A Randomized, Multicenter, Open-Label, Phase 2 Study of Givastomig (TJ033721) in Combination With Nivolumab and Chemotherapy Versus Nivolumab and Chemotherapy in Participants With Previously Untreated CLDN18.2 Positive and PD-1L Positive Locally Advanced or Metastatic Gastric, Esophageal, or Gastroesophageal Junction Adenocarcinoma

The goal of this clinical trial is to learn if givastomig in combination with standard therapy works to treat adults with cancer in the stomach and/or esophagus (GEA adenocarcinoma). It will also help the researchers to learn more about the safety of givastomig. The main questions it aims to answer are:
* Does the addition of givastomig to standard therapy increase the amount of time that participants survive without progression of their cancer?
* What toxicities do participants experience when taking givastomig?
Participants may be able to take part in the study if they have unresectable or metastatic GEA and if their cancer cells express certain proteins called Claudin 18.2 (CLDN18.2) and PD-L1. Participants whose cancer cells express a protein called HER2 cannot take part.
Up to 180 participants will be randomly assigned to received givastomig at one of two doses in combination with an immunotherapy medicine called nivolumab and chemotherapy OR to receive nivolumab and chemotherapy alone. These therapies will be given primarily via intravenous (into a vein) infusion every 2 or 3 weeks.
Participants will:
* Visit the study treatment center for infusions and/or check-ups and tests every 1-3 weeks
* Report any changes in their symptoms to their study doctors
* Have scans to check for any changes in their cancer every 8-12 weeks

开始日期2026-02-01

申办/合作机构

I-Mab Biopharma US Ltd.

NCT04900818

/ Recruiting临床1期

A Phase 1 Study of TJ033721 in Subjects With Advanced or Metastatic Solid Tumors

This is an open label, multi-center, multiple dose Phase 1 study to evaluate the safety, tolerability, MTD PK, and PD of TJ033721 (givastomig) in subjects with advanced or metastatic solid tumors.

开始日期2021-06-29

申办/合作机构

I-Mab Biopharma US Ltd.

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100 项与 Givastomig 相关的临床结果

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100 项与 Givastomig 相关的专利（医药）

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项与 Givastomig 相关的文献（医药）

2025-12-01·CLINICAL CANCER RESEARCH

A First-in-Human Study of Givastomig, a CLDN18.2 and 4-1BB Bispecific Antibody, as Monotherapy in Patients with CLDN18.2-Positive Advanced or Metastatic Solid Tumors

Article

作者: Spencer, Kristen ; Deng, Yanhong ; Park, Jinyoung ; Wang, Zhenning ; Berlin, Jordan ; Liu, Funan ; Lim, Yangmi ; Kratz, Jeremy ; Jeon, Juyeun ; Girda, Eugenia ; Sabbatini, Peter ; Feller, Laura ; Chung, Jou-Ku ; Kim, Sunnie ; Dayyani, Farshid ; Klempner, Samuel J. ; Ku, Geoffrey ; Meng, Yuan ; Ahlers, Christoph M. ; Xu, Claire (Cong) ; Liang, Xinjun ; Shen, Lin ; Deng, Ting ; Powderly, John ; Liu, Xuejun ; Liu, Tianshu ; Pan, Hongming ; Schneider, Reva

Abstract:

Purpose::

Givastomig is a bispecific antibody that targets CLDN18.2 and conditionally activates local 4-1BB–expressing T cells. This first-in-human study evaluated the safety, tolerability, pharmacokinetics, pharmacodynamics, and antitumor activity of givastomig in advanced solid tumors.

Patients and Methods::

A total of 75 patients were enrolled. Escalating givastomig doses of 0.1 to 18 mg/kg were evaluated in 36 patients with metastatic or advanced solid tumors. An additional 6 patients per cohort with CLDN18.2-positive (defined as membrane intensity score of ≥1+ on ≥1% of tumor cells) advanced or metastatic gastric cancer, gastroesophageal junction cancer, or gastroesophageal carcinoma (GEC) were treated with 5 to 15 mg/kg givastomig across four cohorts. Fifteen patients with CLDN18.2-positive GEC were then enrolled to the 12 mg/kg dose expansion cohort.

