The goal of this Phase 1 clinical study is test tumor infiltrating lymphocytes (known as C-TIL051) with NKTR-255 and anti-PD1 therapy for subjects with refractory non-small cell lung cancer.
The purpose of this study is to:
1. Test the safety and ability for subjects to tolerate the TIL therapy
2. Measure to see how the NSCLC responds to the TIL therapy
Participants will be asked to:
* Provide a tumor sample prior to the start of any treatment which will be used to make the C-TIL051.
* Receive standard of care treatment until their lung cancer no longer responds
* When necessary, the C-TIL051 will be manufactured by the sponsor and sent back to the site
* Subject will then receive chemotherapy (called lymphodepletion) for 3 days followed by 2 days of rest
* C-TIL051 will then be infused on day 0 followed by NKTR-255 (IL-15) about 12 to 24 hours later
* Pembrolizumab will be administered every 3 weeks for up to 2 years
NKTR-255 is a novel polymer-conjugated human IL-15 receptor agonist molecule designed to increase the proliferation and survival of memory CD8+ T cells and enhance the formation of long-term immunological memory which may lead to sustained anti-cancer immune response. The combination of NKTR 255 and TIL's could improve proliferation and persistence of cellular therapies leading to enhanced anti-tumor activity.

开始日期2024-02-29

申办/合作机构

AbelZeta Pharma, Inc.

[+1]

NCT05664217

/ Terminated临床2/3期

A Phase 2/3, Randomized, Double Blind, Placebo-controlled, Multicenter Study of NKTR-255 vs Placebo Following CD19-directed CAR-T Cell Therapy in Patients With Relapsed/Refractory Large B-cell Lymphoma

Nektar Study 18-255-01 was a Phase 2/3, randomized, double blind, placebo-controlled, multicenter study of NKTR-255 versus placebo following CD19-directed CAR-T cell therapy in patients with R/R LBCL. This study was to be run in 2 parts: Phase 2 (Stage 1) and Phase 3 (Stage 2).
This study evaluated the safety and efficacy of NKTR-255 following CD19-directed chimeric antigen (CAR)-T cell therapy in patients with relapsed or refractory (R/R) large B-cell lymphoma (LBCL).
NKTR-255 was an investigational IL-15 receptor agonist designed to boost the immune system's natural ability to fight cancer. T cells are infection fighting blood cells that can kill tumor cells. Chimeric antigen (CAR)-T cell product consists of genetically engineered T-cells, modified to recognize CD19, a protein on the surface of cancer cells. These CD19-specific T cells may help the body's immune system identify and kill CD19-positive cancer cells. Giving NKTR-255 following the treatment with CD19 CAR-T cell therapy may work better in treating large B-cell lymphoma than either drug alone.

开始日期2023-02-23

申办/合作机构

Nektar Therapeutics

NCT05632809

/ Recruiting临床2期IIT

REStoring lymphoCytes Using NKTR-255* After chemoradiothErapy in Solid Tumors (RESCUE)

To learn about the effects of the investigational drug NKTR-255 in combination with the standard drug durvalumab on locally advanced NSCLC when given after CRT.

开始日期2023-01-10

申办/合作机构

The University of Texas MD Anderson Cancer Center

[+1]

100 项与 NKTR-255 相关的临床结果

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100 项与 NKTR-255 相关的转化医学

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100 项与 NKTR-255 相关的专利（医药）

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项与 NKTR-255 相关的文献（医药）

2025-12-09·Blood Advances

NKTR-255 enhances complete response following CD19 CAR T-cell therapy in patients with relapsed/refractory large B-cell lymphoma

Article

作者: Chaudhry, Sohail ; Castilla-Llorente, Cristina ; Perales, Miguel-Angel ; McGuirk, Joseph ; Dahiya, Saurabh ; Marcondes, A. Mario Q. ; Diefenbach, Catherine ; Xu, Heng ; Essell, James ; Ahmed, Sairah ; Zalevsky, Jonathan ; Liu, Yi ; Tagliaferri, Mary A. ; DiPersio, John ; Fanton, Christie ; Lee, Zachary H. ; Miklos, David ; Turtle, Cameron J.

Autologous T-cells engineered to express CD19-directed chimeric antigen receptor (CAR) have shown high overall response rates in treatment-refractory large B-cell lymphoma (LBCL). However, more than half of patients do not attain a durable response and will eventually relapse. Thus, strategies to improve long-term efficacy of CAR T-cell products are needed. In this phase 2, randomized, double-blind, placebo-controlled, multicenter study of NKTR-255 versus placebo following CD19 CAR T-cell therapy, eligible patients with R/R LBCL were treated with one of two FDA-approved CAR T-cell products, axicabtagene ciloleucel (axi-cel) or lisocabtagene maraleucel (liso-cel). In total, 15 patients received CD19 CAR T-cell therapy and received study treatment, 11 patients were randomized to the NKTR-255 group (5 at 1.5 µg/kg; 3 at 3.0 µg/kg; 3 at 3 µg/kg then 6 µg/kg cycle 2+) and 4 to placebo. NKTR-255 post CD19 CAR T-cell administration led to augmented CR rates with 8 of 11 (73%) in the NKTR-255 group versus 2 of 4 (50%) in the placebo group reaching complete response rate at month 6 (CR6). Clinical response was accompanied by re-expansion of CD8+ CAR T-cells. The most common (≥20%) grade ≥3 NKTR-255-related adverse events were decreased neutrophil, platelet, and lymphocyte counts; all resolved without clinical sequelae. No cytokine-release-syndrome (CRS) or immune-effector-cell-associated-neurotoxicity-syndrome (ICANS) were reported in the NKTR-255 group. NKTR-255 was well-tolerated, safe, and augmented CR6 for LBCL patients. Based on the findings, additional confirmatory studies with NKTR-255 as adjuvant treatment to CAR T-cell, including other cellular therapies, are warranted (ClinicalTrials.gov number NCT05664217).

2025-12-01·Molecular therapy. Oncology

CXCL10-induced chemotaxis of ex vivo-expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma

Article

作者: Tasneem, Kazi L ; Zhu, Hongwen ; Hoang, Hai M ; Marcondes, Mario ; Luo, Wen ; Lee, Dean A ; Eguchi, Shiori ; Behbehani, Gregory K ; Ayello, Janet ; Xu, Changxin ; Cairo, Mitchell S

Osteosarcoma (OSA) has a dismal prognosis despite surgical resection and multiagent chemotherapy. While adoptive natural killer (NK) cell therapies have been successful in hematological malignancies, the application in solid tumors is challenging due to a tumor microenvironment (TME) that impairs NK cell tumor infiltration. Here, we found that ex vivo expansion of NK cells significantly increases the expression of C-X-C motif chemokine receptor 3 (CXCR3), one of the major proteins in the regulation of NK cell chemotaxis. Engineered over-secretion of CXCR3 ligands, C-X-C motif chemokine ligand (CXCL)9, -10, or -11, from OSA cells significantly enhanced expanded NK cell migration toward OSA cells in vitro and infiltration into the TME in vivo, with the highest NK infiltration rate in CXCL10-secreting tumors. Infusions of expanded NK cells significantly reduced (p = 0.02), and concomitant treatment with an interleukin (IL)-15 agonist NKTR-255 further reduced tumor burden and significantly increased survival in mice bearing CXCL10-secreting tumors compared with those with wild-type tumors (p = 0.02). Single-cell RNA sequencing and mass cytometry revealed upregulated apoptosis and transforming growth factor-β (TGF-β) signaling as the potential mechanisms of response/resistance to NK cell therapy in vivo. Our findings highlight potential application of chemokine-enhanced NK tumor infiltration in combination with an IL-15 agonist as a novel approach to effective treatment of OSA.

