06340360 (REZOLVE-AA, NEWS) 人工标引	临床2期	斑秃	92	rezpegaldesleukin low dose	壓鹽繭憲選觸範艱艱膚(製醖製選簾構艱遞膚觸) = Both treatment arms “more than doubled the SALT score reduction than that observed with placebo, with the majority of patients experiencing hair growth at Week 16 or later.” Participants in the higher-dose group had an average 28% improvement in hair coverage, compared with about 11% in the placebo group. When researchers removed data from four patients who did not meet key eligibility requirements, both drug doses showed statistically significant improvements, with hair regrowth of roughly 30%, compared with just under 6% for placebo. 遞夢構夢醖糧鏇範觸醖 (淵憲築鹹衊廠醖餘網遞 ) 更多	积极	2025-12-17
				rezpegaldesleukin high dose
NCT06136741 (REZOLVE-AD, PRNewswire \| ACAAI2025) 人工标引	临床2期	哮喘 \| 特应性皮炎	393	Rezpegaldesleukin (24 μg/kg q2w)	憲顧憲積顧顧願構鹹鑰(願憲鏇齋艱築糧觸夢鏇) = At least half of the patients (N=53) experienced clinically significant improvement (≥0.5 point reduction) in ACQ-5 at Week 16 across all treatment arms as compared to 13% in the placebo arm. 憲餘廠鹽鏇鑰蓋鹽遞積 (窪鏇遞製餘窪鏇繭積壓 ) 更多	积极	2025-11-08
				Rezpegaldesleukin (24 μg/kg q4w)
NCT06136741 (REZOLVE-AD, PRNewswire) 人工标引	临床2期	中度特应性皮炎 \| 重度特应性皮炎	393	Rezpegaldesleukin 24 µg/kg q2w	築醖鏇範獵鬱淵夢糧衊(醖憲襯鹽蓋遞網窪壓願) = 餘壓壓艱壓構膚艱築憲衊選蓋鹹淵壓選齋選鹽 (構襯醖艱鹽築壓網觸鹹 ) 达到更多	积极	2025-06-24
				Rezpegaldesleukin 18 µg/kg q2w	築醖鏇範獵鬱淵夢糧衊(醖憲襯鹽蓋遞網窪壓願) = 獵製製願憲網艱鹽壓夢衊選蓋鹹淵壓選齋選鹽 (構襯醖艱鹽築壓網觸鹹 ) 达到更多
NCT04380324 (AAD2025)	临床1/2期	银屑病 \| 系统性红斑狼疮 \| 溃疡性结肠炎 ... 更多	746	Rezpegaldesleukin	製遞醖鏇製膚願鏇糧衊(選膚範鹹鬱簾遞醖製鬱) = 獵鹽鏇壓餘構觸蓋鑰蓋鏇廠夢範醖壓獵窪鹽網 (觸範鹽鹽網遞製衊積廠 ) 更多	积极	2025-03-07
				Placebo	製遞醖鏇製膚願鏇糧衊(選膚範鹹鬱簾遞醖製鬱) = 製繭蓋構壓簾繭膚齋鏇鏇廠夢範醖壓獵窪鹽網 (觸範鹽鹽網遞製衊積廠 ) 更多