Results::

No dose-limiting toxicities were reported up to 18 mg/kg, and a maximum tolerated dose was not reached. The most common treatment-related adverse events (in ≥10% of patients) were nausea, anemia, fatigue, white blood cell count decrease, vomiting, and increased alanine aminotransferase. Givastomig exposure increased dose proportionally, and soluble 4-1BB approached a plateau above 5 mg/kg. The 12 mg/kg dose was selected for dose expansion. A 16% objective response rate was observed in CLDN18.2-positive GEC above 5 mg/kg (N = 43). CLDN18.2 expression in responders ranged from 11% to 100%.

Conclusions::

Givastomig demonstrated manageable safety, dose-proportional exposure, and antitumor activity in patients with advanced solid tumors, particularly in CLDN18.2-positive GEC. A givastomig dose range of 5 to 12 mg/kg was chosen to combine with nivolumab and chemotherapy in part 2 of the study in frontline metastatic GEC.See related commentary by Pretelli and Garralda, p. 4866

2023-06-01·Journal for immunotherapy of cancer

CLDN18.2 and 4-1BB bispecific antibody givastomig exerts antitumor activity through CLDN18.2-expressing tumor-directed T-cell activation

Article

作者: Zhang, Cheng ; Liu, Xuejun ; Zhu, Andrew X. ; Zhang, Jingwu Z. ; Liao, Haiyan ; Chung, Hyejin ; Jia, Keren ; Zhang, Yanni ; Sheng, Zhen ; Meng, Zhen ; Gao, Jing ; Niu, Yanling ; Shen, Lin ; Liu, Chanjuan ; Sung, Eunsil ; Chen, Xi ; Jiang, Wenqing ; Chen, Chan ; Jung, Jaeho ; Wang, Zhengyi

Background:

Claudin18.2 (CLDN18.2) is a tight junction protein that has been identified as a clinically proven target in gastric cancer. Stimulation of 4-1BB with agonistic antibodies is also a promising strategy for immunotherapy and 4-1BB+ T cells were reported to be present within the tumor microenvironment of patients with gastric cancer. However, hepatotoxicity-mediated by 4-1BB activation was observed in clinical trials of agonistic anti-4-1BB monoclonal antibodies.

Methods:

To specifically activate the 4-1BB+ T cells in tumor and avoid the on-target liver toxicity, we developed a novel CLDN18.2×4-1BB bispecific antibody (termed ‘givastomig’ or ‘ABL111’; also known as TJ-CD4B or TJ033721) that was designed to activate 4-1BB signaling in a CLDN18.2 engagement-dependent manner.

Results:

4-1BB+ T cells were observed to be coexisted with CLDN18.2+ tumor cells in proximity by multiplex immunohistochemical staining of tumor tissues from patients with gastric cancer (n=60). Givastomig/ABL111 could bind to cell lines expressing various levels of CLDN18.2 with a high affinity and induce 4-1BB activation in vitro only in the context of CLDN18.2 binding. The magnitude of T-cell activation by givastomig/ABL111 treatment was closely correlated with the CLDN18.2 expression level of tumor cells from gastric cancer patient-derived xenograft model. Mechanistically, givastomig/ABL111 treatment could upregulate the expression of a panel of pro-inflammatory and interferon-γ-responsive genes in human peripheral blood mononuclear cells when co-cultured with CLDN18.2+ tumor cells. Furthermore, in humanized 4-1BB transgenic mice inoculated with human CLDN18.2-expressing tumor cells, givastomig/ABL111 induced a localized immune activation in tumor as evident by the increased ratio of CD8+/regulatory T cell, leading to the superior antitumor activity and long-lasting memory response against tumor rechallenge. Givastomig/ABL111 was well tolerated, with no systemic immune response and hepatotoxicity in monkeys.

Conclusions:

Givastomig/ABL111 is a novel CLDN18.2×4-1BB bispecific antibody which has the potential to treat patients with gastric cancer with a wide range of CLDN18.2 expression level through the restricted activation of 4-1BB+ T cells in tumor microenvironment to avoid the risk of liver toxicity and systemic immune response.