2024-12-01·Molecular therapy. Oncology

Combinatorial immunotherapy of anti-MCAM CAR-modified expanded natural killer cells and NKTR-255 against neuroblastoma

Article

作者: Cairo, Mitchell S. ; Liao, Yanling ; Mo, Xiaokui ; Overwijk, Willem W. ; Cairo, Mitchell S ; Cripe, Timothy P. ; Luo, Wen ; Gardenswartz, Aliza ; Ayello, Janet ; Rosenblum, Jeremy M ; Marcondes, A. Mario ; Tian, Meijuan ; Overwijk, Willem W ; Marcondes, A Mario ; Cripe, Timothy P ; Chu, Yaya ; Lee, Dean A. ; Rosenblum, Jeremy M. ; Lee, Dean A ; Hoang, Hai

Pediatric patients with recurrent metastatic neuroblastoma (NB) have a dismal 5-year survival. Novel therapeutic approaches are urgently needed. The melanoma cell adhesion molecule (MCAM/CD146/MUC18) is expressed in a variety of pediatric solid tumors, including NB, and constitutes a novel target for immunotherapy. Here, we developed a chimeric antigen receptor (CAR) expressing natural killer (NK) cell-targeting MCAM by non-viral electroporation of CAR mRNA into ex vivo expanded NK cells. Expression of anti-MCAM CAR significantly enhanced NK cell cytotoxic activity compared to mock NK cells against MCAM^high but not MCAM^low/knockout NB cells in vitro. Anti-MCAM-CAR-NK cell treatment significantly decreased tumor growth and prolonged animal survival in an NB xenograft mouse model. NKTR-255, a polymer-conjugated recombinant human interleukin-15 agonist, significantly stimulated NK cell proliferation and expansion and further enhanced the in vitro cytotoxic activity and in vivo anti-tumor efficacy of anti-MCAM-CAR-NK cells against NB. Our preclinical studies demonstrate that ex vivo expanded and modified anti-MCAM-CAR-NK cells alone and/or in combination with NKTR-255 are promising novel alternative therapeutic approaches to targeting MCAM^high malignant NB.