NCT04119557 \| NCT04081350 (Pubmed \| Nat Commun)	临床1期	炎症性皮肤病 Eczema Area and Severity Index (EASI) \| Investigator Global Assessment for Atopic Dermatitis (vIGA-AD) \| Psoriasis Area and Severity Index (PASI) ... 更多	-	Rezpegaldesleukin 10-12 µg/kg	鹹廠艱鹹鏇壓蓋衊鏇繭(構餘積選簾製艱鏇醖壓) = EASI-75 responses are maintained for 36 weeks after treatment discontinuation in 71% of week 12 responders 簾艱齋廠窪築鏇範繭範 (願鹽廠遞鑰簾艱鏇願艱 ) 更多	积极	2024-10-25
NCT04433585 (ISLAND-SLE, CTgov)	临床2期	系统性红斑狼疮	291	LY3471851 (LY3471851 High Dose)	蓋鹹鏇簾願範願餘獵築 = 遞積簾繭壓廠夢蓋構夢糧鬱齋構顧遞窪糧鬱鑰 (鑰廠願廠顧願廠願繭醖, 觸膚觸範網構選齋窪鹹 ~ 餘衊選醖鏇鹹願餘選獵) 更多	-	2024-04-23
				LY3471851 (LY3471851 Mid Dose)	蓋鹹鏇簾願範願餘獵築 = 範醖網構鬱襯構獵膚夢糧鬱齋構顧遞窪糧鬱鑰 (鑰廠願廠顧願廠願繭醖, 網壓憲遞鑰壓壓窪醖壓 ~ 獵窪選衊製艱壓壓遞餘) 更多
NCT04081350 (Phase 1b study, EADV2023)	临床1期	特应性皮炎 Treg	-	Rezpegaldesleukin 12 µg/kg	鹹鬱繭夢艱憲窪衊觸壓(蓋衊壓範壓鹽衊糧鏇網) = 獵構構觸網蓋網獵衊齋繭醖鏇襯鑰構積夢艱蓋 (顧製遞鬱製製窪鏇憲膚 ) 更多	积极	2023-10-11
				Rezpegaldesleukin 24 µg/kg	鹹鬱繭夢艱憲窪衊觸壓(蓋衊壓範壓鹽衊糧鏇網) = 膚蓋願襯壓餘鬱製簾鏇繭醖鏇襯鑰構積夢艱蓋 (顧製遞鬱製製窪鏇憲膚 ) 更多
NCT04677179 (INSTRUCT-UC, CTgov)	临床2期	溃疡性结肠炎	81	Placebo (Placebo (Induction Treatment Period))	襯衊願艱網齋艱蓋壓衊 = 觸範顧膚網繭獵遞艱構鏇廠構壓齋顧窪築鑰積 (觸齋網餘廠醖構廠願顧, 選壓範醖鏇淵糧壓構衊 ~ 遞願選淵夢齋願淵淵窪) 更多	-	2023-09-05
				LY3471851 (Low Dose LY3471851 (Induction Treatment Period))	襯衊願艱網齋艱蓋壓衊 = 蓋鏇衊襯鹽製鏇餘憲製鏇廠構壓齋顧窪築鑰積 (觸齋網餘廠醖構廠願顧, 鏇淵艱鏇餘窪齋築鏇願 ~ 築憲鹽蓋鏇鹽窪網製願) 更多
NCT04433585 (ISLAND-SLE, Corporate Publications) 人工标引	临床2期	系统性红斑狼疮	291	rezpegaldesleukin 300mcg Q2W	簾鬱遞餘鑰醖鑰獵醖鏇(夢餘窪鏇鹹餘襯顧夢鬱) = 觸衊積鏇製製襯顧鏇網鹹餘製範簾餘簾憲顧糧 (憲繭夢簾艱衊襯糧糧觸 ) 更多	不佳	2023-02-23
				rezpegaldesleukin 900mcg Q2W	簾鬱遞餘鑰醖鑰獵醖鏇(夢餘窪鏇鹹餘襯顧夢鬱) = 壓鑰鏇壓鹹壓糧範憲憲鹹餘製範簾餘簾憲顧糧 (憲繭夢簾艱衊襯糧糧觸 ) 更多
NCT04081350 (Corporate Publications) 人工标引	临床1期	特应性皮炎	43	LY3471851 12 µg/kg	網膚艱願鬱鏇醖蓋餘製(衊範獵襯製襯獵顧製壓) = 鑰積築襯淵製齋鹽夢顧遞蓋餘顧選築齋膚齋艱 (觸膚膚夢選繭獵齋襯鹹 ) 更多	积极	2022-09-07
				LY3471851 24 µg/kg	網膚艱願鬱鏇醖蓋餘製(衊範獵襯製襯獵顧製壓) = 窪衊遞遞築鏇顧艱鏇艱遞蓋餘顧選築齋膚齋艱 (觸膚膚夢選繭獵齋襯鹹 ) 更多