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2026-08-01

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）

2026-03-23·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.

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项与 Rezpegaldesleukin 相关的新闻（医药）

2026-09-04

·药研苑

安进依洛尤单抗强化降脂降低高心血管风险患者死亡风险

药品营销避坑”试读：药品导入期管理视频课（试听）药品生命周期管理（案例）药品立项需要注意什么（案例） 2026年8月31日，安进Amgen发布了依洛尤单抗用于既往无心肌梗死和卒中史，高心血管疾病风险患者3期临床试验VESALIUS-CV的死亡率影响结果。 VESALIUS-CV研究共纳入12,257名低密度脂蛋白胆固醇（LDL-C）≥90mg/dL，或非高密度脂蛋白胆固醇（non-HDL-C）≥120mg/dL，或载脂蛋白B≥80mg/dL，患有动脉粥样硬化性心血管疾病（ASCVD）或高危糖尿病，但既往无心肌梗死或卒中史患者。入组患者按1:1比例在稳定、优化降脂治疗的基础上接受依洛尤单抗140mg，每2周一次，或安慰剂。至中位随访4.6年，依洛尤单抗组与安慰剂组相比全因死亡率下降20%（7.9% vs 9.7%, HR 0.80; 95% CI 0.70–0.91; P=0.0005）；依洛尤单抗组的安慰剂组的心血管死亡率分别为2.8%和3.6%（HR 0.79; 95% CI, 0.64–0.98），非心血管死亡率分别为4.2%和5.0%（HR 0.85; 95% CI, 0.71–1.01），未明原因死亡率分别为1.1%和1.4%（HR 0.64; 95% CI 0.45–0.92）（Robert P Giugliano., 2026）。依洛尤单抗（Evolocumab，瑞百安Repatha）为抗PCSK9（前蛋白转化酶枯草杆菌素/kexin9型）单克隆抗体，能够耗竭PCSK9，防止PCSK9与LDLR（低密度脂蛋白受体）的结合。LDLR在肝细胞表面，负责清除低密度脂蛋白胆固醇（LDL-C），PCSK9与LDLR结合后，能够阻止进入肝细胞内的LDLR返回到肝细胞表面，减少肝细胞LDLR的数量，降低肝细胞通过LDLR清除LDL-C的能力。目前国内获批上市PCSK9抑制剂类药物包括依洛尤单抗（Evolocumab）、阿利西尤单抗（Alirocumab）、英克司兰（Inclisiran）、托莱西单抗（Tafolecimab）、伊努西单抗（Ebronucimab）、昂戈瑞西单抗（Ongericimab）和瑞卡西单抗（Recaticimab），其中英克司兰为小干扰RNA（siRNA）类药物。目前只有依洛尤单抗被证明能够降低既往无心肌梗死和卒中史，高心血管疾病风险患者的全因死亡率和心血管死亡率。在阿利西尤单抗ODYSSEY OUTCOMES研究中，对于急性冠状动脉综合征患者，阿利西尤单抗降低了全因死亡率，但未能证明能够降低心血管死亡率（Philippe Gabriel Steg., 2019）。推荐指数：★★★ 推荐原因：依洛尤单抗是目前唯一个被证明能够降低既往无心肌梗死和卒中史，高心血管疾病风险患者全因死亡率和心血管死亡率的PCSK9抑制剂类药物。个人观点，仅限参考。相关阅读：和黄医药赛沃替尼联合方案MET/EGFR晚期NSCLC取得积极结果减重增强抗银屑病疗效，礼来发布替尔泊肽3b临床试验数据近98%梗阻解除，玛伐凯泰梗阻性肥厚型心肌病试验长期研究北京斯利安药业降高同型半胱氨酸药物甜菜碱散获批上市欧康维视申请地塞米松眼用混悬注射液本地化生产沐源生物再次提交牛磺熊去氧胆酸胶囊的首仿上市申请 FDA批准礼来替尔泊肽用于降低成人2型糖尿病心血管事件风险智翔金泰BCMA/CD3双抗纬利妥米获批用于多发性骨髓瘤诺华放射配体镥[¹⁷⁷Lu]特昔维匹肽获批用于性激素敏感性前列腺癌同源康EGFR-TKI氘申艾替尼获批一线治疗晚期非小细胞肺癌强生口服IL-23受体拮抗剂伊可白滞素获批治疗斑块状银屑病和黄医药FGFR抑制剂凡瑞格拉替尼获批用于肝内胆管癌石药EGFR ADC（SYS6010）EGFR突变NSCLC三期试验达到终点转移性胰腺癌生存期翻倍，FDA批准泛RAS抑制剂Daraxonrasib Rezpegaldesleukin用于中重度特应性皮炎2b期研究数据发表相关内容只作为药物研发的参信息。不构成任何与用药咨询有关的建议。如需发稿，您可通过在药研苑公众号下以发送信息的方式将官网或官方公众号的稿件链接和标题发送给我们。我们将择优确定是否发布。