164

项与 Givastomig 相关的新闻（医药）

2026-03-11

·上海衡道医学病理诊断中心

衡道精选|CLDN18.2：实体瘤靶向治疗与病理检测解析

在精准肿瘤学快速发展的背景下，紧密连接蛋白（Claudin, CLDN）家族因其在肿瘤发生发展中的关键作用及靶向治疗潜力，成为业界关注的焦点。其中，CLDN18.2作为该家族的重要成员，凭借其在肿瘤组织中的特异性表达特征，已成为实体瘤靶向治疗的核心靶点之一。本文基于最新临床研究证据及病理检测共识，系统解析CLDN18.2的生物学特性、肿瘤表达模式、临床研发进展及标准化病理判读方法，为临床诊疗与药物研发提供参考。一、CLDN家族概述及CLDN18.2的结构与功能（一）CLDN家族成员特征 CLDNs是构成上皮细胞紧密连接的核心跨膜蛋白家族，在维持细胞极性、屏障功能及信号传导中发挥关键作用。人类CLDN家族包含23个功能明确的成员（CLDN1-23，CLDN13缺失），均具有保守的四跨膜域结构，即两个细胞外环（ECL1、ECL2）、四个α-螺旋跨膜域及胞内N端与C端尾区。根据功能差异，CLDNs可分为屏障形成型（如CLDN1、CLDN3、CLDN18.1）和通道形成型（如CLDN2、CLDN10），部分成员还可通过异源聚合形成选择性离子通道，调控细胞旁物质转运。各家族成员具有严格的组织特异性表达模式，例如CLDN5主要参与血脑屏障构成，CLDN11维持髓鞘电绝缘性，而CLDN18.2则特异性定位于胃黏膜上皮[1]。（二）CLDN18.2的结构与生物学功能 CLDN18基因定位于人类3号染色体q22.3区域，通过选择性剪接产生两种异构体——CLDN18.1和CLDN18.2，二者仅在N端69个氨基酸（含ECL1区域）中存在21个氨基酸差异，其中ECL1的8个氨基酸替换直接影响抗体结合特异性。CLDN18.1 主要表达于肺泡上皮和肺肿瘤，而 CLDN18.2 仅在胃黏膜中表达，并在胃癌、胰腺癌、食管癌、部分卵巢癌和结直肠癌中过表达。CLDN18.2作为非经典型CLDN蛋白，包含264个氨基酸，分子量约27 kDa，其结构特征为：两个细胞外环（ECL1含保守GLW基序及二硫键，是抗体主要结合位点）、四个跨膜域及胞内PDZ结合基序。生理状态下，CLDN18.2特异性表达于正常胃黏膜上皮细胞的紧密连接复合体中，通过与ZO1、ZO2等支架蛋白结合锚定至肌动蛋白细胞骨架，维持胃黏膜屏障功能及酸抵抗能力，防止细胞旁H⁺渗漏。在恶性转化过程中，肿瘤细胞极性丢失导致紧密连接破坏，CLDN18.2表位暴露并异常稳定表达于细胞膜表面，同时通过调控PI3K-AKT、Hippo-YAP等信号通路，促进肿瘤增殖、侵袭及转移[1]。图1：Claudin 18.2结构、功能和表达模式[1] 二、CLDN18.2在人类实体瘤中的表达模式 CLDN18.2的肿瘤表达具有显著的组织特异性和亚型选择性，其阳性率因肿瘤类型、组织学分型及种族差异呈现明显异质性，相关数据均来自大样本临床研究及生物标志物分析：（一）胃肠道肿瘤 1. 胃癌及胃食管结合部癌（GEJ）：作为CLDN18.2表达最主要的肿瘤类型，全球多中心III期临床试验SPOTLIGHT和GLOW的合并分析显示，在4507例胃癌/GEJ癌样本中，CLDN18.2高表达（IHC 2+/3+且阳性细胞比例≥75%）率为38.4%。不同组织亚型中，弥漫型胃癌阳性率最高（48.3%），肠型胃癌为38.8%，混合型为42.9%；印戒细胞癌（SRCC）作为特殊亚型，阳性率可达64.8%。种族差异方面，欧洲及中东人群阳性率为44.0%，中国人群为35.0%，日本人群为24.0%，韩国人群为46.5%[1]。 2. 食管癌：食管腺癌中CLDN18.2阳性率约18.4%-24.8%[2, 3]，而食管鳞状细胞癌中表达较低；胃食管反流病相关食管癌中，炎症微环境可诱导CLDN18.2异常表达[1]。 3. 结直肠癌：总体阳性率极低（单中心回顾性研究805例样本中仅为2.1%），右侧结直肠癌、黏液性/低分化腺癌及错配修复缺陷（dMMR/MSI-H）亚型中阳性占比更高[4]；结肠炎相关结直肠癌中阳性率约27%[5]。 4. 胰腺癌：胰腺导管腺癌（PDAC）中CLDN18.2阳性率为30.4%-50%[6, 7]，且在癌前病变（如胰腺上皮内瘤变、导管内乳头状黏液性肿瘤）中已可检测到表达，提示胰腺上皮的胃型分化可能是恶性转化为高表达CLDN18.2的胰腺导管腺癌的基础[1]。但需注意，在50%阳性率的文章中，CLDN18.2的判读方法为H-score =（1×弱阳性细胞百分比）+（2×中等阳性细胞百分比）+（3×强阳性细胞百分比），计算结果≥5即为阳性。而30.4%阳性率文章中使用的是≥75%肿瘤细胞2+/3+的阳性定义。（二）非胃肠道实体瘤 1. 