A Phase 3, Randomized, Double-Blind, Parallel-Group, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Rezpegaldesleukin (NKTR-358) Monotherapy in the Treatment of Patients ≥ 12 Years of Age With Moderate-to- Severe Atopic Dermatitis

This is an interventional, randomized, parallel group, treatment, Phase 3, double blind study to assess the effect of Rezpegaldesleukin in participants 12 years of age or older with moderate to severe atopic dermatitis, as compared to placebo.
The estimated participant overall duration is approximately 15 months.

开始日期2026-08-07

申办/合作机构

Nektar Therapeutics

NCT07690371

/ Recruiting临床3期

开始日期2026-06-29

申办/合作机构

Nektar Therapeutics

NCT07142252

/ Recruiting临床2期IIT

Rezpegaldesleukin (NKTR-358) in New Onset Type 1 Diabetes Mellitus

This Phase 2 study is a 2-arm, multi-center, double-masked (masking of the participant, care provider and investigator), placebo-controlled, 2:1 randomized 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2026-05-14

申办/合作机构

National Institute of Diabetes & Digestive & Kidney Diseases

100 项与 Rezpegaldesleukin 相关的临床结果

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100 项与 Rezpegaldesleukin 相关的转化医学

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100 项与 Rezpegaldesleukin 相关的专利（医药）

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项与 Rezpegaldesleukin 相关的文献（医药）

2026-11-01·Dermatology and Therapy

Rezpegaldesleukin and Regulatory T Cell Restoration in Immune-Mediated Skin Diseases

Review

作者: Torres, Tiago ; King, Brett ; Domingues, João ; Chovatiya, Raj

Inflammatory skin diseases such as atopic dermatitis (AD), psoriasis, and alopecia areata (AA) are characterized by immune dysregulation involving impaired regulatory T cell (T_reg) function and persistent activation of effector inflammatory pathways. Current targeted therapies largely suppress downstream inflammatory signaling rather than correcting upstream regulatory abnormalities. Rezpegaldesleukin (REZPEG; NKTR-358) is a first-in-class, T_reg-selective interleukin-2 (IL-2) receptor agonist engineered to preferentially expand cluster of differentiation 4 positive (CD4⁺) FOXP3⁺ T_regs while minimizing activation of conventional effector T cells and natural killer (NK) cells. This review summarizes the biological rationale, mechanism of action, and emerging clinical evidence supporting REZPEG across dermatologic indications, particularly AD and AA. In phase 1 and phase 1b studies, REZPEG induced selective and durable T_reg expansion, attenuation of inflammatory biomarkers, and clinical improvements in AD and psoriasis, including prolonged off-treatment responses. In the phase 2b REZOLVE-AD trial, all active dosing regimens significantly improved Eczema Area and Severity Index outcomes versus placebo, with responses maintained or further deepened through week 52 with monthly or quarterly maintenance dosing. In severe AA, the phase 2b REZOLVE-AA trial did not meet its primary endpoint: mean Severity of Alopecia Tool (SALT) reductions at week 36 were 28.2% and 30.3% with REZPEG 24 and 18 µg/kg, respectively, versus 11.2% with placebo (p = 0.186 and p = 0.121). A supportive sensitivity analysis excluding four participants with major eligibility violations reached statistical significance, while hypothesis-generating extension data suggested further hair regrowth through week 52. Across completed studies, REZPEG has demonstrated a favorable tolerability profile, predominantly characterized by mild injection-site reactions, without major safety signals. Collectively, these findings support selective T_reg expansion as a mechanistically novel therapeutic strategy in immune-mediated skin disease, while further controlled studies are needed to define REZPEG's long-term efficacy and therapeutic positioning.

2026-08-01·LANCET

Rezpegaldesleukin treatment of moderate-to-severe atopic dermatitis (REZOLVE-AD): final results from the 16-week induction period of an international, double-blind, placebo-controlled, randomised phase 2b study

Article

BACKGROUND:

Rezpegaldesleukin is an interleukin-2 receptor agonist that selectively expands and enhances the function of regulatory T cells (Tregs), offering a novel therapeutic approach for autoimmune and inflammatory diseases such as atopic dermatitis. We aimed to compare the efficacy and safety analyses of rezpegaldesleukin with placebo in adults with moderate-to-severe atopic dermatitis naive to biological treatments.