siRNA临床3期上市批准

2026-09-04

·药研苑

普乐司兰降低高甘油三酯血症急性胰腺炎风险3期临床数据发布

药品营销避坑”试读：药品导入期管理视频课（试听）药品生命周期管理（案例）药品立项需要注意什么（案例） 2026年8月30日Arrowhead Pharmaceuticals宣布，在2026年欧洲心脏病学会大会期间发布了普乐司兰用于重度高甘油三酯血症（sHTG）3期临床试验SHASTA-3和SHASTA-4的研究结果。 SHASTA-3和 SHASTA-4为全球双盲、安慰剂对照3期临床试验，共纳入757名患者，入组患者随机接受普乐司兰25mg或安慰剂，每3个月一次。共4次。至第12个月，SHASTA-3和SHASTA-4研究普乐司兰组中位血清甘油三酯（TG）分别下降79%和81%（p均<0.0001）；基线TG≥880mg/dL（≥9.94 mmol/L）的患者，普乐司兰组中位TG分别下降85%；普乐司兰组达到TG<500mg/dL（<5.65mmol/L）的比例分别为91%和93%，而安慰剂组分别为51%和50%（p均<0.0001）；普乐司兰组达到TG<150mg/dL（<1.69mmol/L）的比例分别为52%和55%，而安慰剂组分别为7.9%和2.0%（p均<0.0001）。在急性胰腺炎发生风险方面，与安慰剂相比普乐司兰组所有急性胰腺炎事件的发生率降低78%（RR 0.22; 95% CI: 0.07, 0.67; p=0.008），首次急性胰腺炎发生风险降低74%（HR 0.26; 95% CI: 0.09, 0.78; p=0.016）；对于TG≥500mg/dl（5.65 mmol/L）合并急性胰腺炎发作史患者，与安慰剂相比普乐司兰组急性胰腺炎事件的发生率降低91%（RR 0.09; 95% CI: 0.02, 0.41; p=0.002）。此外，普乐司兰还显著降低了APOC3、VLDL-C和非HDL-C。在安全性方面，普乐司兰组和安慰剂组治疗期间不良事件（TEAE）的发生率分别为73%，分别有8.3%和10%发生严重TEAE，分别有1.4%和0.8%患者由于TEAE导致停药；普乐司兰组TEAE发生率≥5%的不良事件包括血糖控制恶化（14.3%）和腹泻（5.6%），安慰剂组分别为8.7%和3.2%；普乐司兰组和安慰剂组注射部位反应的发生率分别为3.2%和2.0%。普乐司兰组发生3例死亡事件，均认为与研究无关。普乐司兰（Plozasiran）是由Arrowhead开发的靶向APOC3（载脂蛋白C-Ⅲ）mRNA的小干扰RNA（siRNA）药物，抑制肝脏表达APOC3。APOC3是极低密度脂蛋白（VLDL）和乳糜颗粒的重要组成成分，能够抑制血浆中甘油三酯的脂蛋白脂肪酶（LPL）代谢通路。因此，抑制肝脏表达APOC3，能够降低VLDL和乳糜颗粒中的APOC3的含量，促进甘油三酯代谢。普乐司兰为GalNAc修饰siRNA类药物，GalNAc为去唾液酸糖蛋白受体（ASGPR）的配体，与肝细胞表面的ASGPR结合，通过胞吞作用实现普乐司兰的内化。 2025年赛诺菲获得普乐司兰钠在大中华区开发和商业化权利。2026年1月普乐司兰钠注射液（瑞达普®）获得国家药品监督管理局（NMPA）批准，在饮食控制基础上，用于降低家族性乳糜微粒血症综合征（FCS）成人患者的甘油三酯水平。推荐指数：★★★ 推荐原因：SHASTA-3和 SHASTA-4研究显示，普乐司兰在降低重度高甘油三酯血症患者急性胰腺炎的发生风险方面，具有积极的意义。个人观点，仅限参考。相关阅读：和黄医药赛沃替尼联合方案MET/EGFR晚期NSCLC取得积极结果减重增强抗银屑病疗效，礼来发布替尔泊肽3b临床试验数据近98%梗阻解除，玛伐凯泰梗阻性肥厚型心肌病试验长期研究北京斯利安药业降高同型半胱氨酸药物甜菜碱散获批上市欧康维视申请地塞米松眼用混悬注射液本地化生产沐源生物再次提交牛磺熊去氧胆酸胶囊的首仿上市申请 FDA批准礼来替尔泊肽用于降低成人2型糖尿病心血管事件风险智翔金泰BCMA/CD3双抗纬利妥米获批用于多发性骨髓瘤诺华放射配体镥[¹⁷⁷Lu]特昔维匹肽获批用于性激素敏感性前列腺癌同源康EGFR-TKI氘申艾替尼获批一线治疗晚期非小细胞肺癌强生口服IL-23受体拮抗剂伊可白滞素获批治疗斑块状银屑病和黄医药FGFR抑制剂凡瑞格拉替尼获批用于肝内胆管癌石药EGFR ADC（SYS6010）EGFR突变NSCLC三期试验达到终点转移性胰腺癌生存期翻倍，FDA批准泛RAS抑制剂Daraxonrasib Rezpegaldesleukin用于中重度特应性皮炎2b期研究数据发表相关内容只作为药物研发的参信息。不构成任何与用药咨询有关的建议。如需发稿，您可通过在药研苑公众号下以发送信息的方式将官网或官方公众号的稿件链接和标题发送给我们。我们将择优确定是否发布。

