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2026-03-25

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

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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）

2026-03-23·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.

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: Furie, Richard ; Levin, Robert ; Diab, Isam ; Fanton, Christie ; Hanan, Nathan ; Chindalore, Vishala ; Zalevsky, Jonathan ; Dickerson, Daniel ; Dixit, Neha ; 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.

193

项与 Rezpegaldesleukin 相关的新闻（医药）

2026-04-22

·武汉华美生物

IL2 的“双刃剑”又出新招：AACR 2026 涌现 PD1/IL2/VEGF 三抗，Nektar 自免数据引热议

白细胞介素-2（IL2）是免疫系统的核心调控者，既能激活效应T细胞（Teff）抗肿瘤，又能维持调节性T细胞（Treg）抑制自身免疫——这种“双刃剑”特性使其成为药物研发的热点，却也因狭窄的治疗窗口让无数药企折戟。近年来，IL2 的改造策略日趋精细。信达生物的 IBI363（α偏向性 PD1/IL2）在肿瘤中展现潜力，而 Nektar 的 rezpegaldesleukin（同样 α偏向性）则在特应性皮炎维持期取得积极数据，但诱导期仍见关节痛等副作用，疗效不及 Dupilumab，凸显了 IL2 在自免领域的窗口局限。与此同时，2026 年 AACR 大会上，四款 PD1/IL2/VEGF 三特异性药物集中亮相。其中韩国 Y-Biologics 的 AR170 设计巧妙：通过 VEGF 诱导的二聚化协同增强 PD-1 阻断，并利用顺式 IL-2 变体实现 PD-1 依赖的 T 细胞激活，在体外显著促进 CD8⁺ T 细胞增殖，动物模型中抗肿瘤效果优于 PD-1×VEGF 双抗。 IL2 疗法的未来，关键在于“活性”的精准拿捏——过强则毒性，过弱则无效。从单药到双抗再到三抗，这场平衡术仍在继续。 1. 背景介绍白细胞介素2（interleukin-2, IL2）是一种关键的免疫调节细胞因子，最初因能促进T细胞增殖而被发现，其在免疫系统平衡中发挥 “双刃剑” 作用：既能激活效应T细胞（Teff）介导抗肿瘤、抗感染免疫，又能维持调节性T细胞（Treg）功能以抑制过度免疫反应 [1]。早期研究显示，高剂量IL2（HD-IL2）可通过激活细胞毒性T细胞和自然杀伤（NK）细胞发挥抗肿瘤作用，是首个被批准用于转移性肾细胞癌（mRCC）和黑色素瘤的免疫疗法 [2,3]。而低剂量IL2则因优先扩增Treg（表达高亲和力IL2受体CD25），被用于自身免疫病和移植排斥的治疗 [4,5]。近年来，IL2与其他免疫调节剂的联合应用及新型制剂的开发成为研究热点 [2,6]。 2. 研究机制 IL2的生物学功能依赖于与IL2受体（IL2R）的结合，其作用具有剂量依赖性和细胞类型特异性，具体机制如下： 01 IL2受体的分型与功能差异 IL2R由CD25（α链）、CD122（β链）和CD132（γ链）组成，不同组合形成三类受体：高亲和力受体（CD25+CD122+CD132）：仅表达于Treg，对 IL2的亲和力最高（Kd≈10⁻¹¹ M）。低剂量IL2（如 0.3-1×10⁶ IU/m²）即可通过该受体持续激活Treg，促进其增殖、存活及功能维持（如FOXP3稳定表达 [4,5]。例如，在慢性GVHD患者中，低剂量IL2治疗4周后，Treg 数量较基线增加8倍以上，且FOXP3 +细胞比例显著升高 [4]。中亲和力受体（CD122+CD132）：表达于Teff、NK细胞和记忆T细胞，亲和力中等（Kd≈10⁻⁹ M）。高剂量IL2（如600,000-720,000 IU/kg）可优先激活该受体，通过增强细胞毒性分子（如穿孔素、颗粒酶）的表达，提升Teff和NK细胞的抗肿瘤/抗感染活性 [3,7]。