METHODS:

REZOLVE-AD was a phase 2b, randomised, double-blind, placebo-controlled study conducted in 107 community research centres or hospitals in ten countries (Australia, Bulgaria, Canada, Croatia, Czechia, Germany, Hungary, Poland, Spain, and the USA). Eligible patients were adults (aged 18 years or older) with confirmed atopic dermatitis (American Academy of Dermatology Consensus Criteria) diagnosed at least 12 months before enrolment, with moderate-to-severe disease activity defined by an Eczema Area and Severity Index (EASI) score of at least 16·0, validated Investigator Global Assessment for Atopic Dermatitis (vIGA-AD) score of at least 3 (moderate), and at least 10% affected body surface area. Patients were randomly allocated (3:3:3:2) to receive subcutaneous rezpegaldesleukin 24 μg/kg or rezpegaldesleukin 18 μg/kg every 2 weeks, rezpegaldesleukin 24 μg/kg every 4 weeks, or placebo for 16 weeks during the induction period. Randomisation was done by an independent vendor using Randomisation and Trial Supply Management methodology via an interactive response system and was stratified by baseline disease severity (vIGA-AD 3 [moderate] vs 4 [severe]) and geographical region (North America vs rest of world). All patients, investigators, and those assessing outcomes were masked to treatment assignment. Outcomes for the induction period were assessed through week 16 and are included in this report. The primary endpoint was percentage change from baseline in EASI score at week 16. Efficacy and safety analyses were conducted in all randomly assigned patients exposed to study treatment, excluding those enrolled at two sites closed due to Good Clinical Practice non-compliance, both of which received notification of closure approximately 300 days before database lock. All missing data were imputed with multiple imputation. The trial was registered with ClinicalTrials.gov (NCT06136741).

FINDINGS:

398 patients were enrolled between Nov 15, 2023, and Jan 9, 2025. A total of 393 patients were analysed (104 in the rezpegaldesleukin 24 μg/kg every 2 weeks group, 106 in the rezpegaldesleukin 18 μg/kg every 2 weeks group, 110 in the rezpegaldesleukin 24 μg/kg every 4 weeks group, and 73 in the placebo group); 203 (52%) patients were female and 190 (48%) were male. All three rezpegaldesleukin groups met the primary endpoint. Rezpegaldesleukin showed dose-dependent improvements compared with placebo in mean percentage change in EASI from baseline at week 16: -61% (SE 3·8) for rezpegaldesleukin 24 μg/kg every 2 weeks, -58% (3·8) for rezpegaldesleukin 18 μg/kg every 2 weeks, and -53% (3·7) for rezpegaldesleukin 24 μg/kg every 4 weeks versus -31% (4·5) for placebo. Treatment differences versus placebo were -30 percentage points (95% CI -41·3 to -18·0; p<0·0001) for rezpegaldesleukin 24 μg/kg every 2 weeks, -27 percentage points (-38·5 to -15·7; p<0·0001) for rezpegaldesleukin 18 μg/kg every 2 weeks, and -22 percentage points (-33·3 to -10·3; p=0·0002) for rezpegaldesleukin 24 μg/kg every 4 weeks. Treatment-emergent adverse events observed in at least 5% of rezpegaldesleukin-treated patients (n=320) and greater than placebo (n=73) included injection-site reaction (223 [70%] vs three [4%]), eosinophilia (25 [8%] vs two [3%]), pyrexia (20 [6%] vs two [3%]), headache (20 [6%] vs three [4%]), upper respiratory tract infections (19 [6%] vs four [5%]), and arthralgia (16 [5%] vs one [1%]). Nearly all (>99%) injection-site reactions were mild to moderate in severity and resolved. There was no evidence of an increased risk of serious or severe adverse events, and no deaths were reported during the induction period.

