A Pilot, Phase II Study With a Prospective, Randomized, Cross-Over, Placebo-Controlled, Double-Blind Design to Assess the Short-Term Effects of Tolvaptan Plus Placebo vs Tolvaptan Plus Octreotide LAR Combination Therapy in ADPKD Patients With Normal Kidney Function or Hyperfiltration

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a leading cause of End Stage Kidney Disease (ESKD) worldwide. Elevated levels of 3', 5' - cyclic AMP (cAMP) play a central role in the pathogenesis and progression of the disease. Vasopressin antagonists and somatostatin analogues, which indirectly reduce adenyl cyclase 6 activity, have been found to markedly reduce renal tubular cell proliferation and cyst growth in experimental models of ADPKD. In combination, the two treatments show a clear additive effect and may significantly reduce renal cystic and fibrotic volume as well as cAMP levels to wild type levels.
The vasopressin antagonist Tolvaptan and the somatostatin analogue Octreotide share a similar renoprotective effect also in human disease.
Both medications effectively slow total kidney and cystic volume (TKV and TCV, respectively) growth and glomerular filtration rate (GFR) decline in patients with ADPKD. The short-term effect of both medications appear to be larger when the GFR is normal or even higher than normal and kidney volumes are still relatively stable. On the basis of experimental data, it is conceivable that Tolvaptan and Octreotide LAR should have an additive effect also in human disease, during initial treatment as well as in the long-term. To address the working hypothesis of an additional short-term effect of Tolvaptan and Octreotide, we propose to run a pilot, explorative, randomized, placebo-controlled, clinical trial with a Cross-Over Design to compare the short-term effects of Tolvaptan monotherapy and Tolvaptan plus Octreotide LAR combination therapy on TKV as assessed by MRI, and on GFR as directly measured by the iohexol plasma clearance technique in ADPKD patients with normal (80 to 120 ml/min/1.73m2) kidney function or even kidney hyperfiltration (GFR ≥120 ml/min/1.73m2).

开始日期2018-12-12

申办/合作机构

Istituto di Ricerche Farmacologiche Mario Negri

[+1]

NCT03057509

/ Withdrawn临床1期IIT

A Pilot Study Of Ga-68-DOTA-TOC Imaging In Participants With Small Bowel Carcinoid Tumors

This research study is designed to evaluate a type of scan called Ga-68-DOTA-TOC positron emission tomography (PET) scanning as a way of assessing carcinoid tumors.

开始日期2018-11-01

申办/合作机构

The General Hospital Corp.

NCT02874326

/ Unknown status临床2期IIT

An Uncontrolled, Pilot-study Assessing the Efficacy of Octreotide Long-acting Release to Decrease Transfusion Requirements and Endoscopy Frequency in Patients With Rendu-Osler-Weber and Gastrointestinal Bleeding

The purpose of this study is to determine whether long-acting octreotide is safe and effective in the treatment of patients with Rendu-Osler-Weber (e.g. HHT).
The study hypothesis is that octreotide is safe and will reduce transfusion requirements and endoscopy frequency in ROW patients with refractory anaemia due to bleeding gastrointestinal telangiectasias.

开始日期2016-10-01

申办/合作机构

Radboud University Medical Center

[+1]

100 项与 Octreotide depot (GP Pharm SA) 相关的临床结果

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100 项与 Octreotide depot (GP Pharm SA) 相关的转化医学

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100 项与 Octreotide depot (GP Pharm SA) 相关的专利（医药）

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项与 Octreotide depot (GP Pharm SA) 相关的文献（医药）

2026-08-01·EClinicalMedicine

[177Lu]Lu-DOTA-TATE plus long-acting octreotide in patients with newly diagnosed, advanced, grade 2–3, gastroenteropancreatic neuroendocrine tumours: preplanned and post-hoc efficacy analyses from the randomised, phase 3 NETTER-2 trial

Article

作者: Capdevila, Jaume ; Herrmann, Ken ; de Herder, Wouter W ; Zhang, Yufen ; Singh, Simron ; Halfdanarson, Thorvardur R ; García-Burillo, Amparo ; Kunz, Pamela L ; Folitar, Ilya ; Tafuto, Salvatore ; Oh, Do-Youn ; Ferone, Diego ; Filice, Angelina ; Halperin, Daniel ; Deshayes, Emmanuel ; Chasen, Beth ; Yoo, Changhoon ; Sansovini, Maddalena ; Falk, Stephen ; Gerard, Laura ; Pavel, Marianne ; Lastoria, Secondo ; Myrehaug, Sten

Background:

In the phase 3 NETTER-2 study, first-line [¹⁷⁷Lu]Lu-DOTA-TATE (hereafter ¹⁷⁷Lu-DOTATATE) significantly improved progression-free survival in patients with advanced, well-differentiated, higher grade 2-3 (Ki67 ≥10% and ≤55%), somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumours (GEP-NETs). Median progression-free survival was 22·8 months (95% CI 19·4-not estimable [NE]) with ¹⁷⁷Lu-DOTATATE vs 8·5 months (7·7-13·8) in the control arm. Here, we report subgroup analyses, including preplanned assessments of efficacy by NET grade (G) and site of origin; further post-hoc analyses are reported in the main text.

Methods:

In this open-label, parallel-group study, patients from nine countries were randomised 2:1 to receive four cycles of ¹⁷⁷Lu-DOTATATE plus octreotide long-acting repeatable (LAR) 30 mg every 8 weeks then octreotide LAR 30 mg every 4 weeks, or high-dose octreotide LAR 60 mg every 4 weeks. The primary endpoint (progression-free survival) was previously reported. Tumours were assessed at baseline, week 16, week 24, then every 12 weeks until disease progression or death. Preplanned subgroup analyses used blinded independent centrally reviewed data. The study is registered with ClinicalTrials.gov, NCT03972488, and is completed.

Findings:

Between Jan 22, 2020, and Oct 13, 2022, 261 patients were screened; 35 were excluded due to screen failure, and 226 were randomised. ¹⁷⁷Lu-DOTATATE (n = 151) reduced risk of disease progression/death vs control (n = 75) regardless of NET grade/origin (hazard ratio [95% CI]: G2 NET 0·31 [0·18-0·53]; G3 NET 0·27 [0·14-0·49]; pancreatic NET 0·34 [0·20-0·56]; gastrointestinal NET 0·23 [0·12-0·46]). Median progression-free survival in months (95% CI) with ¹⁷⁷Lu-DOTATATE was: G2 NET 29·0 (21·8-NE); G3 NET 22·2 (13·9-27·8); pancreatic NET 19·4 (16·6-24·9); gastrointestinal NET NE (22·6-NE). ¹⁷⁷Lu-DOTATATE improved objective response rate vs control regardless of NET grade/origin.

Interpretation:

These findings support the use of first-line ¹⁷⁷Lu-DOTATATE for patients with advanced, well-differentiated, higher grade 2-3 (Ki67 ≥10% and ≤55%), somatostatin receptor-positive GEP-NETs, and for whom chemotherapy is not considered the most appropriate treatment option, regardless of NET grade (2/3) or origin (pancreas/gastrointestinal).

Funding:

Advanced Accelerator Applications, a Novartis Company.

2026-05-06·Revista medica del Instituto Mexicano del Seguro Social

[Efficacy of octreotide LAR and lanreotide autogel in acromegaly assessed by SAGIT].

Article

作者: Núñez-Martínez, Francisco Javier ; Chávez-Lárraga, Alejandro de Jesús ; Hernández-Salazar, Enrique ; Martínez-Sánchez, Brian Humberto ; Velasco-Santos, Jorge Isaac

Background:

Biochemical control has been the main objective in the treatment of acromegaly; however, GH and IGF-1 levels do not necessarily translate into clinical response, as they fail to account for the complexity of symptoms and patients' perceptions. The SAGIT instrument was developed to assist in assessing the status and evolution of the disease in patients with acromegaly and facilitate decision-making.

Objective:

To compare the efficacy of octreotide LAR and lanreotide autogel in managing patients with acromegaly using the SAGIT instrument.

Material and methods:

Observational, unicentric study, conducted in 2022 at a referral hospital in León, Guanajuato, Mexico.

Results:

Of 37 patients evaluated, 26 were included. 13 (50%) received lanreotide autogel and 11 (42.3%) received octreotide LAR. Disease control, as measured by IGF-1 levels, was achieved in 10 patients (42.3%). When assessing control using the SAGIT instrument, 8 patients (30.7%) met control criteria. Octreotide LAR showed greater disease control as assessed by SAGIT compared to lanreotide autogel (p = 0.043).

Conclusions:

Based on the SAGIT instrument, octreotide LAR is more effective for disease control in patients with acromegaly than in those patients treated with lanreotide. The preferential use of octreotide LAR could be recommended in resource-limited settings.

2026-04-30·Journal of Gastrointestinal Oncology

Transarterial embolization combined with octreotide long-acting release in treating rectal neuroendocrine tumor liver metastases: a single-institutional experience.

Article

作者: Xu, Li-Chao ; Zhao, Qing ; Xu, Jun-Yan ; Chen, Jie ; Liang, Yun ; Chen, Luo-Hai ; Li, Cui-Xian ; Tang, Wei

Background:

Liver metastasis is a critical factor of mortality and morbidity in patients with neuroendocrine tumor, and effective management strategies remain a clinical challenge. The treatment regimen of transarterial embolization (TAE) combined with octreotide long-acting release (LAR) for the subgroup of rectal neuroendocrine tumor liver metastases (NETLMs) have not been specially investigated. This study aims to evaluate the efficacy and factors of hepatic progression-free survival (HPFS) and treatment response in patients with rectal NETLMs receiving TAE plus octreotide LAR therapy.

Methods:

This was a retrospective study, which enrolled 84 patients with rectal NETLMs receiving the combination therapy of TAE and octreotide LAR between January 2022 and December 2024. Patients' data were reviewed to evaluate prognostic factors of HPFS and treatment response by the univariate and multivariate Cox proportional hazards models and logistic regression models.

Results:

The median HPFS was 11.1 months. Partial response (PR) in 71 patients (84.5%), stable disease (SD) in 9 patients (10.7%), and progressive disease (PD) in 4 patients (4.8%) were observed. The objective response rate (ORR) was 84.5% in the cohort. In the multivariate Cox regression model, hepatic tumor burden (HTB) ≤25% [hazard ratio (HR) =4.188, P=0.02] was an independent risk factor for HPFS. In the multivariate logistic regression model, tumor border [odds ratio (OR) =0.069, P=0.01] was a positive prognostic factor of treatment response, while ¹⁸F-fluorodeoxyglucose-positron emission tomography-computed tomography (¹⁸F-FDG PET-CT) (OR =11.919, P=0.003) and Ki-67 (OR =6.469, P=0.018) were negative prognostic factors.