低亲和力受体（CD122+CD132，无CD25）：亲和力最低（Kd≈10⁻⁷ M），主要在免疫激活后期发挥作用，参与免疫记忆的形成 [1]。 02 剂量依赖性的免疫调节效应高剂量IL2（HD-IL2）的免疫激活作用：刺激Teff增殖与分化：增强其对肿瘤细胞的识别和杀伤。在黑色素瘤研究中，HD-IL2联合gp100疫苗使抗原特异性CD8+ T细胞数量增加，客观缓解率（ORR）从6%提升至16% [3]。激活NK细胞：可促进NK细胞分泌 IFN-γ，增强其对肿瘤细胞的抗体依赖细胞毒性（ADCC）。例如，在神经母细胞瘤模型中，IL2与抗GD2抗体联合可显著提高NK细胞对肿瘤细胞的杀伤活性 [8]。低剂量IL2的免疫抑制作用：选择性扩增Treg：通过维持Treg的FOXP3表达和抑制功能，降低过度免疫反应。在HCV诱导的血管炎中，低剂量IL2使Treg占CD4+ T细胞的比例从基线的5%升至15%，同时抑制促炎因子（如 IL-17、TNF-α）的分泌 [9,10]。调节免疫平衡：通过提高Treg:Tcon（常规T细胞）比值（从0.07升至0.39），抑制自身反应性T 胞的活化。在慢性GVHD患者中，该比值升高与皮肤硬化、肝功能异常等症状改善显著相关 [4]。 03 与其他分子的协同机制与疫苗联合：肽疫苗可激活抗原特异性T细胞，而IL2通过提供共刺激信号促进其增殖，二者协同使黑色素瘤患者的中位总生存期从11.1个月延长至17.8个月 [3]。与HDAC抑制剂联合：可抑制Treg的免疫抑制功能（如减少IL-10 分泌），与HD-IL2联合后，mRCC患者的ORR从20-25%提升至37%，中位PFS从4.2个月延长至13.6个月 [2]。与免疫检查点抑制剂联合：低剂量ipilimumab（抗 CTLA-4）可解除T细胞的免疫抑制，与HD-IL2协同激活Teff，在免疫耐药的黑色素瘤中实现18.2%的ORR，且部分患者缓解持续超过37个月 [7]。 3. 信号通路 IL2通过与不同类型的受体结合激活特异性信号通路，其效应因细胞类型和IL2剂量存在显著差异： 01 JAK-STAT通路（主要调控Treg功能） IL2与高亲和力受体（CD25+CD122+CD132）结合后，招募并激活JAK1和JAK3激酶，促使STAT5磷酸化并形成二聚体进入细胞核，调控FOXP3、CD25等基因的表达，这是维持Treg存活、增殖及功能的核心通路 [8,15]。低剂量IL2可优先激活该通路，在慢性GVHD患者中，治疗4周后Treg中FOXP3的表达量较基线增加2.3倍，且这一效应在持续治疗中得以维持 [4]。 02 PI3K-Akt通路（主要调控细胞增殖与存活） PI3K-Akt通路主要由中亲和力受体（CD122+CD132）介导，IL2结合后通过Src家族激酶激活PI3K，生成PIP3并招募Akt使其磷酸化，进而抑制凋亡分子（如Bad）并激活增殖相关基因（如Cyclin D1），最终促进Teff和NK细胞的存活与增殖 [1]。在黑色素瘤治疗中，高剂量IL2使Teff中磷酸化Akt水平升高1.8倍，细胞增殖指数（Ki67+）增加40%，直接增强抗肿瘤免疫应答 [3]。 03 MAPK通路（辅助调控免疫细胞活化） IL2通过Ras-Raf-MEK-ERK级联反应激活该通路，尤其在高剂量IL2处理的Teff中显著。ERK磷酸化后进入细胞核，促进IL-2、IFN-γ等细胞因子的转录，增强效应T细胞的细胞毒性功能 [1]。例如，在gp100疫苗联合IL2的治疗中，Teff分泌的IFN-γ较单药IL2组增加2.1倍，与肿瘤杀伤活性增强直接相关 [3]。 04 通路交叉调控 JAK-STAT与PI3K-Akt通路的平衡决定免疫应答方向：低剂量IL2优先激活JAK-STAT通路（Treg优势），高剂量则同时激活PI3K-Akt通路（Teff优势） [1]。此外，IL2激活的STAT5可与NF-κB通路协同，在NK细胞中上调穿孔素等细胞毒性分子的表达，进一步增强免疫效应 [8]。 4. 相关疾病 IL2的异常调控会导致免疫失衡、信号通路紊乱等，与多种疾病的发生发展密切相关： 01 恶性肿瘤1.肾细胞癌（RCC）肿瘤微环境中IL2信号的减弱是RCC免疫逃逸的重要机制：肿瘤细胞可分泌IL-10等抑制因子，下调T细胞表面CD122的表达，导致Teff对IL2的敏感性降低，抗肿瘤免疫应答减弱 [2,11]。HD-IL2单药治疗转移性透明细胞RCC的ORR为20-25%，中位PFS4.2个月，但完全缓解患者生存期可超5年；与entinostat联合后ORR提升至37%，中位PFS延长至13.6个月，因entinostat可逆转Treg的免疫抑制功能，增强IL2对Teff的激活 [2,11]。2.