INTERPRETATION:

Over the 16-week induction period, rezpegaldesleukin treatment resulted in significant and clinically meaningful improvements across multiple clinical endpoints, including the primary endpoint of EASI percentage change from baseline, in comparison with placebo. Rezpegaldesleukin had a clinically favourable adverse event profile in adult patients with moderate-to-severe atopic dermatitis, supporting its further development as a novel Treg-enhancing biological treatment.

FUNDING:

Nektar Therapeutics.

2026-03-23·Cureus Journal of Medical Science

Biologic Monotherapies for Moderate-to-Severe Atopic Dermatitis: A Systematic Review and Bayesian Network Meta-Analysis of Established and Investigational Agents

Review

作者: Babul, Najib ; Soliman, Yssra ; Babul, Arya ; Mehta, Devina ; Hussain, Momina

Biologic therapies targeting maladaptive type 2 inflammation have transformed the management of moderate‑to‑severe atopic dermatitis (AD); however, comparative evidence integrating both approved and next‑generation investigational agents remains limited. This Bayesian network meta‑analysis (BNMA) provides the first unified evaluation of all biologic monoclonal antibodies approved as monotherapy for AD (dupilumab, lebrikizumab, tralokinumab) together with emerging immunotherapies, including amlitelimab, rademikibart, rezpegaldesleukin, rocatinlimab, telazorlimab, temtokibart, and zumilokibart, across key efficacy measures. A PRISMA‑2020-compliant systematic review and PROSPERO‑registered protocol (CRD420251162704) identified phase 2-3 randomized, double‑blind, placebo‑controlled trials reporting week‑16 outcomes (week‑24 for rocatinlimab). A Bayesian random‑effects NMA estimated relative risks (RRs) for EASI‑75, EASI‑90, IGA‑AD 0/1, and ≥4‑point improvement in itch Numeric Rating Scale (NRS). Treatment hierarchy was evaluated using both Bayesian (SUCRA) and frequentist (P‑score) approaches. Seventeen randomized controlled trials (RCTs) involving more than 6,000 patients were included in the analysis. Dupilumab demonstrated the most consistent and reliable efficacy across all evaluated endpoints, including improvements in EASI-75, EASI-90, IGA-AD 0/1, and itch NRS. Among investigational therapies, rocatinlimab showed a notable signal for deep clinical responses, although the available evidence remains limited and less precise. Other emerging agents, including rademikibart, temtokibart, and zumilokibart, demonstrated encouraging efficacy profiles, whereas telazorlimab showed comparatively modest clinical benefit. Ranking analyses consistently positioned dupilumab as the most reliable and highest-performing therapy overall, followed by rocatinlimab. Overall, biologic therapies were generally well tolerated in the short term; however, dupilumab remains the only agent supported by extensive long-term safety data extending up to a decade. This analysis relied on indirect comparisons anchored to short‑term placebo‑controlled induction periods, limiting assessment of long‑term safety and durability, particularly for mechanistically distinct agents such as rezpegaldesleukin, a regulatory T cell (Treg) pathway agonist, and rocatinlimab, an OXO pathway inhibitor. Evidence for several emerging therapies was restricted to small phase 2 trials, resulting in wide credible intervals (Crls) and lower certainty in comparative rankings. Trial heterogeneity in baseline severity, ethnic composition, and geographic setting may have introduced residual confounding despite sensitivity and meta‑regression analyses. These factors should be considered when interpreting relative efficacy estimates This NMA demonstrates that dupilumab remains the most reliable and effective biologic monotherapy for moderate‑to‑severe AD, supported by the greatest precision, reproducibility, and long‑term safety. Rocatinlimab shows promising investigational efficacy but requires efficacy and long-term safety validation. Zumilokibart, rademikibart, and temtokibart emerge as additional candidates with encouraging activity, whereas telazorlimab showed limited clinical benefit. Collectively, these findings provide a comprehensive comparative framework to inform biologic selection and therapeutic sequencing.