Conclusions:

The therapeutic strategy of TAE combined with octreotide LAR were effective in patients with rectal NETLMs, especially in those with HTB ≤25%. Selected patients with Ki-67 ≤10%, negative ¹⁸F-FDG PET-CT and clear tumor border could derive prognostic advantage from the combination treatment.

项与 Octreotide depot (GP Pharm SA) 相关的新闻（医药）

2026-09-04

·药梦想DrugDream

从奥曲肽显像、PSMA诊疗到靶向α治疗，多肽核药37年研发进化史（1989—2026）

EDITOR'S NOTE导读｜多肽核药不是“多肽+核素”，而是一套系统工程从1989年首个人体受体显像，到2026年PSMA治疗前移、靶向α治疗、FAP环肽与中国原创RGD核药并行推进，多肽与拟肽核药已经从核医学中心里的示踪剂，演化为精准肿瘤药物的重要平台。 ·多肽核药真正的起点，不是某一种核素，而是1989年人类首次用放射性标记奥曲肽在体内“看见”受体阳性肿瘤。 ·37年的主线，是六次范式迁移：生理肽→稳定类似物、直接标记→螯合平台、平面显像→定量PET、诊断→治疗、单靶点→多靶点、β治疗→α治疗。 ·经典多肽核药的获批版图仍高度集中于SSTR轴；PSMA虽属于以Glu-urea-Lys为核心的拟肽型小分子边界赛道，却已建立PET筛选—¹⁷⁷Lu治疗—适应证前移的完整标杆，不能从产业主线中略去。 ·截至2026年9月3日，Pluvicto已从经ARPI和紫杉烷治疗后的mCRPC，前移至延迟紫杉烷的mCRPC，并进一步联合ARPI进入转移性激素敏感/雄激素通路调节初治阶段；中国获批的⁹⁹ᵐTc-3PRGD2则把整合素αvβ3推进到全球首个获批药物层面。 ·多肽核药不是“多肽+核素”的简单拼接。靶点密度、配体药理、螯合稳定性、停留时间、剂量学与供应链必须同时成立。 ·2026年的几起事件说明：阳性III期不是上市终点；同类诊断药的性能优势也不能绕开市场独占；漂亮的剂量学更不等于足够的临床获益。图1｜多肽核药37年的六次范式迁移药梦想编辑部制图；依据[3-65]所列论文、监管文件与临床登记核验。 PROLOGUE序章｜一条多肽，两个命运 1989年，鹿特丹团队在《柳叶刀》报告：将¹²³I标记到Tyr³-octreotide后，可以用γ相机在人体内定位内分泌相关肿瘤。那不是第一种多肽药，却是一个新药物逻辑的开端——多肽不再只负责激动或拮抗受体，而是成为把“放射性信号”送到病灶的导航头。[3] 从那一刻到2026年，37年间，多肽核药完成了从显像到治疗、从β粒子到α粒子、从单一SSTR靶点到多个受体与微环境靶点的扩张。真正被工程化的，不只是一条肽链，而是一套由靶点、配体、连接臂、螯合剂、核素、剂量学、生产与临床路径共同构成的系统。这也解释了为什么核药行业经常出现看似矛盾的场景：同一个配体，换一种核素就改变配送半径；临床III期达到主要终点，仍可能因CMC与生产场地检查收到完整回复函；诊断性能获得认可，也可能因孤儿药市场独占无法上市。多肽核药的终点从来不只是“结合得好”。边界说明｜本文所称“多肽核药”，限定为由肽或明确的肽模拟配体承担靶点识别，并携带诊断或治疗核素的放射性药物。FAP-2286属于环肽，纳入经典多肽主线；PSMA-11、PSMA-617等以Glu-urea-Lys为核心，严格说属于拟肽型小分子放射性配体。本版将PSMA作为不可忽略的相邻标杆完整纳入，但不把其产品数量并入经典多肽核药统计；喹啉类FAPI仍仅作比较。 DISCOVERY一、1973—1994：先有稳定的受体配体，才有可用的分子导航1. 生理信号不是药物平台：somatostatin太短命 1973年，Brazeau等从下丘脑中分离出能够抑制生长激素释放的somatostatin，并确认其14个氨基酸的结构。[1]但天然肽在体内快速降解，半衰期只有数分钟：它适合解释生理，却不适合承担长时间的体内导航。 1982年，Bauer等报道环状八肽SMS 201-995，也就是后来被命名为octreotide的奥曲肽。它保留了对生长激素抑制的活性，又显著延长作用时间。[2]这一改造的研发意义并不只在于“做出长效多肽”，而是首次提供了一个足够稳定、可继续接上放射性标记模块的受体配体骨架。2. 1989：受体第一次成为全身可视的生物标志物 ¹²³I-Tyr³-octreotide证明了SSTR可以被体内显像，但直接碘化也暴露出代谢不稳定、制备繁琐和可用时间窗短等问题。[3-5]随后，DTPA-D-Phe¹-octreotide把¹¹¹In稳定地带到配体上，标记过程变得更可操作，肾脏清除也更可预测。 1994年，¹¹¹In-pentetreotide以OctreoScan获FDA批准。它建立了多肽核药的第一个商业闭环：用受体表达选择病人、发现全身病灶，并影响手术和系统治疗决策。[6]但它仍受限于SPECT分辨率、长成像流程和较高的肝脾背景。下一次跃迁，需要一个能同时容纳多种金属核素的化学接口。 CHELATION PLATFORM二、1994—2001：DOTA把“一个示踪剂”变成“可换弹头的平台”1. 从DTPA到DOTA，改变的是产品架构 DTPA适合¹¹¹In，却不是所有治疗性金属核素的理想容器。宏环螯合剂DOTA带来的关键价值，是让同一类肽配体可以装载⁶⁸Ga、⁹⁰Y、¹⁷⁷Lu乃至后来的²²⁵Ac。于是，药物被拆成三个相对独立又彼此耦合的模块：靶向肽、连接/螯合模块和放射性核素。模块化并不意味着随意替换。核素的离子半径、配位化学和标记条件会反过来改变成药性；连接臂的亲水性、电荷和空间构型又会改变血液清除、肾摄取与受体结合。所谓“同一配体换核素”，本质上仍是一项需要重新验证的药物工程。2. 显像开始变成治疗：⁹⁰Y-DOTATOC建立PRRT雏形 1990年代后半期，DOTA-Tyr³-octreotide（DOTATOC）进入临床治疗探索。⁹⁰Y释放高能β粒子，组织射程较长，能够形成“交叉火力”，对受体表达不完全均一的大体积病灶具有理论优势；但缺少适合常规定量成像的伴随γ射线，也使精细剂量学更困难。[7,8] 这一阶段真正定义了PRRT——peptide receptor radionuclide therapy。它不是传统外照射的小型化，而是先由受体显像确认靶点，再由同一生物学通路把辐射剂量送入全身病灶。诊断与治疗第一次使用了同一套靶点语言。图2｜多肽核药的模块化产品架构药梦想编辑部制图；依据DOTA肽诊疗一体化通用架构与[7-14,51]核验。 PET & PRRT三、2001—2015：⁶⁸Ga负责“看清”，¹⁷⁷Lu负责“打准”1. ⁶⁸Ga-DOTA肽把受体显像带入PET时代 2001年前后，⁶⁸Ga-DOTATOC的人体研究显示，PET可以获得更高的空间分辨率、更快的检查流程和半定量参数。[9,10] ⁶⁸Ge/⁶⁸Ga发生器还提供了一条不完全依赖大型回旋加速器的生产路径。对研发而言，PET不只是“图像更漂亮”，而是把靶点阳性从定性判断推进到可量化、可比较、可用于治疗筛选的生物标志物。随后DOTATATE、DOTATOC、DOTANOC形成差异化的SSTR亚型结合谱。它们之间并不存在脱离场景的绝对优劣：诊断灵敏度、正常器官背景、治疗配对和注册路径共同决定产品价值。2. ¹⁷⁷Lu-DOTATATE解决了可视剂量与可控射程 ¹⁷⁷Lu释放中等能量β粒子，同时伴随可用于SPECT成像的γ射线；6.65天的物理半衰期也与DOTA肽的肿瘤滞留和跨区域配送更匹配。鹿特丹团队从2003年起连续报告¹⁷⁷Lu-DOTATATE的剂量学、疗效和安全性，2008年的大样本经验进一步奠定其临床基础。[11-14] 但PRRT从来不是无差别照射。DOTA肽经肾小球滤过后可在近端小管重吸收，肾脏因此长期被视为关键风险器官；骨髓剂量又限制累积活度。赖氨酸/精氨酸输注、分次给药、个体剂量学和长期血液学随访，都是药物本体之外的组成部分。3. 诊疗一体化的本质：不是同一瓶药，而是同一条决策链用⁶⁸Ga-DOTATATE确认SSTR阳性，再用¹⁷⁷Lu-DOTATATE治疗，是“theranostics”最典型的临床表达。严格地说，诊断剂与治疗剂并非完全相同：核素、比活度、给药质量、制备和质量控制均不同；但两者共享同一靶点假设，使治疗前筛选、治疗中剂量学和治疗后评估能够串成闭环。 REGULATORY VALIDATION四、2016—2020：从中心自制到全球注册，SSTR轴完成产业化 2016年，⁶⁸Ga-DOTATATE（Netspot）获FDA批准，⁶⁸Ga-DOTATOC（SomaKit TOC）获欧盟批准；2017年Lutathera获欧盟批准，2018年获FDA批准。NETTER-1在进展性中肠NET中证明，¹⁷⁷Lu-DOTATATE相较高剂量octreotide LAR显著延长PFS并提高缓解率，完成了从单中心经验到随机III期证据的跨越。[15-19] 2019年，University of Iowa申报的Ga 68 DOTATOC Injection获FDA批准，适用于成人及儿童SSTR阳性NET定位；2020年，⁶⁴Cu-DOTATATE（Detectnet）获批。⁶⁴Cu的12.7小时半衰期扩大了集中生产与配送的时间窗口，也支持更晚时相成像。[20,21] 这段历史容易被简化成“换了更先进的核素”。更准确的说法是：受体生物学、DOTA化学、发生器/回旋加速器、无菌生产、跨中心一致性、影像判读与随机临床试验在同一时期成熟，才把学术中心的示踪剂变成可复制的药品。图3｜SSTR多肽核药关键里程碑（1989—2026）药梦想编辑部制图；批准年份依据FDA、EMA官方资料[6,16-21,23]，临床节点依据[3,8-15,22,27-28]。表1｜已获主要监管机构批准的代表性多肽及拟肽类靶向核药年份产品/通用名靶点与配体核素角色主要注册节点 1994OctreoScan¹¹¹In-pentetreotideSSTR；奥曲肽类似物 SPECT诊断美国FDA批准；开启受体显像产品化 1999NeoTect⁹⁹ᵐTc-depreotideSSTR；六肽类似物 SPECT诊断美国FDA批准；后停止商业销售，非因安全/有效性撤回 2016Netspot⁶⁸Ga-DOTATATESSTR2；TATE PET诊断美国FDA批准 2016SomaKit TOC⁶⁸Ga-DOTATOCSSTR2；TOC PET诊断欧盟集中批准 2017/2018Lutathera¹⁷⁷Lu-DOTATATESSTR2；TATE β⁻治疗欧盟/美国批准；2024年美国扩至≥12岁 2019Ga 68 DOTATOC InjectionSSTR2；TOC PET诊断美国FDA批准，成人及儿童 2020Detectnet⁶⁴Cu-DOTATATESSTR2；TATE PET诊断美国FDA批准；较长半衰期改变配送半径 2020Ga 68 PSMA-11⁶⁸Ga-gozetotidePSMA；Glu-urea-Lys拟肽 PET诊断美国FDA批准；首个PSMA靶向PET药物 2021Pylarifypiflufolastat ¹⁸FPSMA；拟肽型小分子 PET诊断美国FDA批准；扩大PSMA PET配送与可及性 2022/2025/2026Pluvicto¹⁷⁷Lu-vipivotide tetraxetanPSMA；PSMA-617拟肽配体 β⁻治疗美国FDA批准；由后线mCRPC前移至mAPMN/S联合ARPI 2026锝[⁹⁹ᵐTc]佩昔瑞特加肽⁹⁹ᵐTc-3PRGD2整合素αvβ3；二聚RGD环肽 SPECT/CT诊断中国NMPA批准；肺癌区域淋巴结转移辅助检查资料来源：FDA、EMA、NMPA/国家药监局公开文件[6,16-21,23,25,43-44,56,58,60-61]。