黑色素瘤部分黑色素瘤细胞通过突变或表观修饰抑制IL2通路相关基因（如JAK3、STAT5）的表达，使Teff增殖受阻，同时肿瘤浸润Treg高表达CD25，竞争性结合IL2，进一步削弱免疫应答 [3,7]。HD-IL2联合gp100肽疫苗治疗HLA-A0201阳性患者的ORR为16%，高于单药HD-IL2的6%，因疫苗激活的抗原特异性T细胞更易响应IL2的增殖信号；对免疫耐药患者，HD-IL2联合低剂量ipilimumab和nivolumab的ORR为18.2%，因检查点抑制剂可解除T细胞的“刹车”，与IL2协同恢复抗肿瘤活性 [3,7]。3.神经母细胞瘤神经母细胞瘤细胞表面高表达GD2抗原，但其微环境中IL2浓度不足，导致NK细胞的ADCC效应受限 [8]。dinutuximab联合IL2和GM-CSF可增强NK细胞的ADCC效应，但SIOPEN试验显示，与单独dinutuximab相比，添加IL2并未显著提高3年无事件生存率（56%vs60%），且3-4级毛细血管渗漏综合征发生率更高（11-13%vs3-6%），可能因IL2过度激活单核细胞释放炎症因子 [8]。 02 自身免疫病与移植相关疾病1.慢性移植物抗宿主病（GVHD）异基因造血干细胞移植后，供体来源的Teff因IL2信号亢进而攻击宿主组织，同时Treg数量或功能缺陷（如FOXP3表达不稳定），无法有效抑制过度免疫 [4]。对糖皮质激素耐药的患者，每日皮下注射IL2（1×10⁶IU/m²）8周后，52%患者达到部分缓解，因IL2优先扩增Treg，使Treg:Tcon比值从0.07升至0.39，恢复免疫平衡 [4]。2.HCV诱导的血管炎 HCV感染可诱导B细胞产生cryoglobulin，激活补体系统和中性粒细胞，同时Treg功能受损（IL2-JAK-STAT5通路活性降低），导致自身反应性T细胞过度活化 [9,10]。10例患者接受IL2治疗后，8例症状改善，因IL2增强Treg的FOXP3表达和抑制功能，降低炎症基因（TNF-α、IL-6）的表达 [9,10]。3.多发性硬化（MS） MS患者中枢神经系统中浸润的T细胞对IL2的敏感性异常升高，通过PI3K-Akt通路过度增殖，同时NK细胞因IL2供应不足而功能低下，无法清除自身反应性T细胞 [12]。抗CD25抗体（daclizumab）可阻断IL2与Treg的结合，使游离IL2优先激活NK细胞，减少T细胞浸润，临床试验显示其使年复发率从0.46降至0.21 [12]。 03 感染性疾病1.HIV感染 HIV可靶向破坏CD4+T细胞，导致IL2分泌减少，同时病毒蛋白（如Nef）可干扰IL2R的组装，使剩余CD4+T细胞对IL2的应答减弱，免疫重建受阻 [13]。IL2可促进CD4+T细胞增殖，但INSIGHT-ESPRIT试验显示，IL2联合抗逆转录病毒治疗并未降低机会性感染或死亡风险；仅在基线CD4+T细胞<200/μL的亚组中，IL2治疗使主要终点事件减少22%，因低水平CD4+T细胞更依赖IL2进行恢复 [13]。 5. 药物最新研究进展近期，IL-2药物研发取得了多项重要进展。Nektar Therapeutics公司开发的新型IL-2类药物Rezpegaldesleukin在治疗中至重度特应性皮炎的2b期临床试验中取得成功，显著降低了湿疹面积和严重程度指数（EASI），并显示出良好的安全性。Teva与复星医药达成合作，共同开发TEV-56278，这是一种抗PD-1抗体与IL-2融合的免疫疗法，旨在提高抗肿瘤活性并降低毒性。Asher Bio的IL-2候选药物AB248也正在进行1a/1b期临床试验，用于治疗多种晚期实体瘤，并计划与双特异性T细胞接合剂联合用于小细胞肺癌。还有多款IL-2药物处于临床前或临床研究阶段，部分列举如下： *数据来源于Patsnap 通过优化IL-2的靶向性和剂量，研究人员正在努力克服传统IL-2疗法的副作用，同时探索其在更多疾病中的应用潜力。 6. 华美生物IL-2相关产品推荐 ● IL-2重组蛋白 Recombinant Human Interleukin-2 (IL2) (Active); CSB-MP011629HU Recombinant Mouse Interleukin-2 (Il2) (Active); CSB-MP011629MOd9 Recombinant Macaca fascicularis Interleukin-2 (IL2) (Active); CSB-MP640916MOVd9 ● IL-2抗体 ● IL-2 ELISA试剂盒参考文献： [1] Bluestone JA. The Yin and Yang of Interleukin-2–Mediated Immunotherapy. N Engl J Med. 2011;365:2129-2131. [2] Pili R, et al. A randomized, open-label, phase II study of high-dose interleukin 2 vs high-dose interleukin 2 plus entinostat in renal cell carcinoma. 