2026-09-03

·E药经理人

又一中国药企弯道超车的机会来了！

首款Treg疗法获批上市、首个CAR-Treg进入人体试验阶段、首批大药企重金下注......2026年，调节性T细胞（Treg）终于从实验室里的热门“潜力股”，走到了产业化的临界点。 2025年10月，诺贝尔生理学或医学奖授予Mary E. Brunkow、Fred Ramsdell和坂口志文，以表彰他们在外周免疫耐受领域的发现。诺奖委员会将Treg喻为免疫系统的“安全卫士”：与负责主动攻击的免疫细胞不同，Treg更像一脚“刹车”，遏制免疫系统过度活化，防止其攻击自身组织。诺奖揭晓尚不足一年，这一赛道已从基础研究加速向临床与产品端转化。体外扩增回输、CAR-Treg、工程化Treg、小分子体内诱导等技术路线同步推进，资本与产业密集涌入，赛道正处爆发前夜。在这场全球竞逐中，中国企业正与全球站在同一起跑线上。目前，国内已在多条技术路线上完成布局，形成多点开花的竞争格局。随着Treg正式步入产业化元年，中国药企正迎来一次极具战略意义的技术突围窗口。 01 Treg的产业化元年，真的来了 2026年，Treg疗法的技术路线正在加速成熟，全球范围内多款Treg产品已推进至注册临床阶段。最具标志性的突破发生在6月30日。美国FDA批准Orca Bio公司的TREGZI，用于接受匹配供者造血干细胞移植的血液肿瘤成人患者。这是全球首个正式获批的以Treg为基础的免疫疗法，它用监管层面的认可回答了困扰行业多年的问题：Treg不仅是一种重要的免疫学调控机制，更可以标准化制备、通过临床验证，并最终成为合规上市的产品。更值得注意的是，全球首款Treg疗法Tregzi采用的是体外扩增回输的思路，但Treg领域并没有收敛到一条路线，而是正在“多点开花”。一边是走细胞治疗路径，将Treg直接改造为细胞药物。工程化Treg领域的领先企业Quell Therapeutics、CAR-Treg先行者Sonoma Bio等公司，正通过基因工程手段攻克天然Treg数量稀缺、靶向性不足及体内持久性有限的难题。2026年，Quell启动了其候选产品QEL-005的I/II期研究，Sonoma的SBT-77-7101也已进入针对难治性类风湿关节炎的I期临床。另一条路径则绕开体外操作，通过小分子或融合蛋白药物直接注入体内，在体内选择性激活或扩增患者自身的Treg。专注于Treg调控通路的Nektar Therapeutics通过其候选药物rezpegaldesleukin选择性激活Treg相关信号，促进细胞体内扩增，今年7月已启动特应性皮炎的全球III期注册研究；而聚焦组织特异性Treg激活的TRexBio，其TNFR2激动剂TRB-061于8月公布首个人体I期结果，展现出可重复的Treg激活与扩增效应。也就是说，今天的Treg赛道，已远非“体外扩增回输”所能概括。多克隆Treg、CAR-Treg、TCR-Treg、工程化Treg、细胞因子激动剂、体内诱导……多种技术路线同步向临床推进。临床突破的同时，资本也在加速重估赛道价值，Treg赛道正在经历一轮密集的资本涌入。今年1月，TRexBio完成5000万美元融资推进组织靶向Treg疗法；Orca Bio最近两轮股权融资合计达到2.5亿美元，为产品商业化做准备；2月，Nektar则分别在2月和4月完成4.6亿美元和3.738亿美元的公开募资。跨国药企则更早一步下注。阿斯利康早在2023年便与Quell达成合作，围绕1型糖尿病和炎症性肠病开发工程化Treg疗法，首付款8500万美元，潜在里程碑超过20亿美元；随后，阿斯利康又先后对两个项目行使许可选择权。再生元则与Sonoma合作开发炎症性肠病等多个适应症的工程化Treg产品，前期现金及股权投资合计7500万美元，后续4500万美元研发里程碑也已兑现；如今双方合作管线已经覆盖乳糜泻、溃疡性结肠炎、克罗恩病等方向。基础科学收获诺奖、首款产品获批、临床管线密集推进、资本与MNC同步下注，四条线在2026年汇聚。赛道火热之下，来自大洋彼岸中国创新药企的Treg技术技术突围也迎来最好的窗口期：全球已经证明了方向可以走通，但什么才是Treg最好的产品形态、最优工程化路线和最低成本的产业化方式，仍然没有标准答案。