PSMA产品为拟肽型小分子边界赛道；不同国家/地区商品状态可能变化。 EARLIER LINE & ANTAGONISM五、2021—2024：PRRT前移，但“更强结合”也带来新的剂量学代价1. NETTER-2把PRRT推向一线，却没有自动改写所有标签 2024年公布的NETTER-2纳入新诊断、晚期、分化良好的高G2/G3 GEP-NET患者。¹⁷⁷Lu-DOTATATE联合octreotide LAR将中位PFS从8.5个月提高至22.8个月，分层HR为0.276。[22]同年，FDA把Lutathera扩展至12岁及以上SSTR阳性GEP-NET，成为美国首个获批用于该年龄段的放射性药物。[23] 但临床阳性不等于全球标签同步扩展。2025年，企业撤回了在欧盟申请的一线新诊断适应证扩展。[24]因此，截至本文截止日，不应把NETTER-2结果直接改写为“Lutathera已在全球获批一线治疗”。证据、标签和指南，是三套相关但不同的坐标。2. SSTR拮抗剂：结合位点更多，不代表给药方案可以照搬受体激动剂会内化，曾被认为天然更适合递送核素；随后研究发现，拮抗剂虽然不依赖内化，却可能结合更多受体构象与位点，获得更高肿瘤摄取。⁶⁸Ga-OPS202和¹⁷⁷Lu-satoreotide tetraxetan由此进入临床。 2019年的I期研究中，¹⁷⁷Lu-satoreotide tetraxetan显示45%的最佳总体缓解率，但第二周期后7例中4例出现4级血液学毒性，研究一度暂停并下调累积骨髓剂量与第二周期活度。[29]后续I/II期通过降低每周期活度和个体剂量学改善安全性。[30]这是一条重要的工程规则：肿瘤摄取提高时，必须重新定义骨髓、肾和脾的剂量上限，不能把激动剂方案机械复制到拮抗剂。 TARGETED ALPHA THERAPY六、2014—2026：α粒子不是β粒子的“高配版” β粒子射程通常覆盖多个细胞直径，适合通过交叉火力弥补病灶内受体不均一；α粒子线性能量传递高、射程短，能够造成复杂DNA双链断裂，更适合微小病灶和耐受β治疗后的克隆。2014年，²¹³Bi-DOTATOC在β-PRRT难治NET中的首次人体经验，证明了受体靶向α治疗可以产生临床缓解。[31]随后²²⁵Ac-DOTATATE/DOTATOC的临床探索扩展。[32] 然而，²²⁵Ac会经历多级衰变并释放多个α粒子。每次衰变产生的反冲能量可能把子体核素踢出螯合剂；自由子体的再分布会把剂量带到非靶器官。²¹²Pb则可作为体内α发生器，经²¹²Bi等子体释放α辐射。两者都要求研发团队同时回答配位稳定性、子体滞留、微剂量学和核素供应问题。 ²¹²Pb-DOTAMTATE的首次人体I期研究在推荐II期方案的前10例中观察到80%的客观影像学缓解，且总体耐受性可控；这一结果需要在更大样本中确认。[33] 2025年，AlphaMedix的II期研究宣布在PRRT初治和既往PRRT暴露队列均达到预设主要疗效终点。[34]另一方面，²²⁵Ac-DOTATATE（RYZ101）的ACTION-1正在既往¹⁷⁷Lu治疗后进展的SSTR阳性GEP-NET中推进I b/III期，2026年发表的剂量学结果支持其肿瘤/正常组织剂量比。[35,36] PSMA又提供了另一条α治疗验证路径。2016年，²²⁵Ac-PSMA-617的首批临床病例显示出在晚期前列腺癌中产生深度分子应答的潜力；2024年WARMTH Act多中心回顾性研究汇总488例mCRPC患者，中位OS为15.5个月、中位PFS为7.9个月，但在有记录的347例中，68%于首周期后报告口干。[62,63]这组非随机数据不能替代注册试验，却把PSMA α治疗的机会与唾液腺毒性同时摆到了台面上。 α治疗的合理定位，更可能是按病灶尺度、既往β治疗、受体异质性与器官风险分层，而非全面替代¹⁷⁷Lu。真正的比较问题不是“α和β谁更强”，而是“哪种射程和LET与这个患者的病灶空间结构最匹配”。图4｜常见诊断与治疗核素的“物理时钟” 药梦想编辑部制图；半衰期取近似值，依据IAEA核数据与公开核药资料[51,53]核验。 BEYOND SSTR七、从SSTR到PSMA与多靶点：下一代平台在寻找可复制的诊疗闭环1. PSMA：不是经典肽，却定义了“显像筛选—治疗—前线扩展”的工业标杆 PSMA由FOLH1编码，是细胞膜上的谷氨酸羧肽酶II；其催化口袋位于细胞外，配体结合后可发生内化。主流PSMA核药不是线性肽或环肽，而是以Glu-NH-CO-NH-Lys（Glu-urea-Lys）为药效团的拟肽型小分子：PSMA-11在药效团后连接Ahx与HBED-CC，PSMA-617则通过连接臂接入DOTA，从而兼容诊断或治疗性金属核素。[54,55]分类上它处于多肽药与小分子核药的边界，研发逻辑却与多肽核药高度同构。 2013年前后的⁶⁸Ga-PSMA-11人体PET研究显示，前列腺癌复发与转移灶可在低背景下被清晰识别。[54] FDA于2020年批准Ga 68 PSMA-11，2021年批准¹⁸F-piflufolastat（Pylarify）；后者凭借¹⁸F更长的物理半衰期和集中配送能力扩大了PSMA PET的可及性。[56]更重要的是，PSMA PET不只承担“看见病灶”，还成为¹⁷⁷Lu-PSMA治疗前确认靶点表达的入组门槛。治疗端的转折来自VISION。该III期研究在既往接受ARPI和紫杉烷治疗的PSMA阳性mCRPC中，将¹⁷⁷Lu-PSMA-617加入标准治疗，使中位OS从11.3个月延长至15.3个月，HR 0.62；FDA据此于2022年批准Pluvicto。[57,58] 2025年，PSMAfore又把其推进至适合延迟紫杉烷的mCRPC，中位rPFS为9.3个月对5.6个月，HR 0.41；OS差异在当时分析中未达统计学显著，且对照组60%交叉接受治疗。[59,60] 2026年7月31日，FDA基于PSMAddition批准Pluvicto联合ARPI用于PSMA阳性的转移性雄激素通路调节初治或敏感型前列腺癌——也就是此前通常所称的mHSPC。试验各组572例，中位rPFS均尚未达到，HR为0.72；OS数据仍不成熟。[61]从复发定位、后线mCRPC、紫杉烷前mCRPC再到mHSPC，PSMA走出的不是一次获批，而是一条由诊断筛选牵引治疗适应症持续前移的产品生命周期。 α治疗正在接棒下一轮迭代。²²⁵Ac-PSMA-617已从早期病例和回顾性队列进入前瞻性剂量探索，相关项目还包括²²⁵Ac-PSMA-I&T等；但口干、骨髓和肾毒性、α核素供应、衰变子体行为及治疗后PSMA异质性，仍决定其能否建立可注册的获益—风险比。[62-65] PSMA给多肽核药最重要的启示不是“照抄一个热门靶点”，而是同时打通靶点生物学、可规模化PET、治疗选择阈值、核素供应、随机III期和适应证前移。2. 整合素αvβ3：2026年，中国把RGD肽推进到首个获批产品整合素αvβ3参与肿瘤血管生成和侵袭，RGD序列提供了天然的识别起点。⁹⁹ᵐTc-3PRGD2由两个环RGD单元组成，通过多价效应提高结合与体内成像表现。2016年的前瞻性临床研究显示，其对肺癌淋巴结转移的特异性高于¹⁸F-FDG PET/CT，而敏感性相近。[42] 2026年4月，国家药监局通过优先审评审批程序批准锝[⁹⁹ᵐTc]佩昔瑞特加肽注射液及配套药盒，用于可疑肺癌患者区域淋巴结转移的辅助检查。[43]北京协和医院披露，I—III期临床研究在全国11家三甲医院共纳入409例受试者，并将其称为我国首个自主研发的放射性1类创新药、全球首个获批的整合素αvβ3靶向药物。[44] 它的战略意义不只是一款SPECT显像剂获批。⁹⁹ᵐTc发生器与SPECT/CT在中国拥有更广的医院覆盖，意味着创新核药可以从既有基础设施切入，而不必把所有价值都押在PET或治疗核素上。适应证选择——肺癌区域淋巴结分期——也比“泛肿瘤显像”更接近可验证的临床决策。3. FAP-2286：FAP赛道中，环肽与小分子走出不同药代路线 FAP主要表达于多种实体瘤的癌相关成纤维细胞。很多FAPI属于喹啉类小分子，肿瘤摄取快但治疗所需的长滞留并不总是理想；FAP-2286则是FAP结合环肽，设计目标之一就是延长肿瘤停留。[37] 截至2026年9月3日，诺华将¹⁷⁷Lu-FAP-2286以AAA614列为实体瘤II期项目。[39] 2026年发表的LuMIERE早期临床结果继续评估其安全性、剂量学与初步活性。[38]这条路线的核心问题不是“FAP是否广泛表达”，而是正常组织表达、肿瘤间质可及性和治疗窗口能否在不同瘤种中重复。4. GRPR、CCK2R、GLP-1R、uPAR与αvβ6：有信号，还需要有临床位置 GRPR在前列腺癌、乳腺癌等实体瘤中表达。¹⁷⁷Lu-NeoB的I期结果显示了可接受的器官剂量学，并确定9.25 GBq为推荐II期剂量；但诺华在2026年停止推进该项目，公开报道指出早期临床数据不足以支持继续开发，且并非发现新的安全问题。[40,41]这提醒行业：低正常器官摄取和可给药剂量，只回答了“能不能打”，没有回答“是否值得继续打”。 CCK2R在甲状腺髓样癌中表达，¹⁷⁷Lu-PP-F11N的I期研究提示肾与骨髓剂量较低，但胃壁可能成为剂量限制器官；2024年的0b期研究通过抑制中性内肽酶提高肿瘤吸收剂量，显示“体内肽酶调控”也可成为核药工程的一部分。[49,50] GLP-1R靶向的exendin-4在良性胰岛素瘤显像中形成了较强证据。2016年前瞻性队列中，⁶⁸Ga-NOTA-exendin-4灵敏度为97.7%；2024年多中心研究显示其诊断准确率94.4%，高于常规DOTA-SSA PET/CT及其他常规影像。[45,46]但强肾摄取、给药期低血糖管理以及恶性胰岛素瘤受体谱差异，仍限制其简单产品化。 uPAR肽AE105在2015年完成⁶⁴Cu-DOTA-AE105首次人体PET；αvβ6结合肽也已进入首次人体显像。[47,48]它们共同说明：能在人类肿瘤中成像，只是转化链条的中点。下一步必须证明影像能改变活检、分期、用药或手术决策，或者能够筛出真正从治疗核素获益的人群。图5｜多肽/拟肽核药靶点临床成熟度地图（截至2026年9月3日）药梦想编辑部制图；依据[33-65]公开论文、企业管线与监管资料核验。表2｜主要多肽及拟肽类靶点平台与研发状态靶点代表配体诊断/治疗核素截至截止日阶段主要研发瓶颈 SSTR2奥曲肽/奥曲肽酸类似物⁶⁸Ga、⁶⁴Cu / ¹⁷⁷Lu、⁹⁰Y、²¹²Pb、²²⁵Ac 诊断与β治疗已上市；α治疗进入关键临床肾、骨髓、脾；受体异质性 PSMA（边界）Glu-urea-Lys拟肽配体（PSMA-11/PSMA-617等）⁶⁸Ga、¹⁸F / ¹⁷⁷Lu、²²⁵Ac PET诊断与β治疗已上市；2026年治疗前移至mAPMN/S；α进入临床唾液腺、肾、骨髓；异质性与阴性病灶；²²⁵Ac供应整合素αvβ3RGD环肽/二聚体¹⁸F、⁶⁸Ga、⁹⁹ᵐTc 中国诊断药已上市炎症摄取、病灶尺度与适应证价值 FAPFAP-2286环肽⁶⁸Ga / ¹⁷⁷Lu AAA614处于II期（实体瘤）正常组织FAP、肿瘤滞留与骨髓剂量 GRPRNeoB等拮抗肽⁶⁸Ga / ¹⁷⁷Lu 早期临床；NeoB项目2026年停止推进胰腺生理摄取；剂量学到疗效的转化 CCK2Rminigastrin类似物PP-F11N¹¹¹In / ¹⁷⁷Lu I期/0b期探索胃壁剂量、肽酶降解 GLP-1Rexendin-4类似物⁶⁸Ga、¹¹¹In 胰岛素瘤临床显像证据成熟，尚未形成主流上市产品肾摄取、低血糖管理、良恶性差异 uPAR / αvβ6AE105 / A20FMDV2与αvβ6-BP⁶⁴Cu、¹⁸F 首次人体及早期显像靶点异质性、快速清除与临床定位资料来源：[33-50,54-65]。