卵巢癌：转移性卵巢黏液癌中，源自上消化道的肿瘤阳性率为56.6%，而源自下消化道的肿瘤阳性率为0%；卵巢交界性黏液性肿瘤中也可见CLDN18.2异常表达[1]。 2. 非小细胞肺癌（NSCLC）：阳性率约3.7%，主要集中于早期、低增殖亚型，且与甲状腺转录因子1（TTF-1）表达呈负相关[8]。但这篇文章中，CLDN18.2的阳性定义为肿瘤细胞的染色强度与阳性细胞比例乘积的评分在 2–9 分区间。 3. 胆道系统肿瘤：Claudin18表达率为29.5%（70/237），其中胆囊癌（62.5%；20/32）和肝外胆管癌（53.4%；31/58）的表达率最高，而肝内胆管癌（12.9%；19/147）的表达率最低（P < 0.0001）。在所有病例中，检测到 Claudin18 阳性（2+/3+≥40%）的比例为5.5%（13/237），其中胆囊癌（15.6%；5/32）最为常见，其次是肝外胆管癌（8.6%；5/58）和肝内胆管癌（2.0%；3/147）（P = 0.0045）[9]。（三）原发灶与转移灶表达一致性及肿瘤异质性 SPOTLIGHT和GLOW研究显示，原发灶与转移灶的CLDN18.2表达高度一致[10]。但也有文献显示，高达25%的病例中CLDN18.2的表达在原发肿瘤和转移肿瘤中存在不一致性，其中腹膜转移灶阳性率（44.3%）及一致性（31.4%）最高，肝脏转移灶阳性率（17.9%）及一致性（12.8%）最低[11]。另外，对胃癌中CLDN18.2的研究表明，在约60%的病例中存在肿瘤内部的异质性[11]。三、CLDN18.2靶向药物的临床研发进展（一）已获批药物佐妥昔单抗（Zolbetuximab）：全球首个获批的CLDN18.2靶向药物，为嵌合IgG1单克隆抗体，通过特异性结合CLDN18.2的ECL1区域，介导抗体依赖性细胞毒性（ADCC）和补体依赖性细胞毒性（CDC）。基于III期SPOTLIGHT和GLOW试验数据，该药物联合化疗（mFOLFOX6或CAPOX）用于HER2阴性、CLDN18.2高表达（≥75%肿瘤细胞2+/3+）局部晚期不可切除或转移性胃癌/GEJ癌一线治疗，可显著改善患者生存期（中位OS分别为18.23个月和14.39个月），已于2024年获美国FDA、欧盟EMA及中国NMPA批准上市。其伴随诊断试剂Ventana CLDN18（43-14A）RxDx IHC检测同步获批，用于患者筛选。（二）部分在研阶段药物 1. 单克隆抗体：Osemitamab（TST001）作为高亲和力人源化IgG1抗体，通过Fc区域去岩藻糖基化增强ADCC活性，I/IIa期TranStar102试验显示，联合CAPOX治疗CLDN18.2阳性（≥10%肿瘤细胞1+/2+/3+）胃癌/GEJ癌，客观缓解率（ORR）达65.4%；ASKB589联合CAPOX及PD-1抑制剂的I期试验中，ORR为80%，目前已进入III期临床。 2. 抗体药物偶联物（ADC）：CMG901（MMAE payload，DAR=4）在I期试验中，针对经多线治疗的CLDN18.2阳性胃癌/GEJ癌，2.2 mg/kg剂量组ORR达42%，且在腹膜转移、PD-1抑制剂经治患者中仍有效；SYSA1801（MMAE payload）治疗晚期胃癌的ORR为47.1%，目前也已进入III期临床。 3. 双特异性抗体：Givastomig（CLDN18.2/4-1BB）通过肿瘤特异性T细胞激活机制，在I期试验中ORR为16.6%，且对低表达CLDN18.2的肿瘤仍有活性，目前已进入II期临床；Q-1802（CLDN18.2/PD-L1）在I期试验中未观察到剂量限制性毒性，部分患者达到部分缓解。 4. CAR-T细胞疗法：CT041作为第二代CLDN18.2特异性CAR-T细胞，在I期试验中治疗经多线治疗的胃癌/胰腺癌患者，ORR达48.6%，中位PFS为3.7个月，目前已完成关键II期确证试验并进入上市申请阶段。作为该关键II 期临床试验的病理合作方，衡道病理通过精准的病理阅片与判读提供核心数据支撑，为治疗方案的有效性与安全性验证筑牢关键基础。图2：针对CLDN18.2的各种靶向治疗策略[1] 四、CLDN18.2的病理判读方法与阳性定义 CLDN18.2的病理检测结果直接决定患者靶向治疗资格，其判读方法的标准化和阳性定义的明确化是精准筛选获益人群的关键。目前临床检测以免疫组织化学（IHC）为金标准，相关技术规范和判读标准已在《胃癌Claudin18.2临床检测专家共识（2025版）》及国际多中心研究中形成明确共识[10]。（一）检测标本与前期处理规范 1. 标本类型：手术切除标本和活检标本。进展期胃癌推荐取材6-8块，多点取样可以提高检测的准确性。原发灶及转移灶标本均可用于CLDN18.2检测。送检标本需保证至少50个存活肿瘤细胞（细胞学标本≥100个），否则需在报告中注明。 2. 