2023. [3] Schwartzentruber DJ, et al. gp100 Peptide Vaccine and Interleukin-2 in Patients with Advanced Melanoma. N Engl J Med. 2011;364:2119-2127. [4] Koreth J, et al. Interleukin-2 and regulatory T cells in graft-versus-host disease. N Engl J Med. 2011;365:2055-2066. [5] Zhao X, et al. Prophylactic use of low-dose interleukin-2 early post-transplantation: a randomised study. 2015. [6] Amaria RN, et al. OBX-115, an interleukin 2-sparing engineered tumor-infiltrating lymphocyte cell therapy, in patients with immune checkpoint inhibitor-resistant melanoma. 2025. [7] Tarhini AA, et al. High dose bolus interleukin-2 and concurrent low dose ipilimumab followed sequentially by nivolumab in patients with advanced melanoma. 2025. [8] Matthay KK. Interleukin 2 plus anti-GD2 immunotherapy: helpful or harmful? Lancet Oncol. 2018;19:1549-1551. [9] Oo YH, et al. Low-Dose Interleukin-2 and HCV-Induced Vasculitis. N Engl J Med. 2012;366:1353-1354. [10] Saadoun D, et al. Regulatory T-Cell Responses to Low-Dose Interleukin-2 in HCV-Induced Vasculitis. N Engl J Med. 2011;365:2067-2077. [11] Chow S, et al. HIGH-DOSE INTERLEUKIN-2 ARMED WITH PATHOLOGY-BASED SELECTION CRITERIA: A REAL OPTION IN TREATMENT OF METASTATIC RENAL CELL CARCINOMA. Ann Oncol. 2014;25(suppl 4):iv294. [12] Saidha S, et al. Anti-interleukin-2 receptor alpha for multiple sclerosis? Lancet. 2013;381:2141-2142. [13] Sellier P, et al. Interleukin-2 Therapy in Patients with HIV Infection. N Engl J Med. 2010;362:270-271. --END-- 关于我们武汉华美生物工程有限公司成立于2007年12月，是一家以科研试剂生产、诊断试剂原料供应为核心，集自主研发、生产、营销为一体的生物高新技术企业。华美生物拥有多项先进的核心技术，致力于为全球高等院校、政府研究机构、诊断试剂生产厂家以及生物制药公司提供高质量产品与高水平的技术服务。经过18年的不懈努力，华美生物旗下现拥有两大子品牌，CUSABIO与科赛格（CUSAg）。其中，CUSABIO主要经营科研试剂产品，包括重组蛋白、抗体、基因、试剂盒等产品。目前，CUSABIO已开发15000+重组蛋白，涵盖了从人类到其他常见物种的疾病相关的药物靶点抗原和生物标志物。此外，为鼎力相助抗体药研发，针对多次跨膜蛋白，华美生物还搭建了病毒样颗粒 (VLPs)、去垢剂和Nanodisc三大技术平台，较大程度上解决了全长跨膜蛋白制备难的问题。在看你就赞赞我！