阶段为公开信息快照；PSMA为拟肽型小分子边界赛道，在研产品均未获批，除表中明确标注者外。 2026 INFLECTION八、2026：五个事件，把多肽与拟肽核药的真实门槛同时暴露出来事件一｜COMPETE阳性，ITM-11仍收到FDA完整回复函 COMPETE是首个将PRRT与everolimus直接比较的国际随机III期研究。¹⁷⁷Lu-edotreotide把中位PFS从14.1个月延长至23.9个月，HR 0.67；ORR为22%对4%，3/4级治疗相关不良事件为18%对40%。[27] 但2026年8月7日，FDA对ITM-11 NDA发出完整回复函。ITM披露，问题集中于CMC与第三方商业生产设施检查，FDA未指出临床、非临床或安全性数据缺陷。[28]这不是对COMPETE结果的否定，而是一个更现实的结论：核药的临床价值必须被一个可验证、可放大、可审计的制造与供应系统承接。事件二｜Deqtynet并非“效果不够”，而是撞上孤儿药市场独占 ⁶⁴Cu-oxodotreotide（Deqtynet）申请在欧盟用于SSTR阳性病灶PET显像。EMA在2026年最终拒绝上市申请，公开文件的关键理由是SomaKit TOC仍享有孤儿药市场独占，申请方未能证明足以适用豁免。[26] 这一案例把产品策略前移到立项阶段：同靶点、同用途、相邻适应症的核药，不仅要比较灵敏度、分辨率和配送窗口，还要在进入关键临床前完成孤儿药相似性、临床优越性与市场独占的路径设计。事件三｜NeoB有良好剂量学，仍无法跨过组合价值门槛 NeoB的早期临床论文在2026年正式发表，证明GRPR靶向¹⁷⁷Lu治疗可以达到可接受的器官剂量并找到推荐剂量。[40]但当项目需要进入乳腺癌等成熟治疗领域时，比较对象不再是“无药可用”，而是CDK4/6抑制剂、内分泌治疗、ADC等不断演进的标准方案。项目停止提醒我们：核药不能只在自身剂量学体系内证明优秀，还要在真实竞争格局中证明增量获益。事件四｜⁹⁹ᵐTc-3PRGD2获批，证明基础设施也可以定义创新与全球资本最关注的¹⁷⁷Lu和²²⁵Ac不同，中国的标志性突破来自⁹⁹ᵐTc和SPECT/CT。[43,44]这不是“技术代际较低”，而是把核素可得性、医院覆盖和明确临床问题对齐。对于需要规模化落地的诊断核药，基础设施适配本身就是产品创新的一部分。事件五｜Pluvicto再前移，PSMA RLT进入mHSPC 2026年7月，PSMAddition让¹⁷⁷Lu-PSMA-617联合ARPI从去势抵抗阶段进一步前移至转移性激素敏感/雄激素通路调节初治阶段，rPFS风险下降28%，但OS仍不成熟。[61]这标志着放射性配体治疗开始与更早期、疗程更长且竞争更拥挤的系统治疗正面组合，也把长期骨髓/肾安全性、治疗中心容量、PSMA PET筛选和¹⁷⁷Lu供应同时放大为商业化问题。 ENGINEERING QUESTIONS九、立项前必须回答的六个工程问题多肽核药项目常被拆给多肽化学、放化、核医学和临床团队分别优化。真正的失败往往发生在接口：配体改造提高亲和力，却增加肾摄取；换成长半衰期核素扩大配送，却让非靶组织停留产生额外剂量；提高比活度减少肽质量，又可能放大辐射自分解。六个问题必须在同一张目标产品概况中回答。图6｜多肽核药立项前的六个工程问题药梦想编辑部制图；结合[28-30,33,35-41,49-53]所示临床、CMC与监管案例总结。其中最容易被低估的是第六问。普通小分子药的成品可以库存数月，多数放射性药物的价值却在钟表上持续衰减。批次失败、航班延误、医院排程变化都会直接转化为患者无法按时给药。2026年的ITM-11案例已把这一点从运营风险提升为注册风险。[28] 因此，多肽核药的CMC策略不应等到临床III期后补课。核素来源与杂质谱、螯合前体的关键质量属性、无菌工艺、放射化学纯度、比活度、货架期、容器相容性、运输与院内放行，都应在临床路径和商业半径确定之前锁定。EMA也在2025—2026年推动放射性药品质量指南修订，监管关注正在从“能否制得”转向全生命周期一致性。[52] CHINA COORDINATE十、中国坐标：从一款原创诊断药，到完整诊疗生态还差什么？ ⁹⁹ᵐTc-3PRGD2的获批说明，中国已经能够完成原创多肽核药从靶点、分子设计到I—III期和注册生产的全链条闭环。[43,44]但诊断产品的成功不能自动外推到治疗核药。治疗端需要稳定的¹⁷⁷Lu/²²⁵Ac供应、更高等级的热室和无菌灌装、患者级剂量学、辐射防护、跨区域冷链/危化物流以及能够承接长期随访的核医学中心网络。截至2026年9月3日，本次公开资料核验未发现¹⁷⁷Lu-DOTATATE已获NMPA上市批准的官方公告；国内已有多条仿制、改良与创新管线处于申报或临床阶段，但项目状态变化较快，应以CDE/NMPA登记与企业正式公告为准。PSMA的全球进展进一步说明，与其只追问“谁会成为中国Lutathera或Pluvicto”，更值得追问的是：谁能把核素、前体、PET筛选、生产网络、中心准入和患者流做成同一套可复制系统。中国的另一项机会在于靶点与基础设施的本土匹配。⁹⁹ᵐTc适配广泛的SPECT网络；⁶⁸Ga适合发生器和区域化生产；⁶⁴Cu提供集中配送窗口；¹⁷⁷Lu兼顾治疗与剂量学；²²⁵Ac则更依赖上游产能和子体控制。立项不能从“热门核素”出发，而应从目标医院网络与适应证患者流出发。 CONCLUSION结语｜下一款成功的多肽核药，不会只是一条更高亲和力的肽回看1989—2026，SSTR的成功并不是因为奥曲肽拥有某个无法复制的化学奇迹，而是它同时满足了四个条件：肿瘤中有足够而相对稳定的受体表达；配体能够快速到达并长时间留在病灶；诊断影像可以选择患者；治疗核素和临床基础设施能够承接全身性给药。PSMA虽然不是经典多肽靶向剂，却把这四个条件做成了更完整的工业标杆，并在2026年把RLT推进到mHSPC。下一代多肽核药可能来自FAP、GRPR、CCK2R、GLP-1R、uPAR、αvβ6或新的受体，也可能来自更优的SSTR/PSMA配体、白蛋白结合策略、肽酶抑制、双靶点或α/β序贯治疗。但它们必须跨越的，不再只是“有没有肿瘤摄取”，而是能否建立足够宽的治疗窗口、足够清楚的临床位置和足够可靠的供应系统。多肽决定去哪里，核素决定如何释放能量；剂量学决定能走多远，制造与注册决定能否真正抵达患者。37年的进化，最终把多肽核药从一张受体显像图，变成了一整套精准治疗工业。 REFERENCES参考文献与核验来源 [1] Brazeau P, et al. 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Broadening horizons with 225Ac-DOTATATE targeted alpha therapy for GEP-NET. Eur J Nucl Med Mol Imaging. 2020;47:934-946. https://pubmed.ncbi.nlm.nih.gov/31707430/ [33]Delpassand ES, et al. Targeted alpha-emitter therapy with 212Pb-DOTAMTATE: first-in-humans dose-escalation trial. J Nucl Med. 2022;63:1326-1333. DOI: 10.2967/jnumed.121.263230. https://pubmed.ncbi.nlm.nih.gov/34992153/ [34]Orano Med. AlphaMedix achieved all primary efficacy endpoints in Phase 2 study. 2025. https://www.oranomed.com/en/resources/news/2025/alphamedixtm-212pb-dotamtate-achieved-all-primary-efficacy-endpoints-in-phase-2-study [35]ClinicalTrials.gov. ACTION-1: 225Ac-DOTATATE (RYZ101), NCT05477576. https://clinicaltrials.gov/study/NCT05477576 [36]Sgouros G, et al. Dosimetry Results from the Phase 1b/3 ACTION-1 Trial of [225Ac]Ac-DOTATATE. J Nucl Med. 2026. https://pubmed.ncbi.nlm.nih.gov/42242867/ [37]Zboralski D, et al. Preclinical evaluation of FAP-2286 for FAP-targeted radionuclide imaging and therapy. Eur J Nucl Med Mol Imaging. 2022. https://pubmed.ncbi.nlm.nih.gov/35608703/ [38]McConathy J, et al. Targeting FAP with [177Lu]Lu-FAP-2286: LuMIERE phase 1/2 results. Clin Cancer Res. 2026. DOI: 10.1158/1078-0432.CCR-25-4356. https://pubmed.ncbi.nlm.nih.gov/42223513/ [39]Novartis. Novartis Pipeline: AAA614, radioligand therapy targeting FAP, Phase 2. Accessed 2 Sep 2026. https://www.novartis.com/research-development/novartis-pipeline [40]Mittra ES, et al. Phase 1 Study of [177Lu]Lu-NeoB in GRPR-expressing advanced solid tumors. J Nucl Med. 2026;67:262-268. DOI: 10.2967/jnumed.125.270411. https://pubmed.ncbi.nlm.nih.gov/41344852/ [41]Fierce Biotech. Novartis drops phase 2-stage radioligand NeoB. Jul 2026. https://www.fiercebiotech.com/biotech/novartis-drops-phase-2-stage-radioligand-therapy-commitment-modality-unchanged [42]Zheng K, et al. 99mTc-3PRGD2 SPECT/CT for diagnosis of lymph node metastasis in lung cancer. Radiology. 