274

项与 Rezpegaldesleukin 相关的新闻（医药）

2026-10-27

·BioSpace

Nektar Therapeutics to Announce Financial Results for the Third Quarter on Thursday, November 12, 2026, After Close of U.S.-Based Financial Markets

SAN FRANCISCO , Oct. 27, 2026 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) will announce its financial results for the third quarter ended September 30, 2026 on Thursday, November 12, 2026, after the close of U.S.-based financial markets. Howard Robin, President and Chief Executive Officer, will host a conference call to review the results beginning at 5:00 p.m. Eastern Time/2:00 p.m. Pacific Time. This press release and live audio-only webcast of the conference call can be accessed through a link that is posted on the Home Page and Investors section of the Nektar website: The web broadcast of the conference call will be available for replay through December 12, 2026. To access the conference call, please pre-register here . All registrants will receive dial-in information and a PIN allowing them to access the live call. 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 atopic dermatitis, alopecia areata, and Type 1 diabetes mellitus. Nektar's pipeline also includes 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 is headquartered in San Francisco, California. For further information, visit and follow us on LinkedIn . Contacts For Investors: Vivian Wu 628-895-0661 VWu@nektar.com Corey Davis, Ph.D. LifeSci Advisors 212-915-2577 cdavis@lifesciadvisors.com For Media: Susan Roberts LifeSci Communications 202-779-0929 sroberts@lifescicomms.com View original content to download multimedia: SOURCE Nektar Therapeutics

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2026-10-23

·PRNewswire

Nektar Therapeutics Reports Inducement Grants Under Nasdaq Listing Rule 5635(c)(4)

SAN FRANCISCO, Oct. 23, 2026 /PRNewswire/ -- Nektar Therapeutics (NASDAQ: NKTR) today announced that, on October 20, 2026, the Organization and Compensation Committee of Nektar's Board of Directors granted non-qualified stock options to purchase an aggregate of 45,750 shares of its common stock and 2,775 restricted stock units (RSUs) to sixteen newly-hired employees under Nektar's 2025 Inducement Plan, as amended. Nektar's 2025 Inducement Plan was adopted by its Board of Directors on November 6, 2025 and amended on September 23, 2026 to increase the number of shares of common stock reserved and available for issuance under the plan by 250,000 shares, for a total of 500,000 shares. The plan is used exclusively for the grant of equity awards to individuals who were not previously an employee or non-employee director of Nektar (or following a bona fide period of non‑employment), as an inducement material to such individual's entering into employment with Nektar, pursuant to Nasdaq Listing Rule 5635(c)(4). The stock options have an exercise price per share equal to $39.22, which is equal to the closing price of Nektar's common stock on October 20, 2026. The stock options have an eight-year term and will vest over four years with 1/4th of the shares vesting on the one-year anniversary of the employee's grant date and 1/48th of the shares vesting monthly thereafter over the next three years, subject to each employee's continued employment with Nektar on such vesting dates. The RSUs vest over four years with 1/4th of the shares vesting following the one-year anniversary of the employee's grant date and 1/16th of the shares vesting quarterly thereafter over the next three years, subject to each employee's continued employment with Nektar on the applicable vesting dates. The stock options and RSUs are subject to the terms and conditions of Nektar's 2025 Inducement Plan, as amended, and the terms and conditions of the stock option and RSU agreement covering the grant. 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 atopic dermatitis, alopecia areata, and Type 1 diabetes mellitus. Nektar's pipeline also includes 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 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", "can," "develop," "potential," "expand," "address," "may," "plan" and similar references to future periods. Examples of forward-looking statements include, among others, statements regarding the safety and efficacy profile and therapeutic potential of, and future development plans for, rezpegaldesleukin, NKTR-0165, NKTR-0166, and NKTR-422, and potential patient preferences and market adoption related thereto, and plans and timing of future clinical trials and data releases. 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 and NKTR-422 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 and NKTR-422 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 and NKTR-422 are in various stages of preclinical and clinical development, the risk of failure is high and can unexpectedly occur at any stage of development, and there can be no assurance that any such drug candidate will obtain regulatory approval; (iv) data reported from ongoing clinical trials may be preliminary or interim and may change as additional patient data become available or as continuing observations, verifications and analysis are completed; (v) the timing of the initiation or completion 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 filings with the Securities and Exchange Commission (SEC), including the risks and uncertainties described under the heading "Risk Factors" in our most recent Annual Report on Form 10-K or Quarterly Report, as such risks and uncertainties may be amended or supplemented by our other filings with the SEC . 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. Contacts For Investors: Vivian Wu 628-895-0661 [email protected] Corey Davis, Ph.D. LifeSci Advisors 212-915-2577 [email protected] For Media: Susan Roberts LifeSci Communications 202-779-0929 [email protected] SOURCE Nektar Therapeutics 21% more press release views with Request a Demo