2026-04-22

·PRNewswire

Nektar Therapeutics Announces Pricing of Upsized $325 Million Public Offering

SAN FRANCISCO, April 21, 2026 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR), a clinical-stage biotechnology company focused on the development of innovative medicines in the field of immunotherapy, today announced the pricing of its upsized underwritten public offering of $325 million of shares of its common stock. Nektar is selling 3,532,609 shares of common stock at a public offering price of $92.00 per share. The gross proceeds to Nektar from the offering are expected to be approximately $325 million, before deducting underwriting discounts and commissions and estimated offering expenses. In addition, Nektar has granted the underwriters a 30-day option to purchase up to an additional 529,891 shares of its common stock at the public offering price per share, less underwriting discounts and commissions. All of the securities being sold in this offering are being offered by Nektar. The offering is expected to close on April 23, 2026, subject to the satisfaction of customary conditions. Nektar intends to use the net proceeds from the offering for general corporate purposes, which may include research and development, clinical development (including Phase 3 trials for rezpegaldesleukin in atopic dermatitis and alopecia areata) and manufacturing costs to support the advancement of its drug candidates, as well as other general corporate purposes. Jefferies, TD Cowen, and Piper Sandler are acting as joint bookrunning managers for the offering. Citigroup is also acting as a bookrunner for the offering. The securities described above are being offered pursuant to a shelf registration statement on Form S-3ASR (No. 333-291466) that was filed with the U.S. Securities and Exchange Commission (the "SEC") on November 12, 2025 and automatically became effective upon filing. This offering is being made only by means of a prospectus supplement and an accompanying prospectus that form a part of the registration statement. A final prospectus supplement related to and describing the terms of the offering will be filed with the SEC and will be available on the SEC's website located at . Copies of the final prospectus supplement and an accompanying prospectus related to the offering may also be obtained, when available, from Jefferies LLC, Attention: Equity Syndicate Prospectus Department, 520 Madison Avenue, New York, NY 10022, by telephone at (877) 821-7388, or by email at [email protected]; TD Securities (USA) LLC, c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, NY 11717 or by email at [email protected]; Piper Sandler & Co., 350 North 5th Street, Suite 1000, Minneapolis, MN 55401, Attention: Prospectus Department, by telephone at (800) 747-3924, or by email at [email protected]; or Citigroup, c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, NY 11717 (Tel: 800-831-9146). This press release shall not constitute an offer to sell or a solicitation of an offer to buy nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of that state or jurisdiction. 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 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 is headquartered in San Francisco, California. Cautionary Note Regarding Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, which can be identified by words such as: "will," "expect," "develop," "potential," "plan," and similar references to future periods. Examples of forward-looking statements include, among others, statements regarding expected gross proceeds from the offering, the anticipated use of proceeds from the offering and completion and timing of the public offering. Nektar intends such forward-looking statements to be covered by the safe harbor provisions for forward-looking statements contained in Section 21E of the Securities Exchange Act of 1934 and the Private Securities Litigation Reform Act of 1995. Forward-looking statements are neither historical facts nor assurances of future performance. Instead, they are based only on Nektar's current beliefs, expectations, and assumptions. 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 the control of Nektar. The 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 the actual results to differ materially from those indicated in the forward-looking statements include, among others, the risks and uncertainties set forth in Nektar's most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 13, 2026 as well as the risks identified in the registration statement and the preliminary prospectus supplement relating to the offering. Any forward-looking statement made by Nektar in this press release is based only on information currently available to Nektar and speaks only as of the date on which it is made. Nektar undertakes 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. 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