2016;281:958-966. https://pubmed.ncbi.nlm.nih.gov/27479638/ [43]中国食品药品国际交流中心（摘自国家药监局）. 国家药监局批准锝[99mTc]佩昔瑞特加肽注射液及药盒上市. 2026-04-08. https://www.ccfdie.org/zryyxxw/yaop/jgdt/webinfo/2026/04/1774303181120733.htm [44]北京协和医院. 实现从0到1：99mTc-3PRGD2获批上市. 2026-04-16. https://www.pumch.cn/detail/45308.html [45]Luo Y, et al. GLP-1 receptor PET/CT with 68Ga-NOTA-exendin-4 for insulinoma. J Nucl Med. 2016;57:715-720. https://pubmed.ncbi.nlm.nih.gov/26795291/ [46]Boss M, et al. Improved Localization of Insulinomas Using 68Ga-NODAGA-Exendin-4 PET/CT. J Nucl Med. 2024;65:1959-1964. DOI: 10.2967/jnumed.124.268158. https://pubmed.ncbi.nlm.nih.gov/39419553/ [47]Persson M, et al. First-in-human uPAR PET: Imaging of cancer aggressiveness with 64Cu-DOTA-AE105. Theranostics. 2015. https://pubmed.ncbi.nlm.nih.gov/26516369/ [48]Hausner SH, et al. Evaluation of an integrin αvβ6-binding peptide using 18F PET in metastatic carcinoma. J Nucl Med. 2019. https://pubmed.ncbi.nlm.nih.gov/30401687/ [49]Rottenburger C, et al. Cholecystokinin 2 receptor agonist 177Lu-PP-F11N for radionuclide therapy of medullary thyroid carcinoma. J Nucl Med. 2020. https://pubmed.ncbi.nlm.nih.gov/31519804/ [50]Nock BA, et al. Neutral endopeptidase inhibition increases tumor doses of [177Lu]Lu-PP-F11N in humans: LUMED phase 0b. 2024. https://pubmed.ncbi.nlm.nih.gov/38581480/ [51]Fani M, Maecke HR, Okarvi SM. Radiolabeled peptides: valuable tools for the detection and treatment of cancer. Theranostics. 2012;2:481-501. https://pmc.ncbi.nlm.nih.gov/articles/PMC3364555/ [52]EMA. Guideline on radiopharmaceuticals, Revision 2 consultation documents. 2025-2026. https://www.ema.europa.eu/en/radiopharmaceuticals-scientific-guideline [53]IAEA Nuclear Data Services. Medical Portal: radionuclide decay and production data. Accessed 2 Sep 2026. https://nds.iaea.org/medportal/ [54]Afshar-Oromieh A, et al. PET imaging with a [68Ga]gallium-labelled PSMA ligand for the diagnosis of prostate cancer: biodistribution in humans and first evaluation of tumour lesions. Eur J Nucl Med Mol Imaging. 2013;40:486-495. DOI: 10.1007/s00259-012-2298-2. https://pubmed.ncbi.nlm.nih.gov/23179945/ [55]Afshar-Oromieh A, et al. The theranostic PSMA ligand PSMA-617 in the diagnosis of prostate cancer by PET/CT: biodistribution in humans, radiation dosimetry, and first evaluation of tumor lesions. J Nucl Med. 2015;56:1697-1705. DOI: 10.2967/jnumed.115.161299. https://pubmed.ncbi.nlm.nih.gov/26294298/ [56]FDA. FDA approves second PSMA-targeted PET imaging drug for men with prostate cancer; includes first approval of Ga 68 PSMA-11 on 1 Dec 2020 and approval of Pylarify in 2021. https://www.fda.gov/drugs/news-events-human-drugs/fda-approves-second-psma-targeted-pet-imaging-drug-men-prostate-cancer [57]Sartor O, et al. Lutetium-177-PSMA-617 for metastatic castration-resistant prostate cancer (VISION). N Engl J Med. 2021;385:1091-1103. DOI: 10.1056/NEJMoa2107322. https://pubmed.ncbi.nlm.nih.gov/34161051/ [58]FDA. Drug Trials Snapshot: PLUVICTO; original approval 23 Mar 2022. https://www.fda.gov/drugs/drug-trials-snapshots/drug-trials-snapshots-pluvicto [59]Morris MJ, et al. 177Lu-PSMA-617 versus a change of androgen receptor pathway inhibitor therapy for taxane-naive mCRPC (PSMAfore). Lancet. 2024;404:1227-1239. DOI: 10.1016/S0140-6736(24)01653-2. https://pubmed.ncbi.nlm.nih.gov/39293462/ [60]FDA. FDA expands Pluvicto's metastatic castration-resistant prostate cancer indication. 28 Mar 2025. https://www.fda.gov/drugs/resources-information-approved-drugs/fda-expands-pluvictos-metastatic-castration-resistant-prostate-cancer-indication [61]FDA. FDA approves lutetium Lu 177 vipivotide tetraxetan with ARPI therapy for metastatic androgen pathway modulation-naive or -sensitive prostate cancer. 31 Jul 2026. https://www.fda.gov/drugs/resources-information-approved-drugs/fda-approves-lutetium-lu-177-vipivotide-tetraxetan-androgen-receptor-pathway-inhibitor-therapy [62]Kratochwil C, et al. 225Ac-PSMA-617 for PSMA-targeted alpha-radiation therapy of metastatic castration-resistant prostate cancer. J Nucl Med. 2016;57:1941-1944. DOI: 10.2967/jnumed.116.178673. https://pubmed.ncbi.nlm.nih.gov/27390158/ [63]Sathekge MM, et al. Actinium-225-PSMA radioligand therapy of metastatic castration-resistant prostate cancer (WARMTH Act): a multicentre, retrospective study. Lancet Oncol. 2024;25:175-183. DOI: 10.1016/S1470-2045(23)00638-1. https://pubmed.ncbi.nlm.nih.gov/38218192/ [64]ClinicalTrials.gov. AcTION: 225Ac-PSMA-617 in PSMA-positive prostate cancer, NCT04597411; and AAA817 plus ARPI, NCT06855277. Accessed 3 Sep 2026. https://clinicaltrials.gov/study/NCT04597411 ; https://clinicaltrials.gov/study/NCT06855277 [65]ClinicalTrials.gov. FPI-2265 (225Ac-PSMA-I&T) in PSMA-positive mCRPC, NCT06402331. Accessed 3 Sep 2026. https://clinicaltrials.gov/study/NCT06402331声明｜本文用于药物研发与行业研究交流，不构成诊疗建议或投资建议。核药的批准适应证、给药条件与安全要求，请以所在国家或地区最新监管标签为准。