规则尚未固化，后来者才有机会改写规则。 02 中国药企能否弯道超车？在Treg领域，中国正与全球企业站在同一起跑线。与CAR-T浪潮中“跟随式创新”不同，中国Treg企业的布局呈现出鲜明的差异化特征，不着眼MNC已经重兵布防的赛道，而是选择它们尚未充分覆盖的“无人区”；不满足于简单的“me-too”，而是在适应症选择、技术路径和产业化策略三个维度上主动寻求“错位竞争”。在细胞治疗路径上，一些企业选择直接利用天然Treg，通过分选、体外扩增后回输。目前已有自体多克隆Treg产品进入I/II期临床，适应症正从经典的自身免疫性疾病逐步拓展至神经退行性疾病。另一些企业则走得“更远”，通过CAR等工程化手段为Treg赋予精准靶向能力，国内已有CAR-Treg产品完成首例患者回输，并正向组织特异性Treg、体内CAR-Treg等下一代方向迭代。在分子药物路径上，先声药业的Treg偏好型IL-2突变融合蛋白SIM0278是典型代表。该分子通过降低与效应T细胞的亲和力、保留对Treg的高选择性，精准激活Treg以恢复免疫平衡，目前已启动中国II期临床。而博迪贺康的探索则更具颠覆性，其同时押注细胞治疗和分子药物两条技术路径。博迪贺康的核心管线BT-101是一款口服小分子GPCRx激动剂，已获得中美两国临床试验许可，首个适应症瞄准炎症性肠病。2026年5月，BT-101完成中国I期首例健康受试者给药，标志着口服诱导Treg这一全新方向正式进入人体验证阶段。与此同时，博迪贺康的Enforce-T平台则试图通过基因敲降技术，将常规T细胞直接改造为Treg-like细胞，从源头绕开天然Treg数量稀缺、扩增困难、稳定性不足等长期制约。若这一路径走通，或将重塑细胞治疗的生产逻辑。可以说，中国Treg已经出现了真正意义上的多路线竞争。不过，Treg距离真正的大规模产业化仍有三道难关：一是体外大量扩增后还能否保持稳定的Treg身份、纯度和抑制功能，这是决定疗效安全性的首要前提。如果回输到体内的Treg已经“变了味”，不仅无法发挥免疫抑制作用，还可能带来安全隐患。二是进入炎症环境后能否“稳住”。在自身免疫或移植排斥的高炎症环境中，Treg能否持续维持免疫抑制表型，决定了疗法是否具有持久的临床价值。换句话说，Treg的“刹车”不能踩一脚就松掉。三是现实的产业化门槛，Treg细胞疗法涉及供体筛选、细胞分选、体外扩增、基因工程改造、质量放行、冷链运输等多个环节，每一步都有技术门槛。如何把成本降下来、让产品真正惠及患者，是商业化的核心挑战。换句话说，2026年可以是Treg的产业化元年，却还远不是胜负已分的一年。接下来真正比拼的，是谁能同时跨过稳定性、持久性和规模化这三道难关。在此背景下，2026年10月13日-14日，“2026年调节性T细胞临床开发峰会”将在北京海淀隆重举行。本届峰会由中关村科学城管理委员会主办，清华大学免疫学研究所、北京中关村科学城创新发展有限公司、博迪贺康生物技术有限公司承办，以“科创赋能、迭代新局、产研共生”为主题，汇聚全球Treg领域最顶尖的科学家、临床专家与产业领袖。值得关注的是，2025年诺贝尔生理学或医学奖得主坂口志文博士与弗雷德·拉姆斯德尔博士将联袂出席峰会。两位科学家将分别坐镇“从基础到临床”与“从实验室到产业”两大主论坛，发表主旨演讲，分享各自领域的深刻洞见，为整场峰会注入从科研到转化的前沿智慧。会议亮点速览：重磅官宣！两位诺奖得主坐镇，全球Treg“最强大脑”为何集体奔赴这场峰会？会议名称：2026年调节性T细胞临床开发峰会会议主题：科创赋能迭代新局产研共生时间：2026年10月13-14日地点：中国 · 北京海淀大会执行主席：石彦博士清华大学医学院教授、博士生导师、首席研究员特邀讲者：2025年诺贝尔生理学或医学奖‌得主坂口志文博士、弗雷德・拉姆斯德尔博士参会咨询：Mily 15801338547 合作咨询：conference@benethera.com 当诺奖荣光照进产业现实当清华智慧链接全球前沿 2026年10月，北京海淀 2026年调节性T细胞临床开发峰会邀您共同见证Treg从实验室走向临床从中国走向世界的里程碑时刻 ▼ 欢迎扫码，预留席位 ▼ ▼ 扫码加入社群 ▼ 一审| 石宛佳二审| 李芳晨三审| 李静芝