标本处理：标本离体后30分钟内需进行固定，最长不超过1小时，固定液体积为组织体积的4-10倍。手术标本固定24-48小时，活检标本固定6-8小时，避免过度固定或固定不足导致抗原丢失。 3. 对照设置：每次检测需设立阳性对照（正常胃小凹上皮，呈3+强染色；肠上皮化生区域上皮，呈1+/2+弱至中度染色）、阴性对照（固有层淋巴细胞、间质细胞，无染色）及空白对照（PBS替代一抗）；手术标本优先选择带正常胃黏膜的蜡块作为内部对照，活检或转移灶标本需设置外部阳性对照。（二）抗体选择与检测平台目前临床常用的CLDN18.2 IHC检测抗体包括Pan-CLDN18抗体和CLDN18.2特异性抗体，不同抗体的性能特征及适用场景存在差异： 1. 43-14A（Ventana）：识别CLDN18的C端区域，无亚型特异性，但因胃组织中CLDN18.1表达可忽略，故可特异性反映CLDN18.2表达，为SPOTLIGHT、GLOW等III期试验采用的抗体。全球27个实验室参与的环形研究证实，该抗体在Ventana平台上的分析性能（准确性、精密度、灵敏度、特异度）均≥85%，且实验室间一致性良好（Cohen’s kappa 系数达良好至优秀水平）[12]。 2. EPR19202（Abcam）：CLDN18.2特异性抗体，识别N端1-100位氨基酸，与43-14A在高表达样本中一致性良好，但灵敏度略低一点[10]。 3. 其他抗体：14G11（Transcenta）、DS-3（AskGene）、14F8（CARsgen）等均在不同临床试验中应用，需根据试剂盒推荐的检测平台进行验证后使用。（三）判读标准与阳性定义[10] CLDN18.2 IHC判读需结合染色强度、阳性细胞比例及染色定位综合评估，核心标准如下： 1. 染色定位：仅细胞膜线性染色（完全/部分膜、基底外侧膜或顶端膜）或微腔染色视为阳性，胞质染色、核染色及颗粒状膜染色不纳入评分。 2. 染色强度评分：参照HER2“放大规则”分为4级：0（无染色）、1+（弱染色）、2+（中等染色）、3+（强染色）。 3. 阳性细胞比：计数所有浸润性癌成分中的阳性细胞占比，排除癌前病变（肠上皮化生、上皮内瘤变）及间质成分。（四）判读注意事项 1. 弥漫型胃癌判读需避免将阴性肿瘤细胞误判为间质细胞，印戒细胞癌仅计数明确的线性膜表达； 2. 当2+/3+阳性细胞比例处于60%-80%临界区间时，建议由第二位病理医师共同评估； 3. 标本存在电灼损伤、固定不良或肿瘤细胞不足时，应判定为检测结果无效，建议重新取样； 4. 联合检测时需注意与HER2、PD-L1等生物标志物的表达重叠性。结语 CLDN18.2作为实体瘤精准治疗的核心靶点，其生物学特性明确、肿瘤表达特异性高，已形成从病理检测到靶向治疗的完整临床转化链条。随着更多靶向药物进入临床后期开发，标准化的IHC检测流程、统一的判读标准及规范的阳性定义将成为保障治疗效果的关键。衡道病理严格遵循CAP（美国病理学家协会）以及指南、共识的标准化要求，依托丰富的病理医生资源、完善的质量控制体系及系统化人员培训，可实现对CLDN18.2的精准量化评估，有效规避检测异质性带来的误差，为CLDN18.2靶向治疗的患者筛选、疗效预判及预后评估提供最可靠的生物学依据。未来，随着检测技术的迭代与临床研究的深入，CLDN18.2有望在更多实体瘤亚型中实现治疗突破，为患者带来新的生存希望。图3：胃癌的CLDN18.2 IHC染色图（衡道中心实验室供图）图4：胰腺癌的CLDN18.2 IHC染色图（衡道中心实验室供图）参考文献： 1.Izuma N, Changsong Q, Yang C et al. Claudin 18.2 as a novel therapeutic target. Nat Rev Clin Oncol 2024; 21. 2.Svetlana P, Adrian Georg S, Su Ir L et al. The expression of the tight junction protein and therapeutical target Claudin 18.2 is heterogeneously distributed within esophageal and gastric adenocarcinoma. Sci Rep 2025; 15. 3.Valeska M, Florian G, Erdem C et al. Claudin 18.2 expression in esophageal adenocarcinoma and its potential impact on future treatment strategies. Oncol Lett 2020; 19. 