临床3期孤儿药

2025-11-27

·和黄医药官微

和黄医药将于2025年欧洲肿瘤内科学会 (ESMO) 亚洲年会和2025年美国血液学会 (ASH) 年会公布临床数据

中国香港、上海和美国新泽西州: 2025年11月27日，星期四: 和黄医药 (中国) 有限公司 (简称 "和黄医药" 或 "HUTCHMED") (纳斯达克/伦敦证交所: HCM; 香港交易所: 13) 今日宣布和黄医药自主研发的化合物的数项研究的最新及更新后的数据将于2025年12月5日至7日在新加坡召开的欧洲肿瘤内科学会 (ESMO) 亚洲年会，以及2025年12月6日至9日在美国奥兰多召开的美国血液学会 (ASH) 年会上公布。抗CD47单克隆抗体HMPL-A83用于治疗晚期实体瘤的首个人体临床试验结果，以及呋喹替尼联合信迪利单抗用于二线治疗局部晚期或转移性肾细胞癌的FRUSICA-2注册研究中II期部分的结果将于2025年ESMO亚洲年会公布。此外，索凡替尼联合卡瑞利珠单抗和化疗用于一线治疗转移性胰腺癌的II/III期研究中II期部分的结果亦将于大会公布。报告详情如下： 2025年ESMO亚洲年会 - 公司申办的研究标题: 抗CD47单克隆抗体HMPL-A83用于治疗晚期实体瘤患者的一项首次人体剂量递增研究 A first-in-human , dose escalation study of HMPL-A83, an anti-CD47 monoclonal antibody in patients with advanced solid tumors 主要作者: 郭晔 (中国上海) 会议环节: 迷你口头报告 | Mini Oral Session: Developmental therapeutics and precision medicine 摘要编号: 162MO 地点: Hall 407 时间: 2025年12月7日 (星期日) 新加坡时间 11:40 – 11:45 标题: 呋喹替尼单药用于二线治疗局部晚期或转移性肾细胞癌: FRUSICA-2研究中II期部分的结果 Fruquintinib monotherapy as second-line treatment in locally advanced or metastatic renal cell carcinoma: results from phase 2 part of FRUSICA-2 主要作者: 王珊珊 (中国上海) 会议环节: 优选口头报告| Proffered Paper session: Genitourinary tumours 摘要编号: 540O 地点: Hall 402 时间: 2025年12月5日 (星期五) 新加坡时间 14:55 – 15:05 标题: 索凡替尼联合卡瑞利珠单抗、白蛋白结合型紫杉醇和吉西他滨用于一线治疗转移性胰腺癌: 一项随机、开放标签、活性对照的II/III期研究的II期部分结果 Surufatinib in combination with camrelizumab, nab-paclitaxel and gemcitabine as the first-line treatment in metastatic pancreatic cancer: results from phase 2 part of a randomized, open-label, active-controlled, phase 2/3 study 主要作者: 秦叔逵 (中国南京) 会议环节: 海报展示 | Poster Display: Gastrointestinal tumours, non‑colorectal 摘要编号: 375P 标题: 奥希替尼联合赛沃替尼用于治疗EGFR突变伴MET过表达和/或奥希替尼治疗后进展的晚期非小细胞肺癌: SAVANNAH研究的亚洲亚组 Osimertinib + savolitinib in EGFR-mutated advanced non-small cell lung cancer with MET overexpression and/or amplification following progressive disease on osi: SAVANNAH Asian subset 主要作者: Se-Hoon Lee (韩国首尔) 会议环节: 海报展示 | Poster Display: Thoracic tumours, metastatic 摘要编号: 982P 标题: SACHI研究的患者相关结局: 一项赛沃替尼联合奥希替尼对比化疗用于治疗EGFR-TKI治疗后疾病进展的EGFR突变伴MET扩增的晚期非小细胞肺癌的III期研究 Patient-relevant Outcomes from SACHI: a Phase 3 Trial of Savolitinib plus Osimertinib versus Chemotherapy in EGFR-mutant and MET-amplified Advanced NSCLC after Progression on EGFR-TKIs 主要作者: 虞永峰 (中国上海) 会议环节: 海报展示 | Poster Display: Thoracic tumours, metastatic 摘要编号: 984P 标题: SACHI研究中FISH和NGS方法检测的MET扩增分析 Analysis of MET Amplification with FISH and NGS Method in SACHI Trial 主要作者: 孙龙华 (中国南昌) 会议环节: 海报展示 | Poster Display: Thoracic tumours, metastatic 摘要编号: 988P 标题: 接受赛沃替尼联合奥希替尼治疗的EGFR突变伴MET扩增的晚期非小细胞肺癌患者的疾病进展模式 Progression pattern in patients with EGFR-mutant , MET-amplified advanced NSCLC treated with savolitinib plus osimertinib 主要作者: 杨海燕 (中国长沙) 会议环节: 海报展示 | Poster Display: Thoracic tumours, metastatic 摘要编号: 1002P 标题: 一线奥希替尼治疗后疾病进展且伴获得性MET过表达和/或扩增的EGFR突变晚期非小细胞肺癌患者的MET检测和治疗顺序: 一项全球真实世界研究的中期分析 MET testing and treatment sequencing after progression on first line osimertinib in patients with EGFRm advanced NSCLC and acquired MET overexpression and/or amplification: interim analysis of a global real world study 主要作者: Julia Rotow (美国波士顿) 会议环节: 海报展示 | Poster Display: Thoracic tumours, metastatic 摘要编号: 1005P 2025年ESMO亚洲年会 - 研究者发起的研究标题: 呋喹替尼联合TAS-102 (联合或不联合立体定向放射治疗) 用于三线或后线治疗转移性结直肠癌:一项前瞻性II期研究的初步结果 Fruquintinib Combined with TAS-102 with or without SBRT as Third- or Later-Line Treatment in Metastatic Colorectal Cancer: Preliminary Results from a Prospective Phase II Trial 主要作者: 张琛 / 王奕 (中国宁波) 会议环节: 海报展示 | Poster Display: Gastrointestinal tumours, colorectal 摘要编号: 205P 标题: 呋喹替尼联合PD-1抑制剂和西达本胺治疗微卫星稳定型 (MSS) 转移性结直肠癌的疗效和安全性:与真实世界贝伐珠单抗联合抗PD-1抗体和西达本胺组的比较 Efficacy and safety of fruquintinib combined with PD-1 inhibitor and chidamide in MSS mCRC: a comparison with real-world bevacizumab plus anti-pd-1 and chidamide arm 主要作者: 戴广海 / 苟苗苗 (中国北京) 会议环节: 海报展示 | Poster Display: Gastrointestinal tumours, colorectal 摘要编号: 245eP 标题: 呋喹替尼联合FOLFIRI方案用于二线治疗既往接受过贝伐珠单抗治疗的RAS突变的转移性结直肠癌的疗效和安全性 The Efficacy and Safety of Fruquintinib Plus FOLFIRI as Second-line Treatment in Bevacizumab -pretreated RAS-mutated Metastatic Colorectal Cancer 主要作者: 刘振洋 / 杨晓琳 (中国长沙) 会议环节: 海报展示 | Poster Display: Gastrointestinal tumours, colorectal 摘要编号: 250eP 标题: 一项评估呋喹替尼联合伊立替康和卡培他滨用于二线治疗晚期结直肠癌患者疗效的真实世界观察性研究 Real-world Observational Study of Fruquintinib in Combination with Irinotecan and Capecitabine as Second-line Treatment in Patients with Advanced Colorectal Cancer 主要作者: 曲秀娟 / 徐玲 (中国沈阳) 会议环节: 海报展示 | Poster Display: Gastrointestinal tumours, colorectal 摘要编号: 255eP 标题: 匹配调整后的间接比较索凡替尼与高剂量长效奥曲肽用于治疗晚期非胰腺神经内分泌瘤的疗效 Matching-Adjusted Indirect Comparison of Surufatinib versus High-Dose Octreotide LAR in Advanced Extrapancreatic Neuroendocrine Tumors 主要作者: 徐建明 (中国北京) 会议环节: 海报展示 | Poster Display: Gastrointestinal tumours, colorectal 摘要编号: 214P 标题: 索凡替尼联合CAPTEM作为不可切除胰腺神经内分泌瘤患者的转化治疗的疗效和安全性: 一项前瞻性、开放标签研究的数据更新 Efficacy and safety of surufatinib in combination with CAPTEM as conversion therapy in patients with unresectable pancreatic neuroendocrine tumors (pNETs): Data updates from a prospective, open-label study 主要作者: 刘续宝 / 王孜尧 (中国成都) 会议环节: 海报展示 | Poster Display: Gastrointestinal tumours, colorectal 摘要编号: 400P 索乐匹尼布用于治疗慢性原发免疫性血小板减少症成人患者的ESLIM-01中国III期研究的长期结果将于2025年ASH年会上公布。报告详情如下： 2025年ASH年会 - 公司申办的研究标题: ESLIM-01 III期研究: 索乐匹尼布长期治疗慢性原发免疫性血小板减少症成人患者的疗效和安全性最终分析 Phase 3 ESLIM-01 study: Final analysis of efficacy and safety of long-term treatment with sovleplenib in adults with chronic primary immune thrombocytopenia 主要作者: 杨仁池 (中国天津) 会议环节: 口头报告 | Oral Abstract Session 摘要编号: 843 地点: Room OCCC - W304EFGH 时间: 2025年12月8日 (星期一) 美国东部时间 15:15 –15:30 关于呋喹替尼呋喹替尼是一种针对所有三种血管内皮生长因子受体 ("VEGFR")-1、-2和-3的选择性口服抑制剂。VEGFR抑制剂在抑制肿瘤的血管生成中起到至关重要的作用。在中国，呋喹替尼由和黄医药及礼来公司合作研发和商业化，并以商品名爱优特®上市。武田拥有在中国内地、香港和澳门以外进一步开发、商业化和生产呋喹替尼的全球独家许可，并以商品名FRUZAQLA®上市销售。关于HMPL-A83 HMPL-A83是一种研究性IgG4型人源化抗CD47单克隆抗体，能够与CD47高亲和力结合。HMPL-A83能够阻断CD47与信号调节蛋白 (SIRP) α的结合，并干扰癌细胞用来保护其免受免疫系统攻击的"别吃我"信号。和黄医药目前拥有HMPL-A83在全球范围内的所有权利。关于赛沃替尼赛沃替尼是一种强效、高选择性的口服MET酪氨酸激酶抑制剂，在晚期实体瘤中表现出临床活性。赛沃替尼可阻断因突变 (例如外显子14跳跃突变或其他点突变)、基因扩增或蛋白质过表达而导致的MET受体酪氨酸激酶信号通路的异常激活。赛沃替尼由阿斯利康与和黄医药共同开发，并以商品名沃瑞沙®由阿斯利康商业化。关于索凡替尼索凡替尼是一种新型的口服酪氨酸激酶抑制剂，具有抗血管生成和免疫调节双重活性。索凡替尼可通过抑制VEGFR和成纤维细胞生长因子受体 (FGFR) 以阻断肿瘤血管生成，并可抑制集落刺激因子-1受体 (CSF-1R)，通过调节肿瘤相关巨噬细胞，促进机体对肿瘤细胞的免疫应答。索凡替尼在中国市场由和黄医药以商品名苏泰达®上市销售。和黄医药目前拥有索凡替尼在全球范围内的所有权利。关于索乐匹尼布索乐匹尼布是一种探索性的新型、选择性的口服小分子脾酪氨酸激酶 ("Syk") 抑制剂。Syk作为B细胞受体和Fc受体信号传导通路中的一个关键蛋白，是多种亚型的B细胞淋巴瘤及自身免疫疾病的成熟治疗靶点。和黄医药目前保留索乐匹尼布在全球的所有权利。前瞻性陈述本新闻稿包含1995年《美国私人证券诉讼改革法案》"安全港" 条款中定义的前瞻性陈述。这些前瞻性陈述反映了和黄医药目前对未来事件的预期，包括对呋喹替尼、HMPL-A83、索凡替尼、赛沃替尼和索乐匹尼布的治疗潜力的预期，呋喹替尼、HMPL-A83、索凡替尼、赛沃替尼和索乐匹尼布的进一步临床研究计划，对呋喹替尼、HMPL-A83、索凡替尼、赛沃替尼和索乐匹尼布的研究是否能达到其主要或次要终点的预期，以及对此类研究完成时间和结果发布的预期。此类风险和不确定性包括下列假设：入组率、满足研究入选和排除标准的受试者的时间和可用性；临床方案或监管要求变更；非预期不良事件或安全性问题；呋喹替尼、HMPL-A83、索凡替尼、赛沃替尼和索乐匹尼布 (包括作为联合疗法) 达到研究的主要或次要终点的疗效；获得不同司法管辖区的监管批准及获得监管批准后获得上市许可；呋喹替尼、HMPL-A83、索凡替尼、赛沃替尼和索乐匹尼布用于目标适应症的潜在市场，以及资金充足性等。此外，由于部分研究可能依赖于与其他药物 (例如卡瑞利珠单抗和奥希替尼) 联合使用，因此此类风险和不确定性包括有关这些治疗药物的安全性、疗效、供应和监管批准的假设。当前和潜在投资者请勿过度依赖这些前瞻性陈述，这些陈述仅在截至本新闻稿发布当日有效。有关这些风险和其他风险的进一步讨论，请查阅和黄医药向美国证券交易委员会、香港联合交易所有限公司以及AIM提交的文件。无论是否出现新讯息、未来事件或情况或其他因素，和黄医药均不承担更新或修订本新闻稿所含讯息的义务。医疗信息本新闻稿所提到的产品可能并未在所有国家上市，或可能以不同的商标进行销售，或用于不同的病症，或采用不同的剂量，或拥有不同的效力。本文中所包含的任何信息都不应被看作是任何处方药的申请、推广或广告，包括那些正在研发的药物。和黄医药（纳斯达克/伦敦证交所：HCM；香港交易所：13）是一家处于商业化阶段的创新型生物医药公司，致力于发现、全球开发和商业化治疗癌症和免疫性疾病的靶向药物和免疫疗法。自成立以来，和黄医药致力于将自主发现的候选药物带向全球患者，首三个药物现已在中国上市，其中首个药物亦于美国、欧洲和日本等全球各地获批。欲了解更多详情，请访问：www.hutch-med.com/sc。