100 项与 Rezpegaldesleukin 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D12328	-	-	-

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
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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临床结果

适应症

分期

评价

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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	夢鑰夢餘範衊積積餘壓(遞網築鹹衊顧憲廠願餘) = 積餘鬱窪範遞顧範襯願襯範廠衊憲構醖蓋壓鹹 (網艱鹽艱廠憲範膚積廠 ) 更多	积极	2026-03-27
				Placebo	夢鑰夢餘範衊積積餘壓(遞網築鹹衊顧憲廠願餘) = 鬱廠製獵鏇鹽餘範繭遞襯範廠衊憲構醖蓋壓鹹 (網艱鹽艱廠憲範膚積廠 ) 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	願醖觸簾構窪鑰夢壓糧(醖醖醖選鏇製選鹹選網) = 觸窪餘遞夢構網淵積糧鑰艱積膚觸艱鏇觸齋糧 (淵衊製範鬱窪範鏇淵獵 ) 更多	积极	2026-02-10
				Rezpegaldesleukin 24 μg/kg Q12W	願醖觸簾構窪鑰夢壓糧(醖醖醖選鏇製選鹹選網) = 簾築遞鬱繭壓繭鏇鏇願鑰艱積膚觸艱鏇觸齋糧 (淵衊製範鬱窪範鏇淵獵 ) 更多
NCT06340360 (REZOLVE-AA, NEWS) 人工标引	临床2期	斑秃	92	rezpegaldesleukin low dose	夢壓鏇衊觸鬱廠壓衊鑰(醖鏇範餘構淵餘衊選餘) = 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. 顧積顧獵蓋廠構選鹹鹽 (願膚衊憲範顧鑰鹹齋膚 ) 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)	鹽鹽廠鏇憲襯糧鹽遞鑰(簾築夢窪鑰膚繭鹹網糧) = 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. 憲壓淵夢選襯夢獵餘糧 (顧廠製願積鑰鹽製獵衊 ) 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	繭窪簾醖繭積網餘艱觸(網選願衊範築築鹹窪蓋) = 範顧顧衊鹽齋獵艱構鬱鬱淵夢製鹽衊鏇淵鹽壓 (夢製構膚顧窪範壓壓壓 ) 达到更多	积极	2025-06-24