项与 NKTR-255 相关的新闻（医药）

2026-09-17

·RecodeX

复融生物Pre-B轮累计近2亿元：细胞因子能否破解肿瘤免疫耐药与响应率低瓶颈

肿瘤免疫治疗正在经历一场静默的分化。PD-1/PD-L1抑制剂把“免疫系统可以对抗癌症”从假设变成标准疗法之后，行业撞上了一堵并不隐蔽的墙：相当一部分患者对检查点抑制剂原发性耐药，更多患者在初始响应后出现获得性耐药。药企的应对策略一度高度同质化——寻找新的检查点、开发双抗、尝试联合用药。但在这些路径之外，一个更古老的免疫学问题重新浮出水面：如果免疫系统需要被激活，而不是仅仅被“解除刹车”，该用什么分子来完成这一步？细胞因子是这个问题的天然答案之一。IL-2在1992年获批用于转移性肾细胞癌，证明了增强T细胞功能可以治疗肿瘤；但高剂量IL-2带来的毛细血管渗漏综合征和多器官毒性，也让“细胞因子成药”在此后三十年间成为一个反复被提起、又反复被搁置的命题。半衰期短、作用广泛、多效性带来的脱靶毒性，构成了细胞因子药物难以跨越的三重门。苏州复融生物技术有限公司在2026年9月宣布完成Pre-B轮融资第二关交割，金额过亿元。这笔资金由复星医药旗下产业基金复健资本新药基金领投，广发信德、德同资本、常熟开晟、苏州宸枫跟投，苏州寒武纪持续追加投资。加上此前由复旦科创基金领投、常熟国发创投和苏州寒武纪跟投的首关融资，复融生物Pre-B轮两次交割累计近2亿元。凯乘资本担任本轮融资独家财务顾问并继续负责后续融资。这家成立于2019年的临床阶段生物制药公司，正在试图用工程化细胞因子回答PD-1之后的问题。字段内容公司苏州复融生物技术有限公司轮次 Pre-B轮（第二关交割）金额第二关过亿元；Pre-B轮两次交割累计近2亿元投资方第二关：复健资本新药基金（领投）、广发信德、德同资本、常熟开晟、苏州宸枫、苏州寒武纪（追加）；首关：复旦科创基金（领投）、常熟国发创投、苏州寒武纪总部苏州高新区（上海设有研发中心）创始人应天雷（创始人）、纪恩（联合创始人、董事长）官网 https://www.forlongbiotech.comIL-15超级激动剂：用Fbody把“毒性分子”改造成“可给药分子” 复融生物的首发管线FL115是一款工程化IL-15/IL-15Rα-Fbody融合蛋白，公司称其具有“同类最佳”潜力。IL-15的生物学逻辑并不复杂：它能激活自然杀伤细胞和记忆性T细胞，而这两类细胞在肿瘤免疫监视中扮演关键角色。问题在于，天然IL-15的半衰期极短，且系统性给药可能引发广泛的免疫激活。复融生物的解决方案是Fbody®技术——一种经工程化改造的单链Fc。据公司披露，Fbody®在保留FcRn亲和力的同时，消除了与Fcγ受体及补体系统的结合。这个设计的意图很明确：保留FcRn介导的再循环以延长半衰期，同时切断Fcγ受体和补体介导的效应功能，从而降低抗体依赖性细胞毒性和补体依赖性细胞毒性带来的额外风险。从已披露的临床数据看，FL115在晚期实体瘤中的表现构成了复融生物最核心的叙事资产。据公司披露，FL115已在中美多个临床中心完成超过90例晚期实体瘤及非肌层浸润性膀胱癌患者的给药。在已完成的I期临床中，FL115单药治疗的疾病控制率为39%；一例晚期宫颈癌患者疾病稳定超过20个月，两例确认部分缓解患者的缓解持续时间分别超过12个月和10个月。公司特别强调，静脉输注FL115单药是“唯一单药获得部分缓解的IL-15超级激动剂”。这个“唯一”的表述需要审慎对待。它来自公司官网新闻稿，而非独立的第三方头对头研究。IL-15超级激动剂领域并非无人区，Nektar Therapeutics的NKTR-255、ImmunityBio的Anktiva（N-803）等产品都在不同适应症中推进过临床开发。Anktiva已于2024年获得FDA批准用于BCG无应答的非肌层浸润性膀胱癌，这恰恰是FL115正在推进II期临床的适应症。因此，FL115的差异化叙事不能只建立在“唯一单药PR”这一公司口径上，而需要看它在与BCG联用的II期数据中，能否在与已获批产品的间接比较中显示出有意义的疗效或安全性优势。目前，公司称BCG无应答NMIBC适应症的I/II期数据“持续成熟”，但尚未披露具体缓解率数据。PD-1/IL-18双抗：绕开IL-18BP的“诱饵陷阱” FL116是复融生物的第二款候选药物，设计逻辑比FL115更复杂。IL-18是另一个具有抗肿瘤潜力的细胞因子，但它在体内有一个天然的“刹车”——IL-18结合蛋白。IL-18BP会与IL-18结合，阻止其与受体相互作用，从而限制IL-18的免疫激活效应。复融生物的应对策略是构建一个差异化的IL-18文库，据公司披露内含百余条完全不与IL-18BP结合的IL-18突变体。基于此文库开发的FL116，将抗PD-1抗体与这种工程化IL-18突变体融合，形成PD-1/IL-18双特异性抗体融合蛋白。这个设计的巧妙之处在于，它试图同时解决两个问题：用PD-1抗体部分阻断免疫抑制信号，同时用不被IL-18BP中和的IL-18突变体提供免疫激活信号。公司称FL116已在多种对免疫检查点抑制剂耐药的体内肿瘤模型中显示出强大的肿瘤杀伤能力。但“体内肿瘤模型”与人体临床之间隔着巨大的不确定性。目前FL116完成了在非人类灵长类的早期毒理探索和第一个GMP批次生产，尚未进入人体临床试验。公司计划推动FL116进入实体瘤适应症临床试验，并在2027年将FL115及FL116在实体瘤领域推进至临床概念确认研究阶段。这个时间表意味着，FL116距离产生任何可评估的人体数据还有相当距离。技术平台的“可复制性”才是真正的估值锚点复融生物在融资材料中反复强调其建立了四个专有技术平台：Fbody®长效化技术平台、Fc工程化平台、Syntokine®新型人工合成细胞因子平台以及大分子AI智能发现平台。在细胞因子药物开发领域，技术平台的价值不在于它听起来有多完整，而在于它能否被重复用于多个靶点、多个分子的改造，并且每次改造都能产生可预测的药代动力学和药效学结果。从已披露的信息看，复融生物的平台至少在两个方向上得到了产业界的一定程度验证。据公司披露，其已与复宏汉霖、信达生物、人福医药等达成多项研发合作。信达生物和复宏汉霖都是中国头部的创新药企，它们选择与一家临床阶段公司进行研发合作，通常意味着对后者技术平台的某种认可。但合作的具体内容、金额、里程碑和权益分配均未披露，因此这种“验证”的含金量无法独立评估。复旦科创基金在首关融资时的表态也值得注意，其称公司“已获得信达、复宏汉霖等头部药企的研发合作验证”，并将FL115的膀胱癌适应症进入II期视为“成药确定性极高”的依据。