临床2期免疫疗法

2026-04-20

·药明康德

产业新闻 | FDA授予Keytruda/ADC组合疗法优先审评资格；潜在“first-in-class”新药积极临床数据公布……

FDA授予Keytruda/ADC组合疗法优先审评资格！默沙东（MSD）今日宣布，美国FDA已受理其两项补充生物制品许可申请（sBLA），并授予优先审评资格。此次申请涉及抗PD-1疗法Keytruda（pembrolizumab）静脉输注制剂，以及Keytruda Qlex（pembrolizumab和berahyaluronidase alfa）皮下注射制剂。上述两种方案均拟联合辉瑞（Pfizer）和安斯泰来（Astellas）共同开发的抗体偶联药物（ADC）Padcev（enfortumab vedotin），用于治疗适合接受顺铂化疗的肌层浸润性膀胱癌（MIBC）患者。FDA已将该申请的PDUFA目标审评日期定为2026年8月17日。根据新闻稿，若获批，该联合疗法有望成为首个适用于所有MIBC患者（无论是否适合顺铂治疗）的围手术期治疗选择，并可能成为新的标准治疗方案。此次申报主要基于3期KEYNOTE-B15研究结果。数据显示，Keytruda联合Padcev方案在研究参与者中实现了具有统计学显著性且具临床意义的无事件生存期（EFS）和总生存期（OS）改善。之前公布的分析显示，在中位随访33.6个月后，Keytruda联合Padcev达到了研究的主要终点。与新辅助化疗联合手术相比，该方案将EFS事件风险降低47%（HR=0.53，95% CI：0.41–0.70，p<0.0001）。Keytruda联合Padcev组的中位EFS尚未达到，而对照组为48.5个月（95% CI：43.3–NR）。在两年时，约79.4%接受该联合治疗的患者仍存活且未出现疾病进展或复发，而新辅助化疗联合手术组为约66.2%。 Padcev是一种抗体偶联药物，其靶点为Nectin-4，这是一种位于细胞表面并在膀胱癌中高表达的蛋白质。Keytruda则是一种PD-1单克隆抗体，可阻断PD-1与其配体PD-L1和PD-L2之间的相互作用，从而激活T淋巴细胞，以发挥抗肿瘤功效。治疗斑秃，潜在“first-in-class”新药积极临床数据公布 Nektar Therapeutics今日公布其2b期REZOLVE-AA研究中一项盲态16周延长期治疗的新结果。该研究正在评估在研药物rezpegaldesleukin用于治疗重度至极重度斑秃患者。REZOLVE-AA为一项全球研究，共纳入92名重度至极重度斑秃患者，旨在进一步评估该疗法的疗效与安全性。数据显示，在持续每月两次给药的治疗方案下，18 µg/kg和24 µg/kg延长期治疗组分别有29%和31%的患者在第36周至第52周期间新达到斑秃严重度评分工具（SALT）评分≤20（即80%以上的头皮毛发覆盖率），显示出持续治疗带来的进一步获益。与此同时，越来越多患者在多个SALT评估指标上达到具有临床意义的毛发生长标准，且94%的患者完成了延长期治疗。安全性方面，该药物在52周内维持了良好的安全性特征，与此前公布结果一致。上述数据支持rezpegaldesleukin推进至斑秃适应症后期临床开发阶段。 Rezpegaldesleukin是一种潜在“first-in-class”、针对调节性T细胞（Treg）的生物制品，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。 70亿美元！礼来收购基因疗法新锐礼来（Eli Lilly and Company）与Kelonia Therapeutics今日宣布，双方已达成最终协议，礼来将收购Kelonia。