临床2期临床结果

2025-11-27

·GlobeNewswire-Health Care

HUTCHMED Highlights Clinical Data to be Presented at the 2025 ESMO Asia Congress and the 2025 ASH Annual Meeting

HONG KONG and SHANGHAI and FLORHAM PARK, N.J., Nov. 27, 2025 (GLOBE NEWSWIRE) -- HUTCHMED (China) Limited (“HUTCHMED”) (Nasdaq/AIM:HCM; HKEX:13) today announces that new and updated data from several studies of compounds discovered by HUTCHMED will be presented at the European Society for Medical Oncology (“ESMO”) Asia Congress 2025, taking place on December 5-7, 2025 in Singapore, and the American Society of Hematology (“ASH”) Annual Meeting taking place on December 6-9, 2025 in Orlando, USA. Results from a first-in-human study of the anti-CD47 monoclonal antibody HMPL-A83 in advanced solid tumors, as well as from the phase II part of the FRUSICA-2 registration study of the fruquintinib and sintilimab combination as a second-line treatment for locally advanced or metastatic renal cell carcinoma, will be presented at the ESMO Asia Congress 2025. Results from the phase II part of the phase II/III study of surufatinib in combination with camrelizumab and chemotherapy as a first-line treatment for metastatic pancreatic cancer will also be reported. Details of the presentations are as follows: Abstract titlePresenter/Lead authorPresentation detailsESMO Asia Congress 2025 - SPONSORED STUDIES A first-in-human (FIH), dose escalation study of HMPL-A83 (A83), an anti-CD47 monoclonal antibody (mAb) in patients (pts) with advanced solid tumorsYe Guo (Shanghai, China)162MO | Mini Oral session: Developmental therapeutics and precision medicineSunday, December 7, 202511:40 - 11:45 SGTHall 407Fruquintinib monotherapy as second-line (2L) treatment in locally advanced or metastatic renal cell carcinoma (RCC): results from phase 2 part of FRUSICA-2Shanshan Wang (Shanghai, China)540O | Proffered Paper session: Genitourinary tumoursFriday, December 5, 202514:55 - 15:05 SGT Hall 402Surufatinib (S) in combination with camrelizumab (C), nab-paclitaxel and gemcitabine (AG) as the first-line treatment in metastatic pancreatic cancer: results from phase 2 part of a randomized, open-label, active-controlled, phase 2/3 studyShukui Qin (Nanjing, China)375P | Poster Display: Gastrointestinal tumours, non‑colorectalOsimertinib (osi) + savolitinib (savo) in EGFR-mutated (EGFRm) advanced non-small cell lung cancer (NSCLC) with MET overexpression and/or amplification (OverExp/Amp) following progressive disease (PD) on osi: SAVANNAH Asian subsetSe-Hoon Lee (Seoul, Korea)982P | Poster Display: Thoracic tumours, metastaticPatient-relevant Outcomes (PROs) from SACHI: a Phase 3 Trial of Savolitinib (Savo) plus Osimertinib (Osi) versus Chemotherapy (Chemo) in EGFR-mutant (EGFRm) and MET-amplified (METamp) Advanced NSCLC after Progression on EGFR-TKIsYongfeng Yu (Shanghai, China)984P | Poster Display: Thoracic tumours, metastaticAnalysis of MET Amplification (METamp) with FISH and NGS Method in SACHI TrialLonghua Sun (Nanchang, China)988P | Poster Display: Thoracic tumours, metastaticProgression pattern in patients (pts) with EGFR-mutant (EGFRm), MET-amplified (METamp) advanced NSCLC treated with savolitinib (savo) plus osimertinib (osi)Haiyan Yang (Changsha, China)1002P | Poster Display: Thoracic tumours, metastaticMET testing and treatment (tx) sequencing after progression of disease (PD) on first-line (1L) osimertinib (osi) in patients (pts) with EGFRm advanced NSCLC and acquired MET overexpression and/or amplification (OverExp/Amp): Final analysis of a global real-world (rw) studyJulia Rotow (Boston, US)1005P | Poster Display: Thoracic tumours, metastatic ESMO Asia Congress 2025 - INVESTIGATOR-INITIATED STUDIES Fruquintinib Combined with TAS-102 with or without SBRT as Third- or Later-Line Treatment in Metastatic Colorectal Cancer: Preliminary Results from a Prospective Phase II TrialChen Zhang/ Yi Wang(Ningbo, China)205P | Poster Display: Gastrointestinal tumours, colorectalEfficacy and safety of fruquintinib combined with PD-1 inhibitor and chidamide in MSS mCRC: a comparison with real-world bevacizumab plus anti-pd-1 and chidamide armGuanghai Dai/ Miaomiao Gou(Beijing, China)245eP | Poster Display: Gastrointestinal tumours, colorectalThe Efficacy and Safety of Fruquintinib (F) Plus FOLFIRI as Second-line (2L) Treatment in Bevacizumab (Bev)-pretreated RAS-mutated (RAS‑m) Metastatic Colorectal Cancer (mCRC)Zhenyang Liu/ Xiaolin Yang(Changsha, China)250eP | Poster Display: Gastrointestinal tumours, colorectalReal-world Observational Study of Fruquintinib in Combination with Irinotecan and Capecitabine as Second-line Treatment in Patients with Advanced Colorectal CancerXiujuan Qu/ Lin Xu (Shenyang, China)255eP | Poster Display: Gastrointestinal tumours, colorectalMatching-Adjusted Indirect Comparison of Surufatinib versus High-Dose Octreotide LAR in Advanced Extrapancreatic Neuroendocrine TumorsJianming Xu (Beijing, China)214P | Poster Display: Gastrointestinal tumours, colorectalEfficacy and safety of surufatinib in combination with CAPTEM as conversion therapy in patients with unresectable pancreatic neuroendocrine tumors (pNETs): Data updates from a prospective, open-label studyXubao Liu/ Ziyao Wang (Chengdu, China)400P | Poster Display: Gastrointestinal tumours, non‑colorectal Final analysis of long-term results of sovleplenib’s ESLIM-01 China Phase III study in in adult patients with chronic primary immune thrombocytopenia will be presented at the 2025 ASH Annual Meeting. Details of the presentation is as follows: Abstract titlePresenter/Lead authorPresentation details2025 ASH Annual Meeting - SPONSORED STUDIES Phase 3 ESLIM-01 study: Final analysis of efficacy and safety of long-term treatment with sovleplenib in adults with chronic primary immune thrombocytopeniaRenchi Yang (Tianjin, China)843 | Oral Abstract SessionMonday, December 8, 202515:15 - 15:30 EST Room OCCC - W304EFGH About Fruquintinib Fruquintinib is a selective oral inhibitor of all three vascular endothelial growth factor receptors (“VEGFR”) -1, ‑2 and -3. Fruquintinib is co-developed and co-commercialized in China by HUTCHMED and Eli Lilly and Company under the brand name ELUNATE®. Takeda holds the exclusive worldwide license to further develop, commercialize, and manufacture fruquintinib outside mainland China, Hong Kong and Macau, marketing it under the brand name FRUZAQLA®. About HMPL-A83 HMPL-A83 is an investigational IgG4-type humanized anti-CD47 monoclonal antibody that exhibits high affinity for CD47. HMPL-A83 blocks CD47 binding to Signal regulatory protein (SIRP) α and disrupts the “do not eat me” signal that cancer cells use to shield themselves from the immune system. HUTCHMED currently retains all rights to HMPL-A83 worldwide. About Savolitinib Savolitinib is an oral, potent and highly selective MET tyrosine kinase inhibitor that has demonstrated clinical activity in advanced solid tumors. It blocks atypical activation of the MET receptor tyrosine kinase pathway that occurs because of mutations (such as exon 14 skipping alterations or other point mutations), gene amplification or protein overexpression. Savolitinib is being jointly developed by AstraZeneca and HUTCHMED, and commercialized by AstraZeneca under the brand name ORPATHYS®. About Surufatinib Surufatinib is a novel, oral angio-immuno kinase inhibitor that selectively inhibits the tyrosine kinase activity associated with VEGFRs and fibroblast growth factor receptor (FGFR), which both inhibit angiogenesis, and colony stimulating factor-1 receptor (CSF-1R), which regulates tumor-associated macrophages, promoting the body’s immune response against tumor cells. Surufatinib is marketed in China by HUTCHMED under the brand name SULANDA®. HUTCHMED currently retains all rights to surufatinib worldwide. About Sovleplenib Sovleplenib is a novel, investigational, selective small molecule inhibitor for oral administration targeting the spleen tyrosine kinase, also known as Syk. Syk is a major component in B-cell receptor and Fc receptor signaling and is an established target for the treatment of multiple subtypes of B-cell lymphomas and autoimmune disorders. HUTCHMED currently retains all rights to sovleplenib worldwide. About HUTCHMED HUTCHMED (Nasdaq/AIM:HCM; HKEX:13) is an innovative, commercial-stage, biopharmaceutical company. It is committed to the discovery and global development and commercialization of targeted therapies and immunotherapies for the treatment of cancer and immunological diseases. Since inception it has focused on bringing drug candidates from in-house discovery to patients around the world, with its first three medicines marketed in China, the first of which is also approved around the world including in the US, Europe and Japan. For more information, please visit: www.hutch‑med.com or follow us on LinkedIn. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the “safe harbor” provisions of the US Private Securities Litigation Reform Act of 1995. These forward-looking statements reflect HUTCHMED’s current expectations regarding future events, including but not limited to its expectations regarding the therapeutic potential of fruquintinib, HMPL-A83, surufatinib, savolitinib and sovleplenib, the further clinical development for fruquintinib, HMPL-A83, surufatinib, savolitinib and sovleplenib, its expectations as to whether any studies on fruquintinib, HMPL-A83, surufatinib, savolitinib and sovleplenib would meet their primary or secondary endpoints, and its expectations as to the timing of the completion and the release of results from such studies. Such risks and uncertainties include, among other things, assumptions regarding enrollment rates and the timing and availability of subjects meeting a study’s inclusion and exclusion criteria; changes to clinical protocols or regulatory requirements; unexpected adverse events or safety issues; the ability of fruquintinib, HMPL-A83, surufatinib, savolitinib and sovleplenib, including as combination therapies, to meet the primary or secondary endpoint of a study, to obtain regulatory approval in different jurisdictions and to gain commercial acceptance after obtaining regulatory approval; the potential markets of fruquintinib, HMPL-A83, surufatinib, savolitinib and sovleplenib for a targeted indication, and the sufficiency of funding. In addition, as certain studies rely on the use of other drug products such as camrelizumab and osimertinib as combination therapeutics, such risks and uncertainties include assumptions regarding their safety, efficacy, supply and continued regulatory approval. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. For further discussion of these and other risks, see HUTCHMED’s filings with the US Securities and Exchange Commission, The Stock Exchange of Hong Kong Limited and on AIM. HUTCHMED undertakes no obligation to update or revise the information contained in this press release, whether as a result of new information, future events or circumstances or otherwise. Medical Information This press release contains information about products that may not be available in all countries, or may be available under different trademarks, for different indications, in different dosages, or in different strengths. Nothing contained herein should be considered a solicitation, promotion or advertisement for any prescription drugs including the ones under development. CONTACTS Investor Enquiries+852 2121 8200 / ir@hutch-med.com Media Enquiries FTI Consulting –+44 20 3727 1030 / HUTCHMED@fticonsulting.comBen Atwell / Tim Stamper+44 7771 913 902 (Mobile) / +44 7421 898 348 (Mobile)Brunswick – Zhou Yi+852 9783 6894 (Mobile) / HUTCHMED@brunswickgroup.com Panmure LiberumNominated Advisor and Joint BrokerAtholl Tweedie / Emma Earl / Rupert Dearden+44 20 7886 2500 CavendishJoint BrokerGeoff Nash / Nigel Birks+44 20 7220 0500 Deutsche NumisJoint BrokerFreddie Barnfield / Jeffrey Wong / Duncan Monteith+44 20 7260 1000