快速通道

2026-10-23

·Antibody Research

再说PD1/IL2，与常识相悖，IL2针对alpha受体结合增强，未必带来Treg的更强增殖

▎追溯现有的一些指向都在说IL2结合CD25（IL2Rα）增强，会带来Treg的升高，这是惯有而且容易被大众理解的一套理论，但越来越多的数据，可能逐渐会显现出另一种完全不同的实验数据和现象。反而相对更强的IL2Rα结合，更偏向性比例上CD8阳性 T细胞的增殖。这里面我们再次提到NAKTAR的NKTR-358。 NKTR-358（Rezpegaldesleukin，rezpeg）目标是选择性恢复Treg稳态，偏向性激活Treg，但几乎不可能做到。该分子采用阿地白介素〔aldesleukin，商品名Proleukin〕的氨基酸序列，并通过化学方法偶联稳定的聚乙二醇（PEG）基团，拟以低剂量皮下注射给药，同时尽量减少对常规T细胞功能的影响。从现实意义的亲和力来看，NKTR-358的亲和力远不如野生型IL-2。所以NAKTAR只能用相对数据，但具有相对更强的IL-2Rα结合能力，也很难得到数据的支持。如果计算“对α相对于β的亲和力优势”： - rhIL-2：530÷4.3≈123倍。 - NKTR-358：88,000÷7,300≈12倍。相对β，NKTR-358容易结合IL2Rα，但这种相对优势比rhIL-2小，而非更大。也不能解释为“PEG对β结合的削弱比对α更严重”。所以，相比于野生型，反而NKTR-358并不算是偏向性alpha IL-2。野生型相比来看，更像是一款偏向性alpha IL-2。针对一个这样的IL2Rα削减程度更高，而野生型alpha偏向性更强的数据，来看体内T细胞增殖概况，可能并不想大家想象的样子。对于体内数据，我们从下图来看，NKTR-358对于Treg激活是强烈的，但同时对于增殖CD4+ T细胞相比于野生型IL2也更强烈。野生型反而相对均匀增殖的状态，CD8+ T细胞稍有增强的趋势。根据上述计算，显然野生型更为alpha偏向性。其他家也同样得出类似结论，如下图猴子PD数据，TA3便为增强IL2Rα结合的PD1/IL2，增强IL2Rα结合后，反而并没有增强Treg的增殖，而IL2Rα结合弱IL2Rβ/γ结合强的TA1，更能引起Treg的增殖，同时对于整体的CD4+ T细胞引起了超大量的增殖，这可能是毒性的来源，Treg的增殖并不能完全抑制整体CD4的毒性。与此同时，TA3相对应的是CD8阳性T细胞有了比例上的偏向性激活。这其实是完全跟当下理论相反的实验想象。同时，根据外周PBMC检测数据，在未激活的状态下，整体无论是CD4还是CD8，CD25的表达均是非常低，相比于PD1还要低。但激活以后CD25迅速增强。所以，我们返回头来思考，为什么罗氏的PD1/IL2完全削弱alpha结合之后，仍然有很强的毒性。PD1依赖下IL2激活已经足够，而这种激活，甚至是更能激活CD4阳性T细胞。也就是说外周毒性，在未被刺激的情况下，PD1/IL2Rβ/γ也足够主导毒性。β/γ要削弱到合适的位置。 CD25（IL-2Rα）属于Ⅰ型跨膜糖蛋白，由三部分组成：胞外区（extracellular domain）：负责结合 IL-2；单跨膜区（transmembrane domain）；短胞内尾（cytoplasmic tail）。其中胞内尾非常短，缺乏经典信号基序，无明确激活下游通路的结构域。所以CD25单独结合IL-2后不能启动细胞内信号所以，以此CD25在一定程度上可以作为依赖性激活IL-2Rβ（CD122）/γ(CD123)的标志。CD25在存在构成性表达的同时，也有另一种存在形式，就是受到炎症刺激后诱导性上调表达。所以PD1，CD25双依赖激活，理论上是存在的，当然现实中也可以被验证。 IL-2Rα/β/γ作为一个整体调节的话，就是尽可能增强对于IL-2Rα的结合，削弱β/γ本身的激活，使得最大限度的依赖性激活，在不存在IL-2Rα和PD1的时候，完全不被激活。相对来说更优的PD1/IL2，在理论上，就有了存在的可能性了。增强alpha，减弱β/γ。但活性又不能太弱，这样就没有了增殖T细胞的能力。这个窗口是极小的。外周系统中IL-2Rα和PD1的表达相对是微弱的，当遇到炎症环境，两者才会急剧上调表达。这样在外周系统中对于IFN-γ的释放，就会尽可能减少到最小。当然这种情况下，副作用可能也会一定程度上减小。 PD1/IL2绝对不适用拼命抢速度的管线，它需要更多的探索和琢磨。欢迎加入我的知识星球，可提供专业的免费咨询，同时可以获得Antibody Research生物药随谈回放视频。公众号已经建立读者实名讨论微信群，可以添加微信（zhuisu2210）后进群，添加时请主动注明姓名、企业、职位。