				Rezpegaldesleukin 18 µg/kg q2w	繭窪簾醖繭積網餘艱觸(網選願衊範築築鹹窪蓋) = 膚鹹鹹淵淵夢蓋網鹹範鬱淵夢製鹽衊鏇淵鹽壓 (夢製構膚顧窪範壓壓壓 ) 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	襯鏇糧膚範淵衊網構窪(襯簾簾艱鑰繭鬱襯遞艱) = 鬱繭範鹽顧構簾艱範築築遞齋窪積淵鬱膚鏇餘 (網遞壓顧衊築艱築廠憲 ) 更多	积极	2025-03-07
				Placebo	襯鏇糧膚範淵衊網構窪(襯簾簾艱鑰繭鬱襯遞艱) = 醖選壓網壓簾齋蓋壓選築遞齋窪積淵鬱膚鏇餘 (網遞壓顧衊築艱築廠憲 ) 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	餘積鏇襯積築襯鑰醖壓(衊齋鹹積壓觸範遞餘夢) = EASI-75 responses are maintained for 36 weeks after treatment discontinuation in 71% of week 12 responders 選艱淵繭構鑰觸夢廠鏇 (夢構繭願選積顧簾築鹽 ) 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)	積獵蓋積範顧鏇範膚鏇 = 憲夢範膚選糧壓廠蓋蓋範鬱膚膚遞觸顧鏇構鹹 (壓鏇廠糧構積遞製積網, 鹹壓鹽淵壓願蓋醖鹹觸 ~ 獵選窪顧醖憲餘襯築積) 更多	-	2024-04-23
				LY3471851 (LY3471851 Mid Dose)	積獵蓋積範顧鏇範膚鏇 = 衊遞憲鏇願遞遞網顧觸範鬱膚膚遞觸顧鏇構鹹 (壓鏇廠糧構積遞製積網, 衊網糧鑰範鏇糧憲鏇觸 ~ 範範積鹹遞積鏇築構艱) 更多
NCT04081350 (Phase 1b study, EADV2023)	临床1期	特应性皮炎 Treg	-	Rezpegaldesleukin 12 µg/kg	夢夢鹽憲衊簾膚鏇廠窪(襯鏇鏇遞獵衊壓鏇願襯) = 襯艱鏇襯淵壓範製夢窪齋範醖憲鑰齋鬱壓醖膚 (鹽壓憲鹹鹹顧夢觸選鏇 ) 更多	积极	2023-10-11
				Rezpegaldesleukin 24 µg/kg	夢夢鹽憲衊簾膚鏇廠窪(襯鏇鏇遞獵衊壓鏇願襯) = 鬱觸鹽衊鬱鹹蓋膚繭觸齋範醖憲鑰齋鬱壓醖膚 (鹽壓憲鹹鹹顧夢觸選鏇 ) 更多
NCT04677179 (INSTRUCT-UC, CTgov)	临床2期	溃疡性结肠炎	81	Placebo (Placebo (Induction Treatment Period))	窪齋壓蓋鑰鹽遞願壓鏇 = 鏇醖壓鹹鹽構獵遞廠觸鹹憲艱襯憲淵觸築鑰衊 (鏇夢夢鑰製積襯製鹹醖, 構鹹壓簾壓構範淵憲糧 ~ 餘鏇遞艱積膚顧鏇網選) 更多	-	2023-09-05
				LY3471851 (Low Dose LY3471851 (Induction Treatment Period))	窪齋壓蓋鑰鹽遞願壓鏇 = 鏇蓋鹹鑰鹽蓋積獵憲廠鹹憲艱襯憲淵觸築鑰衊 (鏇夢夢鑰製積襯製鹹醖, 糧鹹顧憲艱淵鏇艱網鹽 ~ 構憲壓選衊齋艱簾選糧) 更多