这是投资方的判断，而非事实本身。另一个值得关注的细节是FL115的生产工艺。公司称FL115“生产工艺稳健、成本较低，具备显著的成本优势和定价灵活性”。在细胞因子药物领域，生产成本确实是一个容易被忽视但实际影响重大的变量。IL-15超级激动剂通常需要哺乳动物细胞表达系统生产，如果复融生物确实在产率或纯化工艺上有实质性改进，这将在未来的商业化阶段转化为定价空间。但“成本较低”目前只是公司口径，没有披露具体的单位生产成本或与竞品的比较数据。膀胱癌适应症：一个“聪明”的注册路径选择复融生物将FL115的注册III期临床聚焦于非肌层浸润性膀胱癌的BCG无应答适应症，这是一个值得拆解的战略选择。NMIBC的标准治疗是经尿道膀胱肿瘤切除术加膀胱内灌注卡介苗。但相当一部分患者对BCG无应答，这些患者面临的选择有限：要么接受根治性膀胱切除术，要么尝试替代的膀胱内灌注疗法。FDA在2024年批准Anktiva用于这一适应症，实际上验证了“IL-15通路激活NK细胞和T细胞来清除膀胱内肿瘤”的机制逻辑。复融生物选择BCG无应答NMIBC作为首个注册适应症，至少有三重考量。其一，膀胱内灌注给药可以将药物局部递送到肿瘤微环境，降低系统性暴露和全身毒性风险，这对于细胞因子类药物尤其重要。其二，该适应症已有明确的监管路径和获批先例，临床终点相对清晰。其三，NMIBC患者群体数量可观，且BCG无应答亚群存在明确的未满足需求。但硬币的另一面是，Anktiva已经占据先发位置，FL115进入III期时需要在疗效、给药便利性或安全性上展示出可感知的差异。公司CEO魏东博士在融资新闻中称，BCG无应答NMIBC适应症的I/II期数据“进一步支持其成为该疾病最佳疗法的潜力”，但具体数据尚未公开，这一判断目前无法被外部验证。资本结构：产业资本与高校基金的“双重背书” 复融生物Pre-B轮的投资者名单呈现出一种有意味的结构。第二关领投方复健资本新药基金是复星医药旗下产业基金，其投资逻辑通常不只是财务回报，还包括与复星医药自身管线和产业资源的潜在协同。复健资本新药基金负责人在融资新闻中称复融生物为“国内细胞因子赛道头部标杆企业”，并强调“依托对创新药前沿领域的深度研判”进行投资。这是投资方声明，需要放在产业资本的战略语境中理解。首关领投方复旦科创基金则代表了另一种逻辑。复融生物创始人应天雷是复旦大学基础医学院教授、上海合成免疫工程技术研究中心主任，公司的技术源头与复旦大学的科研体系深度绑定。复旦科创基金的使命是推动复旦大学科技成果转化，其投资复融生物既是财务行为，也是科技成果转化生态的一部分。这种“高校基金+产业资本”的组合，在生物医药早期项目中并不罕见，但复融生物的特别之处在于，它的技术平台确实源自高校实验室的长期积累，而非单纯的license-in或me-too开发。从融资节奏看，复融生物在2023年完成1.1亿元A轮融资后，将FL115推进至临床开发阶段；2026年5月完成Pre-B轮首关，9月完成第二关。两次交割累计近2亿元的规模，对于一家需要同时推进中美两地临床试验、准备III期注册研究的生物制药公司而言，并不算宽裕。III期临床的入组规模、临床运营成本和CMC投入，通常远超I/II期。公司明确将资金用于“推动FL115在NMIBC适应症开展注册III期临床研究”，这意味着Pre-B轮资金的核心用途是烧向一个高成本的临床阶段。风险与待验证假设：数据密度决定叙事成色复融生物的故事建立在几个尚未被完全验证的假设之上。第一个假设是，FL115在BCG无应答NMIBC中的疗效能够达到或超过已获批的Anktiva，并且安全性特征足够有竞争力。目前公司只披露了“数据持续成熟”的定性描述，没有给出具体的完全缓解率或持续时间数据。在注册III期启动之前，这些数据将决定试验设计的统计假设和成功概率。第二个假设是，FL115在晚期实体瘤中的单药活性能够转化为与PD-(L)1抗体联用的协同效应。公司已启动FL115与PD-1抑制剂联用的Ib/II期临床试验，但联合用药的毒性叠加风险和治疗窗口变化是细胞因子联用方案的核心不确定性。IL-15激活NK细胞和记忆性T细胞的机制，与PD-1抑制剂解除T细胞抑制的机制，在理论上互补，但在人体中是否产生协同而不产生不可接受的免疫相关毒性，需要临床数据来回答。第三个假设是，FL116的IL-18突变体策略能够在人体中重现动物模型中的抗肿瘤活性。IL-18BP是人体内源性的负反馈调节机制，绕开它意味着人为延长和增强IL-18信号。这在理论上可以增强抗肿瘤免疫，但也可能打破免疫稳态，带来不可预期的炎症毒性。FL116在非人灵长类中的早期毒理探索据公司称“展现出良好的安全性特征”，但非人灵长类数据与人体安全性之间的转化关系，在细胞因子领域尤其需要谨慎。从更宏观的视角看，复融生物面临的是一个“时间窗口”问题。细胞因子赛道正在升温，全球范围内多个IL-15、IL-2、IL-18相关项目在推进临床。复融生物的技术差异化——Fbody®消除Fcγ受体和补体结合、IL-18突变体绕开IL-18BP——在分子设计层面有清晰的逻辑，但最终决定公司价值的，是这些设计能否在注册临床中转化为可量化的疗效和安全性优势。在数据读出之前，所有的“同类最佳”“标杆潜力”都只是假设。验证边界与可复核指标本文涉及的“首个、唯一、最大、领先”、订单、出货、性能等表述，如无另行说明，均是公司、创始人或投资方在现有公开材料中的披露口径；RecodeX未在本次采集材料中找到独立审计或第三方测试结论，因而不将其视为已经独立确认的事实。文中的产业协同、竞争位置和商业路径属于基于已披露产品与融资用途的编辑分析，不代表相关结果已经实现。技术侧应核验第三方测试条件、样本规模、良率、稳定性及与可比方案一致口径的结果；商业侧应核验去重后的付费客户、可执行合同、收入确认、复购率以及订单转化；资本与产业协同应以工商股权、关联交易、联合开发、采购或量产文件为准。 RecodeX 极客视：复融生物的真正看点，不在于它又完成了一轮近2亿元的融资，而在于它把细胞因子这个被行业反复放弃又反复捡起的领域，重新放回了PD-1之后的核心议程。Fbody®对Fc效应功能的“减法设计”和IL-18突变体对IL-18BP的“绕行策略”，在分子层面都指向同一个目标：让细胞因子从“知道有效但不敢用”变成“可以安全地用”。但分子设计的优雅不能替代临床数据的密度。FL115在NMIBC的II期数据、与PD-1联用的Ib/II期数据，以及FL116进入人体后的安全性信号，将决定这家公司是成为“后PD-1时代”的参与者，还是又一个在细胞因子成药难题前止步的尝试。