根据协议，Kelonia最高可获得70亿美元款项，其中包括32.5亿美元预付款，以及在达到特定临床、监管和商业里程碑后支付的后续款项。此次交易将进一步拓展礼来在遗传医学领域的布局，并获得一项具有广泛应用潜力的新型体内基因递送与整合技术平台。 Kelonia开发了专有体内基因植入系统iGPS，该平台利用特殊工程化慢病毒颗粒，可在体内高效且选择性地进入T细胞，使患者自身在体内生成嵌合抗原受体T细胞（CAR-T）疗法，以治疗相关疾病。公司核心项目KLN-1010是一款潜在“first-in-class”的静脉注射一次性基因疗法，可在体内生成靶向BCMA蛋白的CAR-T细胞，用于治疗复发/难治性多发性骨髓瘤，目前处于1期临床开发阶段。该项目近期临床数据显示初步临床验证及令人鼓舞的耐受性表现。若后续开发顺利，KLN-1010有望通过免除传统体外个体化细胞制备流程及给药前化疗步骤，为多发性骨髓瘤治疗带来显著进展。参考资料： [1] FDA Grants Priority Review for KEYTRUDA® (pembrolizumab) and KEYTRUDA QLEX™ (pembrolizumab and berahyaluronidase alfa-pmph), Each with Padcev® (enfortumab vedotin-ejfv), for Cisplatin-Eligible Patients with Muscle-Invasive Bladder Cancer. Retrieved April 20, 2026 from https://www.businesswire.com/news/home/20260420766130/en/FDA-Grants-Priority-Review-for-KEYTRUDA-pembrolizumab-and-KEYTRUDA-QLEX-pembrolizumab-and-berahyaluronidase-alfa-pmph-Each-with-Padcev-enfortumab-vedotin-ejfv-for-Cisplatin-Eligible-Patients-with-Muscle-Invasive-Bladder-Cancer [2] 52-Week Topline Results from 16-Week Blinded Treatment Extension of REZOLVE-AA Demonstrate Deepening of Responses in Severe-to-Very-Severe Alopecia Areata with Rezpegaldesleukin. Retrieved April 20, 2026 from https://ir.nektar.com/news-releases/news-release-details/52-week-topline-results-16-week-blinded-treatment-extension [3] Lilly to acquire Kelonia Therapeutics to advance in vivo CAR-T cell therapies. Retrieved April 20, 2026 from https://investor.lilly.com/news-releases/news-release-details/lilly-acquire-kelonia-therapeutics-advance-vivo-car-t-cell 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，聚焦全球生物医药健康创新