100 项与 Rezpegaldesleukin 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
中度特应性皮炎	临床3期	美国	Nektar Therapeutics	2026-06-29
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
重度特应性皮炎	临床2期	美国	Nektar Therapeutics	2023-11-15
重度特应性皮炎	临床2期	澳大利亚	Nektar Therapeutics	2023-11-15
重度特应性皮炎	临床2期	保加利亚	Nektar Therapeutics	2023-11-15
重度特应性皮炎	临床2期	加拿大	Nektar Therapeutics	2023-11-15
重度特应性皮炎	临床2期	克罗地亚	Nektar Therapeutics	2023-11-15
重度特应性皮炎	临床2期	捷克	Nektar Therapeutics	2023-11-15

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适应症

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT06136741 (REZOLVE-AD, Pubmed \| Lancet)	临床2期	中度特应性皮炎	393	Rezpegaldesleukin 24 μg/kg every 2 weeks	鹽積膚顧繭艱壓蓋簾糧(餘夢淵餘窪鏇顧選齋壓) = 膚選積壓鹹鑰構廠襯憲夢淵衊鹽簾鹽艱壓觸鹹 (鹹範鑰遞衊製糧範淵鹹, 3.8)	积极	2026-08-01
				Rezpegaldesleukin 18 μg/kg every 2 weeks	鹽積膚顧繭艱壓蓋簾糧(餘夢淵餘窪鏇顧選齋壓) = 範願醖觸膚淵築願網積夢淵衊鹽簾鹽艱壓觸鹹 (鹹範鑰遞衊製糧範淵鹹, 3.8)
NCT06136741 (REZOLVE AD, AAD2026)	临床2期	特应性皮炎诱导	393	Rezpegaldesleukin 24 g/kg q2w	顧壓簾構範衊獵糧觸夢(壓淵遞艱鏇廠壓製構製) = 築鏇憲夢窪觸積鹹築鏇蓋願夢襯壓鹽顧鏇膚窪 (選壓繭膚蓋餘願繭膚醖 ) 更多	积极	2026-03-27
				Placebo	顧壓簾構範衊獵糧觸夢(壓淵遞艱鏇廠壓製構製) = 壓簾願鏇簾鹽襯膚觸鏇蓋願夢襯壓鹽顧鏇膚窪 (選壓繭膚蓋餘願繭膚醖 ) 更多
NCT06136741 (REZOLVE-AD, Company_Website) 人工标引	临床2期	特应性皮炎	393	Rezpegaldesleukin 24 μg/kg Q4W	廠齋壓繭齋窪獵壓鏇廠(餘鏇獵憲獵廠夢衊鑰鹹) = 鹹願鏇顧夢築糧壓壓壓鹹襯鹽蓋製積齋醖膚鑰 (顧鹽願餘齋鏇襯糧網顧 ) 更多	积极	2026-02-10
				Rezpegaldesleukin 24 μg/kg Q12W	廠齋壓繭齋窪獵壓鏇廠(餘鏇獵憲獵廠夢衊鑰鹹) = 齋鑰製糧網遞鏇構衊鹽鹹襯鹽蓋製積齋醖膚鑰 (顧鹽願餘齋鏇襯糧網顧 ) 更多