2026-04-27

·星际微光

Nektar 3.7亿美金超额募资：三线齐发，是“免疫重置”的王者归来，还是2b数据泡沫的最后一舞？

Nektar Therapeutics宣布完成3.738亿美元普通股公开发行，发行价为每股92美元，共出售4,062,500股，其中包括承销商全额行使超额配售权购买的529,891股。募集资金总额尚未扣除承销费用及其他发行开支。Jefferies、TD Cowen、Piper Sandler和Citigroup参与承销。本次发行依据此前向SEC提交并自动生效的S-3ASR搁架注册声明进行。 Nektar是一家临床阶段生物技术公司，聚焦自身免疫和慢性炎症疾病，核心资产REZPEG正在特应性皮炎、斑秃和1型糖尿病临床试验中开发。有问题，问星光智能体！人类基地：从Mercor到中国职场：员工正在训练即将取代自己的AI 投资亮点事实层面看，这是一轮“强势窗口融资”。Nektar本次公开发行共出售4,062,500股普通股，发行价92美元/股，募资总额约3.738亿美元；其中包括承销商全额行使529,891股超额配售权。SEC招股书显示，在超额配售全额行使后，发行后普通股数约为33,742,147股；以4月1日约29,679,647股为基数测算，本轮新增股份带来的稀释约13.7%。公司预计本次发行净募资约3.509亿美元。投资亮点之一，是资金质量和融资时点较好。临床阶段生物科技公司最怕在股价低迷、数据不确定时被迫融资；Nektar此次能以92美元/股完成大额公开发行，并且承销商全额行使超额配售，说明机构端对其核心资产REZPEG后续开发仍有较强需求。更重要的是，公司在2026年2月刚完成4.6亿美元融资，年报披露2025年底现金及投资为2.458亿美元，且未计入2月融资约4.32亿美元净额和ATM融资约4,400万美元；这次再融资后，公司的现金缓冲显著增强。投资亮点之二，是资金用途直接指向关键价值创造节点。本次募资可能用于研发、临床开发，包括REZPEG在特应性皮炎和斑秃中的3期试验，以及生产成本。对一家临床阶段公司而言，3期资金可见度本身就是估值支撑：它降低了短期“缺钱停项目”风险，也使公司在潜在BD、授权或并购谈判中拥有更强议价能力。投资亮点之三，是核心资产机制有差异化。 REZPEG是一种调节性T细胞刺激剂，靶向IL-2受体通路，意图扩增Treg、恢复免疫平衡。相比单纯阻断某一炎症因子的药物，这类“免疫重置/上游调节”逻辑如果在3期得到验证，理论上可能适用于多个自身免疫和炎症疾病。公司披露，REZPEG已获得FDA在中重度特应性皮炎和重度斑秃中的Fast Track资格，并在特应性皮炎、斑秃和1型糖尿病中开发。投资亮点之四，是已有2b期数据形成多适应症验证雏形。在特应性皮炎REZOLVE-AD研究中，公司称393例中重度患者在16周诱导期内相较安慰剂显示EASI改善，并计划在2026年二季度启动3期ZENITH-AD项目。斑秃REZOLVE-AA研究中，92例重度至极重度患者数据支持概念验证；虽然ITT主终点“接近但未达到”统计学显著性，但剔除4名重大入组违规患者后，两剂量组在36周SALT改善上达到统计学显著。投资亮点之五，是商业市场足够大。特应性皮炎患者基数大，公司引用数据显示美国约有3,000万人受影响；若REZPEG能证明疗效、安全性和较低给药频率优势，潜在市场空间不小。斑秃方面，目前治疗选择仍有限，若REZPEG作为非JAK、可自我给药的生物制剂展现更好安全/监测负担，可能形成差异化定位。风险：这次融资本身不是临床成功的证明。主要风险包括：3期失败、2b数据外推不足、斑秃主终点在原始mITT分析中未显著、未来仍有进一步稀释可能、竞争药物持续迭代，以及管理层如何有效使用近几轮大额资金。SEC文件也明确提示，本次发行后新投资者存在即时账面稀释，公司未来仍可能继续融资。这是一笔偏积极的融资事件，核心亮点在于“高价大额融资+超额配售全额行使+3期资金可见度提升+REZPEG多适应症平台化预期”。牛点是资金和数据共同支撑后续3期推进；熊点是估值已明显前置，临床失败或数据不一致会造成剧烈回撤。后续重点看AD三期启动、AA延长期/停药期数据、3期设计、现金消耗速度和是否出现大型药企合作。 Nektar的价值分析 Nektar目前的核心定位，已经从过去较宽泛的药物递送/聚合物技术公司，转向“免疫调节型、自身免疫与慢性炎症疾病公司”。其目标是开发可重新定义自身免疫和炎症疾病治疗范式的新药，并通过恢复免疫稳态来解决免疫失衡问题。公司称其管线重点是“first-in-class”、具备潜在疾病修饰能力的候选药物，这说明其投资故事不再是短期商业化产品驱动，而是围绕差异化机制和中后期临床验证展开。一、产品优势主要集中在核心资产rezpegaldesleukin，即REZPEG/NKTR-358。该药是靶向调节性T细胞的IL-2受体激动剂，正在开发特应性皮炎、斑秃和1型糖尿病等适应症。与只阻断单一炎症因子的药物不同，REZPEG的逻辑是增加Treg数量和功能，从上游调节Th1、Th2、Th17等多条炎症通路。若临床验证成功，它的潜在优势不只是“抗炎”，而是更接近“恢复免疫平衡”。二、技术优势在于Treg生物学的上游调控。 Treg是免疫反应的“主调节器”，Treg水平不足或功能不足可能与自身免疫和炎症疾病相关。 REZPEG通过直接靶向Treg表面的IL-2受体，促进Treg增殖并增强功能。这种机制如果成立，理论上可解释其跨适应症开发潜力：特应性皮炎是皮肤炎症，斑秃涉及毛囊免疫特权崩塌，1型糖尿病涉及免疫系统攻击胰岛β细胞，但三者都可被归入免疫耐受失衡问题。三、平台优势不只体现在REZPEG。公司还布局TNFR2方向的NKTR-0165、双特异性抗体NKTR-0166、CSF1R相关的NKTR-422，以及肿瘤免疫方向的IL-15受体激动剂NKTR-255。 NKTR-0165针对组织特异性Treg，计划用于溃疡性结肠炎、白癜风、多发性硬化等； NKTR-422则试图激活炎症消退相关的巨噬细胞生物学。这说明Nektar的平台叙事是“免疫细胞功能重塑”，而非单一靶点公司。四、服务优势不是传统意义上的医疗服务，而是临床开发与患者支持体系。公司在特应性皮炎和斑秃中有REZOLVE-AD、REZOLVE-AA研究，并提供试验信息、入组标准、研究地点及Medical Affairs联系渠道。公司也披露了扩展使用政策，强调优先通过临床试验获得系统性安全性和有效性数据，同时在个案中考虑伦理、公平、风险和监管要求。五、商业模式目前仍是典型临床阶段biotech模式：通过自研管线推进价值拐点，同时保留合作和授权弹性。值得注意的是，REZPEG由Nektar全资拥有，这提高了未来商业化或BD谈判的经济权益。另一方面，公司有超过三十年创新历史、五项活跃合作，以及通过战略合作产生11个已获批药物的记录，这为其未来寻找大型药企合作、共同开发或区域授权提供了可信背书。六、医疗价值在于瞄准高未满足需求。公司称特应性皮炎影响美国约3000万人；斑秃方面，公司披露美国约70万人当前患有某种形式斑秃，且疾病与生活质量、焦虑抑郁负担相关。若REZPEG能通过较低频率、自我给药方式带来持续疗效，并避免JAK抑制剂类药物的部分安全和监测顾虑，其临床定位可能具备差异化。七、未来前景取决于3期验证。正面看，REZOLVE-AD 2b研究纳入393例中重度特应性皮炎患者，并显示EASI改善；REZOLVE-AA 52周延长期数据显示，18 µg/kg和24 µg/kg组分别有29%和31%患者在36至52周新达到SALT≤20，且安全性描述为总体有利。负面看，这些仍是临床开发阶段数据，候选药物仍有未来安全性、有效性、注册、制造、竞争和审批失败风险；Fast Track也不代表一定获批。 Nektar的投资亮点是：机制差异化、REZPEG全资权益、多适应症扩展潜力、合作历史较强、近期临床数据增强进入后期开发的可信度。