临床2期免疫疗法临床结果引进/卖出临床3期

100 项与 Octreotide depot (GP Pharm SA) 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB00104

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
肢端肥大症	西班牙	GP Pharm SA	-
食道静脉出血	西班牙	GP Pharm SA	-

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
肠梗阻	临床2期	法国	Novartis Pharmaceuticals Corp.	2005-09-01
腹膜癌	临床2期	法国	Novartis Pharmaceuticals Corp.	2005-09-01
晚期前列腺癌	临床2期	意大利	Novartis AG	2004-02-01

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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


ASCO_GI2025	N/A	胃神经内分泌肿瘤辅助 ki67	35	Somatostatin analogs (long-acting releasing octreotide 30 mg)	醖獵顧積廠膚艱觸鹹廠(艱夢遞簾齋製糧繭簾選) = 願繭鬱淵艱製齋醖憲夢築鏇積蓋憲齋製網範鑰 (鹽艱醖簾窪壓窪衊醖壓, 67 ~ NR)	积极	2025-01-23
				Lanreotide 120 mg	醖獵顧積廠膚艱觸鹹廠(艱夢遞簾齋製糧繭簾選) = 鹽壓獵糧齋願網遞齋夢築鏇積蓋憲齋製網範鑰 (鹽艱醖簾窪壓窪衊醖壓, 67 ~ NR)
NCT01538966 (CTgov)	N/A	肢端肥大症	76	Octreotide LAR+Lanreotide+Pegvisomant (High Dose SRL + Weekly Pegvisomant)	襯選範願遞膚鹹衊衊鑰(艱積繭範鏇鹹網衊獵壓) = 願選廠選觸願夢顧壓醖餘鹽鹽遞築夢齋窪鏇廠 (範獵鬱遞網遞簾壓齋蓋, 1,645.49) 更多	-	2023-01-04
				Octreotide LAR+Lanreotide+Pegvisomant (Low Dose SRL + Daily Pegvisomant)	襯選範願遞膚鹹衊衊鑰(艱積繭範鏇鹹網衊獵壓) = 蓋壓窪淵選齋獵觸襯簾餘鹽鹽遞築夢齋窪鏇廠 (範獵鬱遞網遞簾壓齋蓋, 11,158.49) 更多
ASCO_GI2018	N/A	胃肠胰神经内分泌肿瘤一线 \| 二线	273	Octreotide	簾餘壓鏇構顧製憲鏇夢(醖夢積醖衊範衊鏇網願) = 膚醖糧鬱鬱廠鬱築壓築襯鬱簾鹽築壓鹽鏇襯鏇 (簾壓衊顧襯構壓築築鬱, 51%)	-	2018-02-26
Pubmed \| PLoS One	临床2期	胸腺肿瘤新辅助 positive octreotide scans	17	Octreotide LAR	網觸繭繭願鑰製範鏇憲(醖鹽鹹網遞鏇築鑰網顧) = 71% 積襯鬱選襯鬱鏇廠獵醖 (鬱膚鏇觸遞齋鏇壓齋夢 ) 更多	积极	2016-12-16
NCT01371643 (CTgov)	临床4期	垂体腺瘤 \| 肢端肥大症	41	Octreotide LAR (Medical Treatment by Octreotide LAR)	遞膚齋膚鬱夢鹹糧衊遞 = 膚鹽襯窪鏇鏇衊鹹廠顧鹽窪艱築顧簾憲餘願顧 (鬱夢廠觸膚構憲憲艱獵, 膚廠餘選廠網範願獵鹹 ~ 積願鹽膚製鹹製鹹繭願) 更多	-	2016-07-22
				transsphenoidal surgery+Octreotide LAR (Surgical Debulking Followed by Octreotide LAR)	遞膚齋膚鬱夢鹹糧衊遞 = 齋選選衊選願廠衊鑰構鹽窪艱築顧簾憲餘願顧 (鬱夢廠觸膚構憲憲艱獵, 廠積蓋餘憲衊鬱顧窪鏇 ~ 鬱蓋糧顧積構憲襯築網) 更多
ASCO2015	N/A	神经内分泌肿瘤	-	Octreotide LAR	鬱鏇繭淵製網憲衊鑰廠(鑰積鏇顧襯繭餘壓淵廠) = 鏇窪鏇繭遞淵壓廠構餘鏇廠齋選繭憲壓製蓋願 (鑰構顧鑰艱遞糧積窪顧 ) 更多	-	2015-05-20
ASCO_GI2015	N/A	神经内分泌肿瘤	214	Octreotide LAR (Group A)	鏇糧繭襯網餘廠鑰顧餘(獵淵鑰淵壓醖簾鏇範襯) = 顧積齋醖夢齋艱遞顧獵鏇醖範窪淵壓鹽鬱艱夢 (範襯鑰遞範構醖繭鹽鏇, 13.2–31.5)	-	2015-01-20
				Octreotide LAR (Group B)	鏇糧繭襯網餘廠鑰顧餘(獵淵鑰淵壓醖簾鏇範襯) = 壓獵夢構選遞網願範蓋鏇醖範窪淵壓鹽鬱艱夢 (範襯鑰遞範構醖繭鹽鏇, 20.5–51.1)
ASCO2014	N/A	神经内分泌肿瘤	-	Octreotide LAR (OCT-L)	蓋積鹹憲鹽鹽醖淵築繭(淵艱網廠製餘願廠觸鏇) = 範鑰艱遞簾壓艱糧製醖膚遞膚蓋膚餘簾齋齋顧 (範齋廠蓋簾顧鹽壓鹽鹹 )	-	2014-05-20
				No OCT-L	蓋積鹹憲鹽鹽醖淵築繭(淵艱網廠製餘願廠觸鏇) = 鹹窪選齋願鹽鑰選顧鏇膚遞膚蓋膚餘簾齋齋顧 (範齋廠蓋簾顧鹽壓鹽鹹 )
ASCO2014	临床3期	晚期神经内分泌肿瘤	254	Octreotide LAR	願壓範鏇鏇窪願積鬱鹽(憲鬱願鑰願餘鏇廠壓構) = 繭糧繭範觸鹽窪醖鹹製鹽壓獵網鹽憲艱範壓衊 (觸鹽淵蓋獵築願醖憲襯, 32 ~ 52)	-	2014-05-20
NCT00108355 (CTgov)	临床4期	纤维化 \| 腹水	29	Oral tablet (Midodrine placebo)	簾網遞製餘糧構窪選齋(襯築蓋衊壓鏇醖窪鏇範) = 鏇獵獵選範範蓋繭簾鬱築製膚築衊遞醖鬱積鏇 (襯遞壓廠膚築遞餘醖網, 憲鏇網網膚醖醖糧獵構 ~ 鏇製築衊膚顧艱鏇選繭) 更多	-	2014-03-06