4.Shigemasa T, Hidekazu H, Atsuo T et al. Clinicopathological and molecular features of claudin-18 isoform 2 expression in patients with colorectal cancer: a single-center retrospective study. Ther Adv Med Oncol 2024; 16. 5.Mai I, Hiroyuki H, Tomoyuki N et al. Colitis-associated colorectal adenocarcinomas frequently express claudin 18 isoform 2: implications for claudin 18.2 monoclonal antibody therapy. Histopathology 2021; 79. 6.Su Ir L, Caroline F, Adrian Georg S et al. Extent and clinical significance of the therapy-relevant tight junction protein Claudin 18.2 in pancreatic ductal adenocarcinoma - real-world evidence. Transl Oncol 2024; 47. 7.Anna M V, Graziana A, Ilaria G et al. Claudin 18.2: An attractive marker in pancreatic ductal adenocarcinoma. Oncol Lett 2025; 29. 8.Patrick M, Johanna Sofia Margareta M, Karolina E et al. Aberrantly activated claudin 6 and 18.2 as potential therapy targets in non-small-cell lung cancer. Int J Cancer 2014; 135. 9.V A, D S, M R et al. Claudin 18.2: a promising actionable target in biliary tract cancers. ESMO Open 2025; 10. 10.《胃癌Claudin18.2临床检测专家共识》专家委员会. 胃癌Claudin18.2临床检测专家共识(2025版). 中华病理学杂志 2025; 54: 718-725. 11.Antonio S, Alberto T, Samuel J K, Thomas F B. Claudin proteins as emerging therapeutic targets for solid tumours. Nat Rev Cancer 2026. 12.Bharat J, Philippe T, Hans-Ulrich S et al. Global Ring Study to Investigate the Comparability of Total Assay Performance of Commercial Claudin 18 Antibodies for Evaluation in Gastric Cancer. Lab Invest 2023; 104. 药企研发、病理中心实验室业务合作咨询请联系：临床试验业务:曹先生 18603122060临床检验业务:冯先生 15632107654（北区）临床检验业务:李女士 13661913066（南区）衡道医学中国病理行业全链赋能者，以「硬科技+软实力+新基建」重塑病理诊断未来—🔬 国家认证的行业标杆国内首批“三证齐全”的第三方病理诊断中心（CNAS-15189认可/美国CAP认证/五星AAA双评定），全国体量领先的智能实验室，服务千家医疗机构，更以科技援疆践行社会责任。🤝病理CRO服务全球药企研发加速器与跨国知名药械企业共建精准医疗生态圈，依托自主数智设备与千万级样本库年的实力，支撑超百项创新药研发项目，助力跨国药企实现「病理数据-药物疗效」精准映射。 💡智慧数字病理系统科技引擎树立行业智慧数字病理系统新标杆，构建全球消化道病理AI训练数据库，联合瑞金医院发布首部《智慧病理科白皮书》，驱动20+省病理科迈入“智慧病理诊断时代”，5G质控系统年处理标本超百万例。⚙ 智能病理设备衡道智造自主研发数智病理科发展所需核心智能设备，建成病理硬件智能制造产线，国内少数具备“数智化软硬件+诊断服务”全链条能力的病理行业服务商。🌐 10万+病理医者成长平台医学新媒体矩阵原创学术超千篇，千万级课程播放量打造病理人“掌上学院”，从诊断技术到AI应用，助力行业发展和个人提升，赋能病理人终身成长。