主要风险是：核心资产集中度高、斑秃和特应性皮炎竞争激烈、2期信号能否复制到3期仍不确定，以及公司尚未形成稳定商业收入。最关键的观察点：REZPEG在特应性皮炎和斑秃的3期设计、入组速度、疗效终点、安全性以及是否出现大型药企合作。 Treg 许多自身免疫和慢性炎症疾病并非只是某一个炎症因子过度活跃，而是免疫系统内部“效应T细胞”和“调节性T细胞”失衡。 Treg，即调节性T细胞，负责防止免疫系统攻击自身组织，并控制免疫反应强度；Treg数量不足或功能不足，可能参与自身免疫和炎症疾病发生。Nektar因此把治疗目标设定为恢复“Treg稳态”，即维持足够且有功能的Treg群体，使其重新压制异常免疫反应。一、这套科学叙事的最大特点，是“上游免疫调节”而非“下游单通路阻断”。现有许多自身免疫药物通过阻断IL-4、IL-13、IL-17、TNF、JAK等具体通路发挥作用；Nektar则认为Treg位于Th1、Th2、Th17等促炎通路上游，若能增强Treg数量和功能，理论上可以同时调节多条炎症轴，而不是只压制某一个细胞因子。这种方法旨在比单一通路拮抗机制更有效地降低炎症，但这里的关键词是“aims to”，仍属于有待临床验证的治疗假设。二、公司核心资产rezpegaldesleukin，简称REZPEG或NKTR-358，就是这一科学假设的主要载体。 REZPEG是一种作用于Treg表面IL-2受体的生物药，通过直接靶向IL-2受体，促进Treg增殖并提高其功能。 REZPEG可刺激包括FOXP3阳性Treg在内的调节性T细胞增殖，并已布局特应性皮炎、斑秃和1型糖尿病等免疫相关适应症。三、从分子设计角度看，REZPEG的科学基础来自IL-2生物学。 Nature Communications论文显示，IL-2对Treg增殖和生存有重要作用，但传统低剂量IL-2存在治疗窗窄、半衰期短、需要频繁给药以及可能诱导常规T细胞等问题；REZPEG使用重组人IL-2序列并连接PEG基团，设计目标是延长半衰期，并相较普通IL-2更偏向刺激Treg而非Tcon。这个设计若成立，关键优势在于把IL-2从“广泛免疫刺激因子”改造成更偏向“免疫耐受恢复工具”。四、科学逻辑在不同疾病中的应用也较清晰。特应性皮炎通常涉及Th2为主的炎症反应，Nektar认为Treg上游调节可影响Th1、Th2、Th17相关炎症；斑秃中，公司认为炎症环境会导致生长期毛囊免疫特权崩塌，并涉及NKG2D阳性T细胞、NK细胞及自身反应性CD8阳性T细胞，REZPEG目标是降低毛囊局部炎症、恢复免疫特权； 1型糖尿病中，公司则把Treg增强与减缓新发疾病进展相联系。五、这套科学平台的投资吸引力在于：第一，机制具有平台化潜力，不局限于单一疾病；第二，Treg扩增、CD25bright Treg变化等可作为药效学标志物，便于早期验证；第三，如果能证明停药后仍有持续疗效，将明显区别于需要长期持续抑炎的药物。 Nature Communications论文中，REZPEG在两项1b期皮肤炎症研究中采用每两周一次皮下注射，较高剂量特应性皮炎患者12周EASI改善83%，且部分应答在停药后仍维持，并伴随CD25bright Treg持续增加，这支持“免疫稳态恢复”假说，但仍属早期和探索性证据。 Nektar的pipeline 公司并不是围绕某一个适应症布局，而是围绕“免疫调节”布局。其研发管线利用免疫学洞察，开发针对疾病因果生物学和免疫失衡核心机制的新疗法，覆盖自身免疫、慢性炎症和肿瘤免疫等方向。换言之，Nektar的资产组合不是传统“一个靶点打一种病”，而是试图通过调节Treg、TNFR2、CSF1R、IL-15等关键免疫节点，形成可横向扩展的平台型管线。核心资产是Rezpegaldesleukin，简称REZPEG。它同时布局特应性皮炎、斑秃和1型糖尿病，靶点均为IL-2 receptor agonist / regulatory T cell agent。其科学逻辑的描述是：REZPEG作用于调节性T细胞表面的IL-2受体，刺激包括FOXP3阳性Treg在内的调节性T细胞增殖；Treg位于Th1、Th2、Th17等促炎通路上游，因此理论上可比只阻断单一炎症通路的药物更广泛地降低炎症。从投资角度看，REZPEG的优势是“一个机制、多适应症”。特应性皮炎验证的是皮肤慢性炎症；斑秃验证的是毛囊局部免疫特权崩塌；1型糖尿病验证的是自身反应性T细胞攻击胰岛β细胞。三个适应症表面不同，但共同点都是免疫耐受失衡。如果REZPEG在多个疾病中都显示一致疗效，市场会把它看成Treg平台资产，而不是单一皮肤病药物。但风险也在这里：Treg外周扩增不一定等于病灶组织内免疫重塑，尤其在1型糖尿病这类器官特异性自身免疫病中，临床终点更难、验证周期更长。第二个重要资产是NKTR-0165。为独特的双价TNFR2激动抗体，靶向组织特异性Treg，潜在适应症包括溃疡性结肠炎、白癜风和多发性硬化，首个人体临床研究计划于2026年开展。其科学基础是TNFR2优先表达于高度抑制性的组织特异性Treg、B调节细胞、神经元和内皮细胞表面；NKTR-0165选择性刺激TNFR2，而不调节TNFR1信号。 NKTR-0165的战略意义在于，它可能成为REZPEG之后的第二条Treg轴。REZPEG通过IL-2受体扩增Treg，NKTR-0165则通过TNFR2增强组织特异性Treg功能和稳定性。若两者机制互补，公司可从“REZPEG单品公司”升级为“免疫耐受平台公司”。不过，NKTR-0165仍处早期，核心风险是人体安全性、组织选择性和剂量窗口尚未验证；TNFR2生物学复杂，既涉及免疫调节，也可能影响炎症和组织修复，早期数据不能直接外推商业价值。 NKTR-0166是更前沿、也更不确定的项目。一种双功能抗体，整合TNFR2激动表位和一个已在风湿病治疗中验证过的拮抗抗体靶点，用于多种风湿性疾病。这个设计的吸引力在于“一边增强免疫耐受，一边阻断致病通路”，理论上比单纯激动Treg或单纯拮抗炎症因子更强。但这类双功能抗体的开发难点也更高：两个机制的剂量、组织分布、安全性和药代动力学必须同时匹配，否则可能出现疗效不足或毒性增加。 NKTR-422代表公司向炎症消退和纤维化方向扩展。长效CSF1/CSF1R相关生物药，目标是选择性激活炎症消退的生理过程，并驱动抗炎性组织驻留巨噬细胞生物学。这个项目的价值在于切入“炎症后修复”和纤维化，而不是单纯抑炎。若成功，它可能覆盖急慢性炎症、纤维化疾病等更广阔场景。但该领域转化风险高，因为巨噬细胞在不同组织和疾病阶段可能既促炎也抗炎，适应症选择会非常关键。 NKTR-255则是肿瘤免疫方向的保留资产。它是工程化IL-15受体激动剂，旨在增强NK细胞、CD8阳性T细胞、TIL和CAR-T细胞的增殖与存活，目前与Bavencio、Imfinzi、TIL疗法和Breyanzi等联合评估。这个项目与自身免疫管线方向相反：自身免疫是增强免疫耐受，肿瘤是增强效应免疫。其潜在价值在于提高细胞疗法或检查点抑制剂疗效，但IL-15赛道竞争激烈，且联合疗法开发依赖外部合作和清晰的临床信号。 Nektar pipeline的亮点是：核心资产REZPEG已进入多适应症临床验证，后续项目围绕Treg、TNFR2、CSF1R和IL-15形成免疫调节矩阵，具备平台化想象空间。主要短板是：商业化产品缺乏、价值高度依赖REZPEG后期数据，早期项目仍需人体概念验证。后续应重点跟踪REZPEG三大适应症临床数据、NKTR-0165首个人体试验进展、NKTR-255联合疗法信号，以及公司是否能通过合作降低研发资金压力。欲深入了解更多行业洞察，请扫以下二维码加入社群：公司已完成项目星际微光已完成的项目（截至2023.9，仍在继续......）圆满中秋 | 星际微光七年完成100个咨询项目咨询、调研、PR、投资、融资、营销、技术转化项目需求请扫码联系我们：点击“阅读原文”，看看：你的SOP，要贡献出来灭掉自己吗？