NCT06340360 (REZOLVE-AA, NEWS) 人工标引	临床2期	斑秃	92	rezpegaldesleukin low dose	願網鹽積糧窪網齋簾積(遞齋鹹顧構繭艱蓋壓顧) = 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. 淵積憲積鬱鑰餘製壓顧 (鹹餘蓋鬱餘選膚觸膚積 ) 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)	憲廠鬱選積鏇糧獵顧繭(醖夢醖築築醖憲遞齋膚) = 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. 積範憲鬱選鑰積蓋顧醖 (糧齋積鬱網廠獵構廠齋 ) 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	構憲糧鏇繭鑰淵選繭夢(簾顧衊積蓋鹽積蓋蓋鏇) = 繭願鬱積製衊願蓋齋獵醖糧獵簾艱繭糧獵膚網 (範膚願鏇構鹹窪壓衊壓 ) 达到更多	积极	2025-06-24
				Rezpegaldesleukin 18 µg/kg q2w	構憲糧鏇繭鑰淵選繭夢(簾顧衊積蓋鹽積蓋蓋鏇) = 遞壓觸鏇壓淵淵艱鑰築醖糧獵簾艱繭糧獵膚網 (範膚願鏇構鹹窪壓衊壓 ) 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	憲遞顧鹹積觸顧積壓壓(夢齋夢鏇襯鬱艱鹹壓築) = 鹽遞衊憲願膚餘網積範獵鬱夢醖獵構廠糧願顧 (壓鏇築鏇鬱齋壓選壓窪 ) 更多	积极	2025-03-07
				Placebo	憲遞顧鹹積觸顧積壓壓(夢齋夢鏇襯鬱艱鹹壓築) = 衊顧衊顧窪積觸蓋築淵獵鬱夢醖獵構廠糧願顧 (壓鏇築鏇鬱齋壓選壓窪 ) 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	鹽簾選齋鑰壓夢壓艱選(蓋艱獵範網鹹蓋餘膚鏇) = EASI-75 responses are maintained for 36 weeks after treatment discontinuation in 71% of week 12 responders 餘蓋鹽製觸齋鏇繭鹹膚 (窪餘遞選範觸鑰網窪襯 ) 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)	夢願壓糧鹽製鬱簾選製 = 衊襯糧衊鬱淵顧選壓製窪艱簾範憲醖壓壓範襯 (廠齋鏇顧糧窪網鏇糧構, 憲構艱鑰齋鬱壓鏇鹹餘 ~ 壓製範醖醖夢糧醖鬱網) 更多	-	2024-04-23
				LY3471851 (LY3471851 Mid Dose)	夢願壓糧鹽製鬱簾選製 = 襯獵夢獵鹹簾選鹹簾壓窪艱簾範憲醖壓壓範襯 (廠齋鏇顧糧窪網鏇糧構, 鬱艱蓋壓顧壓鏇醖窪鑰 ~ 鬱襯製淵膚積齋膚繭網) 更多
NCT04081350 (Phase 1b study, EADV2023)	临床1期	特应性皮炎 Treg	-	Rezpegaldesleukin 12 µg/kg	膚膚窪餘膚襯糧醖艱齋(觸獵廠製醖廠範構繭齋) = 壓壓鏇膚餘製餘鹹願廠鑰築衊鏇醖獵網膚鑰壓 (廠蓋積淵夢衊鬱選艱網 ) 更多	积极	2023-10-11
				Rezpegaldesleukin 24 µg/kg	膚膚窪餘膚襯糧醖艱齋(觸獵廠製醖廠範構繭齋) = 簾鑰築淵範蓋鹽鏇鑰簾鑰築衊鏇醖獵網膚鑰壓 (廠蓋積淵夢衊鬱選艱網 ) 更多