100 项与 Rezpegaldesleukin 相关的药物交易

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研发状态

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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

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临床结果

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, AAD2026)	临床2期	特应性皮炎诱导	393	Rezpegaldesleukin 24 g/kg q2w	襯積鑰選艱築衊壓觸夢(夢獵範選淵膚選憲餘觸) = 網鏇餘憲築築顧憲獵積襯獵簾簾遞夢襯遞醖構 (繭襯廠網憲製鬱範簾鑰 ) 更多	积极	2026-03-27
				Placebo	襯積鑰選艱築衊壓觸夢(夢獵範選淵膚選憲餘觸) = 醖廠膚製衊襯網遞淵簾襯獵簾簾遞夢襯遞醖構 (繭襯廠網憲製鬱範簾鑰 ) 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	網製範醖鬱襯艱構網構(鹽鹽糧簾夢願襯鏇蓋範) = 範衊窪鬱夢夢繭鹹餘繭顧鹹憲積糧願鬱遞襯窪 (廠觸襯夢鑰艱齋繭糧鏇 ) 更多	积极	2026-02-10
				Rezpegaldesleukin 24 μg/kg Q12W	網製範醖鬱襯艱構網構(鹽鹽糧簾夢願襯鏇蓋範) = 繭淵鏇廠醖顧膚蓋糧鹹顧鹹憲積糧願鬱遞襯窪 (廠觸襯夢鑰艱齋繭糧鏇 ) 更多
NCT06340360 (REZOLVE-AA, NEWS) 人工标引	临床2期	斑秃	92	rezpegaldesleukin low dose	膚觸構簾膚襯壓遞構繭(醖鹹衊顧衊齋鏇鬱艱鬱) = 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. 願製簾壓遞襯夢壓顧簾 (艱窪遞獵膚淵蓋積齋淵 ) 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)	糧顧憲蓋鏇鑰醖簾鏇鹽(鏇積廠簾淵選鹹顧遞餘) = 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. 鑰鹹餘簾獵顧範壓艱願 (窪鬱繭遞醖積獵鏇襯積 ) 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	簾夢蓋繭齋膚獵壓夢鏇(鑰網窪壓選網獵構窪網) = 顧夢憲繭築艱鑰壓衊淵窪衊製築憲艱積網鑰築 (餘糧淵遞齋鏇製艱鹽醖 ) 达到更多	积极	2025-06-24
				Rezpegaldesleukin 18 µg/kg q2w	簾夢蓋繭齋膚獵壓夢鏇(鑰網窪壓選網獵構窪網) = 夢齋憲夢蓋顧廠觸糧鏇窪衊製築憲艱積網鑰築 (餘糧淵遞齋鏇製艱鹽醖 ) 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	繭選壓網鹽壓膚顧願鏇(簾糧壓夢窪糧觸簾築顧) = 鑰鹽願壓齋遞觸廠襯繭鹽構壓願襯築憲範繭遞 (蓋積餘鹽簾構膚網鬱積 ) 更多	积极	2025-03-07
				Placebo	繭選壓網鹽壓膚顧願鏇(簾糧壓夢窪糧觸簾築顧) = 觸觸淵糧製選鏇選顧蓋鹽構壓願襯築憲範繭遞 (蓋積餘鹽簾構膚網鬱積 ) 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	淵夢醖遞鹽積顧獵鬱遞(製繭艱鏇鹽遞顧憲襯獵) = EASI-75 responses are maintained for 36 weeks after treatment discontinuation in 71% of week 12 responders 衊鑰艱鹽鹽獵廠繭壓鬱 (簾蓋構構鑰顧築築築鏇 ) 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)	夢遞壓範艱襯襯網獵鬱 = 鏇積範餘壓夢顧蓋壓醖衊願廠艱鑰積願鬱壓製 (壓範遞憲艱齋鏇衊鏇衊, 襯鬱憲獵衊餘築願構糧 ~ 餘衊衊鑰膚網鑰觸獵醖) 更多	-	2024-04-23
				LY3471851 (LY3471851 Mid Dose)	夢遞壓範艱襯襯網獵鬱 = 餘鑰願獵憲鑰構築淵淵衊願廠艱鑰積願鬱壓製 (壓範遞憲艱齋鏇衊鏇衊, 蓋衊鹽製鑰衊齋簾夢夢 ~ 膚衊窪鬱積襯簾網積選) 更多
NCT04081350 (Phase 1b study, EADV2023)	临床1期	特应性皮炎 Treg	-	Rezpegaldesleukin 12 µg/kg	醖齋餘糧艱觸網鹽衊製(願廠壓願鹽網窪衊簾壓) = 鹽蓋製繭膚鹽艱願夢遞選齋醖膚獵醖餘遞淵簾 (艱淵繭艱積簾鹽鏇夢獵 ) 更多	积极	2023-10-11
				Rezpegaldesleukin 24 µg/kg	醖齋餘糧艱觸網鹽衊製(願廠壓願鹽網窪衊簾壓) = 餘獵夢膚廠鹹範遞網鹹選齋醖膚獵醖餘遞淵簾 (艱淵繭艱積簾鹽鏇夢獵 ) 更多
NCT04677179 (INSTRUCT-UC, CTgov)	临床2期	溃疡性结肠炎	81	Placebo (Placebo (Induction Treatment Period))	繭鏇願糧範窪觸鹽鑰蓋 = 鹽觸蓋製選觸築鬱鏇憲選齋築網鏇製廠觸蓋廠 (願製鹹糧膚鑰觸構憲獵, 壓夢醖齋糧蓋蓋蓋憲網 ~ 餘壓築廠夢齋築繭艱簾) 更多	-	2023-09-05
				LY3471851 (Low Dose LY3471851 (Induction Treatment Period))	繭鏇願糧範窪觸鹽鑰蓋 = 觸網鑰窪艱衊願鹹繭積選齋築網鏇製廠觸蓋廠 (願製鹹糧膚鑰觸構憲獵, 構窪淵構鹹膚鏇壓遞淵 ~ 顧餘願鹽襯顧獵構遞壓) 更多