2026-03-12

·PRNewswire

Nektar Therapeutics Reports Fourth Quarter and Full Year 2025 Financial Results

SAN FRANCISCO, March 12, 2026 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) today reported financial results for the fourth quarter ended December 31, 2025. Cash and investments in marketable securities on December 31, 2025 were $245.8 million as compared to $269.1 million on December 31, 2024. Cash and investments at December 31, 2025 excludes net proceeds of approximately $432 million from the $460 million secondary offering completed by the Company in February 2026, and also excludes net proceeds of $44 million from sales of shares in February and March 2026 under the Company's existing $110 million at-the-market offering facility that was established in November 2025. "2025 was a pivotal year for Nektar as we saw successful and transformative Phase 2 data readouts for rezpegaldesleukin," said Howard W. Robin, President and CEO of Nektar. "The data highlighted the promise and differentiation of our novel Treg mechanism in two inflammatory dermatological disease settings of atopic dermatitis and alopecia areata. In early 2026, we reported the 52-week treatment data for rezpegaldesleukin. These data provide hope that complete clearance of disease could be possible for patients with monthly and quarterly maintenance dosing of rezpegaldesleukin. With our strengthened financial position following the recent financing, we look forward to initiating our Phase 3 program in atopic dermatitis in June of this year, while we continue to advance our earlier TNFR2 agonist antibody and bispecific program toward the clinic." Summary of Financial Results Revenue in the fourth quarter of 2025 was $21.8 million as compared to $29.2 million in the fourth quarter of 2024. Revenue for the full year of 2025 was $55.2 million compared to $98.4 million in 2024. Revenue primarily decreased year-over-year because we no longer recognize product sales due to the December 2024 sale of the Huntsville manufacturing facility, as well as a decrease in non-cash royalty revenue. Total operating costs and expenses in the fourth quarter of 2025 were $49.5 million as compared to $14.8 million in the fourth quarter of 2024. Total operating costs and expenses for 2025 were $195.3 million compared to $203.6 million in 2024. In the fourth quarter of 2024, we recorded a one-time $40.4 million gain from the sale of the Huntsville manufacturing facility. Excluding this gain, operating expenses for the fourth quarter and full year of 2025 decreased due to the elimination of cost of goods sold following the sale of the Huntsville manufacturing facility. R&D expense in the fourth quarter of 2025 was $29.7 million as compared to $28.7 million for the fourth quarter of 2024. For the full year of 2025, R&D expense was $117.3 million compared to $120.9 million in 2024. R&D expense decreased for full year of 2025 primarily due to a decrease in expense for the development of NKTR-255, partially offset by an increase in expense for the development of rezpegaldesleukin. G&A expense was $11.2 million in the fourth quarter of 2025 as compared to $17.1 million in the fourth quarter of 2024. G&A expense was $68.7 million for 2025 compared to $76.8 million in 2024. G&A expense decreased for both the fourth quarter and the full year of 2025 due to decreases in facilities and stock-based compensation expenses. Non-cash restructuring and impairment charges were $8.6 million in the fourth quarter of 2025 and $9.3 million for the full year of 2025, as compared to $1.4 million in the fourth quarter of 2024 and $15.7 million in the full year of 2024. These non-cash charges are related to the declining San Francisco commercial real estate market and real estate lease obligations held by Nektar. In the first quarter of 2025, we began accounting for our investment in the new portfolio company, Gannet BioChem, under the equity method of accounting which calculates our gain or loss based on the change in our share of Gannet BioChem's equity each quarter. This resulted in non-cash losses from the equity method investment of $1.3 million in the fourth quarter of 2025 and $8.7 million for the full year of 2025. Net loss for the fourth quarter of 2025 was $36.1 million or $1.78 basic and diluted net loss per share as compared to net income of $7.3 million or $0.521 basic and diluted earnings per share in the fourth quarter of 2024. Net loss for 2025 was $164.1 million or $9.73 basic and diluted loss per share compared to a net loss of $119.0 million or $8.681 basic and diluted net loss per share in 2024. Excluding the $8.7 million non-cash loss from our equity method investment in Gannet BioChem, and the $9.3 million restructuring and impairment charges, net loss, on a non-GAAP basis, for the full year of 2025 was $146.0 million or $8.66 basic and diluted net loss per share. Recent Business Highlights In February 2026, Nektar established a Research Collaboration with UCSF and Dr. Stephen Hauser for NKTR-0165, a tumor necrosis factor receptor 2 (TNFR2) antibody, in multiple sclerosis. In February 2026, Nektar announced the successful closing of a public offering of its common stock, including the full exercise of underwriters' option to purchase additional shares, raising $460 million in gross proceeds. In February 2026, Nektar presented new maintenance data from the REZOLVE-AD Phase 2b Study in atopic dermatitis, demonstrating durable and new responses with rezpegaldesleukin across key disease measurements with both monthly and quarterly dosing. In December 2025, Nektar announced topline results from the 36-week induction treatment period of the REZOLVE-AA Phase 2b Study, establishing proof-of-concept of rezpegaldesleukin in patients with severe-to-very-severe alopecia areata. In November 2025, Nektar presented a late-breaking oral abstract titled "Rezpegaldesleukin, Novel Treg-Inducing Therapy, Demonstrates Efficacy in Atopic Dermatitis and Asthma in Phase 2b Trial" at the American College of Allergy, Asthma and Immunology's 2025 Annual Scientific Meeting (ACAAI), highlighting statistically significant improvements across key efficacy endpoints in atopic dermatitis and supportive findings in patients with comorbid asthma. 1 The per share amounts have been retrospectively adjusted to reflect a one-for-fifteen reverse stock split completed on June 8, 2025 Upcoming Milestones Data from the 36-week treatment period of the REZOLVE-AA study in patients with alopecia areata were accepted for a presentation in a late-breaking oral session at the American Academy of Dermatology (AAD) 2026 Annual Meeting to be held March 27-31, 2026, in Denver, CO. Topline data to be reported from the blinded 16-week treatment extension period in the Phase 2b REZOLVE-AA study of rezpegaldesleukin in alopecia areata in April 2026. (The Company will enter a quiet period beginning April 1, 2026 and continuing until the public announcement of these data.) Commencement of the Phase 3 studies for rezpegaldesleukin in patients with moderate-to-severe atopic dermatitis in Q2 2026. Presentation of 36-week maintenance data from the Phase 2b REZOLVE-AD study of rezpegaldesleukin in moderate-to-severe atopic dermatitis at a medical conference in second half of 2026. Topline data to be reported from the 24-week off-treatment period in REZOLVE-AA in Q4 2026. Topline data to be reported from the 52-week off-treatment period in REZOLVE-AD in Q1 2027. Initial data from TrialNet-sponsored Phase 2 study of rezpegaldesleukin in Stage 3 New Onset Type 1 Diabetes to be reported in 2027. Preclinical data presentation from the NKTR-0165 (TNFR2 agonist antibody) program to be presented at a scientific conference in second half of 2026. Conference Call to Discuss Fourth Quarter 2025 Financial Results Nektar management will host a conference call to review the results beginning at 5:00 p.m. Eastern Time/2:00 p.m. Pacific Time on March 12, 2026. 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 June 12, 2026. To access the conference call by phone, please pre-register at Nektar Earnings Call Registration. 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 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," "target," "address," "may," "initiate" 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. Contacts: For Investors: Vivian Wu [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期财报临床结果快速通道

100 项与 NKTR-255 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
纵隔大b细胞淋巴瘤	临床3期	美国	Nektar Therapeutics	2023-02-23
大B细胞淋巴瘤	临床3期	英国	Nektar Therapeutics	2022-01-30
非小细胞肺癌	临床2期	-	Nektar Therapeutics	2023-05-30
局部晚期非小细胞肺癌	临床2期	美国	Nektar Therapeutics	2023-01-10
尿路上皮癌	临床2期	美国	Nektar Therapeutics	2022-08-15
膀胱癌	临床2期	美国	Pfizer Inc.	2022-01-30
膀胱癌	临床2期	英国	Nektar Therapeutics	2022-01-30
膀胱癌	临床2期	-	Merck & Co., Inc.	2022-01-30
头颈癌转移	临床2期	英国	Nektar Therapeutics	2022-01-30
转移性结直肠癌	临床2期	英国	Nektar Therapeutics	2022-01-30

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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


NCT05664217 (Pubmed) 人工标引	临床2期	大B细胞淋巴瘤	15	NKTR-255 (received CD19 CAR T-cell therapy)	廠網艱廠願蓋膚築襯鏇(選鑰網齋遞構憲憲願餘) = 艱艱獵夢鑰夢範醖鑰繭構憲願選餘鹹鑰構構糧 (觸夢壓憲蓋淵襯範構鏇 )	积极	2025-08-08
				Placebo (received CD19 CAR T-cell therapy)	廠網艱廠願蓋膚築襯鏇(選鑰網齋遞構憲憲願餘) = 壓簾艱觸膚齋鬱遞鬱鏇構憲願選餘鹹鑰構構糧 (觸夢壓憲蓋淵襯範構鏇 )
NCT05359211 (ICML2025)	临床1期	大B细胞淋巴瘤	23	NKTR-255 plus lisocabtagene maraleucel	觸範顧製鏇範築築襯遞(糧餘鏇醖襯構艱獵製鏇) = 繭鹽壓築艱鏇鏇鏇範觸壓齋製範夢觸構簾壓選 (繭網糧壓選憲襯廠夢蓋, 57.8 ~ 97.3) 更多	积极	2025-06-17
				Liso-cel alone	淵餘鏇壓襯膚廠夢醖製(獵憲獵遞顧餘憲選鏇築) = 襯遞鏇積範壓醖憲簾淵窪衊構構觸範膚糧齋憲 (廠鹹壓壓鹽網壓壓餘網 )
NCT04616196 (CTgov)	临床1/2期	头颈部鳞状细胞癌 \| 结直肠癌	25	Cetuximab+NKTR-255 (Dose Escalation of NKTR-255 Level 1 (1.5 µg/kg) With Cetuximab)	窪鏇鏇淵蓋鬱淵鹽衊鬱 = 衊鏇膚糧築襯構願遞選積範繭鏇襯觸鬱衊範淵 (壓簾繭膚構顧蓋構積鏇, 築範簾餘鑰憲廠窪襯選 ~ 鑰醖鑰齋簾繭憲遞網鑰) 更多	-	2025-06-08
				Cetuximab+NKTR-255 (Dose Escalation of NKTR-255 Level 2 (3.0 µg/kg) With Cetuximab)	窪鏇鏇淵蓋鬱淵鹽衊鬱 = 餘鹽膚鑰鹹醖鑰衊網願積範繭鏇襯觸鬱衊範淵 (壓簾繭膚構顧蓋構積鏇, 艱鏇餘築廠夢範鬱網淵 ~ 廠憲構顧構醖積窪憲壓) 更多
NCT05359211 (S280, EHA2025)	临床1期	大B细胞淋巴瘤 CD19	23	NKTR-255	獵鑰壓選窪餘遞餘網觸(鹹膚夢鏇蓋醖觸簾築憲) = 顧衊製鬱壓壓壓憲壓蓋範膚夢襯窪襯獵夢鬱積 (築廠襯憲選繭廠網觸顧, 42.4 ~ 87.3) 更多	积极	2025-05-14
NCT05664217 (Tandem Meetings ASTCT and CIBMTR2025)	临床2/3期	复发性弥漫性大B细胞淋巴瘤	15	NKTR-255	蓋糧繭簾鏇襯衊鏇範網(觸簾鹽壓顧餘簾艱衊鑰) = 範繭蓋構鏇獵醖廠範鏇範遞餘觸製鏇齋製衊夢 (廠願築餘壓齋艱願遞鏇 ) 更多	积极	2025-02-12
				Placebo	蓋糧繭簾鏇襯衊鏇範網(觸簾鹽壓顧餘簾艱衊鑰) = 廠觸壓衊繭積糧觸選繭範遞餘觸製鏇齋製衊夢 (廠願築餘壓齋艱願遞鏇 )
NCT05664217 (ASH2024) 人工标引	临床2/3期	大B细胞淋巴瘤辅助	15	NKTR-255	衊醖網衊獵鹹蓋憲糧鹽(鏇鹽壓廠醖壓繭鹽範選) = 獵範憲觸觸餘蓋構憲鏇醖膚觸遞鑰鏇淵蓋鹽簾 (鏇鏇壓鑰遞鹹製顧鑰憲 ) 更多	积极	2024-12-07
				Placebo	衊醖網衊獵鹹蓋憲糧鹽(鏇鹽壓廠醖壓繭鹽範選) = 衊簾積選觸襯蓋衊選願醖膚觸遞鑰鏇淵蓋鹽簾 (鏇鏇壓鑰遞鹹製顧鑰憲 ) 更多
NCT05632809 (RESCUE, SITC2024) 人工标引	临床2期	局部晚期非小细胞肺癌	15	NKTR-255 + durvalumab	鏇獵憲淵艱觸蓋獵遞網(選蓋觸願鹽齋醖選獵範) = 餘積壓顧糧鏇廠遞築衊簾醖範遞壓顧願廠廠糧 (膚窪築鑰壓願網壓簾鑰 )	积极	2024-11-05
NCT03233854 (Pubmed) 人工标引	临床1期	难治性 B 细胞急性淋巴细胞白血病	11	NKTR-255Anti-CD19/CD22 CAR-T(Stanford University)	淵築蓋蓋夢積憲遞淵簾(構膚艱簾鏇膚選選繭膚) = None 顧艱窪襯鹹壓憲壓艱範 (憲觸憲淵鹹淵糧醖齋廠 )	积极	2024-07-05
				historical controls
NCT03233854 (Phase I Study of CAR-T Cells + NKTR-255, Tandem Meetings ASTCT and CIBMTR2023)	临床1期	复发难治性急性淋巴细胞白血病	6	CAR-T cells + NKTR-255 (PEG-IL-15)	積願壓醖艱繭願簾膚憲(齋顧簾夢觸築壓獵願齋) = The three patients dosed at DL1 developed fever within 6 hours after the first NKTR-255 cycle with resolution by 24 hours. Additional cycles were associated with transient fever and no additional cytokine-related AEs. One patient treated at DL2 experienced fever and self-limited G3 liver enzyme elevation. 鑰繭窪繭繭網遞築構憲 (顧壓構膚醖糧構遞願繭 )	积极	2023-02-01
				NKTR-255 (DL1: 1.5mcg/kg; DL2: 3mcg/kg)
NCT04136756 (ASH 12021 \| ASH 22021) 人工标引	临床1期	血液肿瘤	14	NKTR 255	簾製餘艱糧顧鬱憲膚遞(遞選獵艱願艱製遞鹹鹹) = 糧餘醖夢簾願憲衊艱壓築獵窪夢繭鹹憲積觸膚 (糧齋鏇積顧製鏇顧鹽醖 ) 更多	积极	2021-11-05