临床研究

2026-03-10

·抗体圈

迷你Biotech，惊天大反转

今天有一个电话会比较重要，关于新桥生物（Nasdq：NBP）资本运作得到的眼科双抗VIS-101的临床IIa期数据发布。新桥生物（原I-MAB）虽然在分家下后拿走的东西不算多，但是好在有一条比较优质的胃癌管线givastomig，只要这条管线能够被顺利孵化出来，2030年将要面对的是120亿美元的市场份额，Lucid Capital Markets分析师给givastomig估值上，仅在胃癌一个适应症峰值就达到27亿美元。在VIS-101发布之前，我们是觉得只要givastomig按部就班顺利走下去，新桥生物肯定有出头的一天。在VIS-101临床IIa期数据发布之后，它目前手里的管线似乎又多了一条爆款预期，可以把它目前新桥的公司向前推进看作两条管线双轮驱动，双子星拉着出海的新桥生物，一同驶向星辰大海。 01 分家后的奋斗史看biotech，不能只看数据，看机制，看管线本身；事实上，管线后面资本运作的故事，远比管线本身推进读出数据要精彩的多。管线是人和分子的博弈，推进管线的过程，靠的是科学家的热血。但人和资本的博弈，往往展现出热血与萧瑟一体两面，一方面是双方的热情定格交易前进的方向，一边是双方复杂且曲折的谈判历程忽快忽慢影响交易前进的速度。让我们从2024年天境生物分家之后开始讲起。臧敬五，2020年上纳斯达克敲钟的人，天境生物的董事长，在2024年这个分家的关口，在国内和国外之间选择了国内，领导天境杭州。而国外I-MAB，董事长变成了康桥资本的创始人傅唯，康桥资本和天境生物什么关系？看下图就知道，第二大股东（第一大股东是云顶新耀，注意，这是个伏笔）。但远远不止如此，事实上，天境的第一桶金——A轮投资的1000万，就是康桥资本给的，此后，康桥资本陆续参与了对天境的B轮和C轮投资，绑定多深不必多赘述。傅唯接过的这个I-MAB，分到的管线中，主要是两类，一类是很早的共同研发的“化石”管线，例如CD47和CD73.CD47还失败了，CD73之后情况也不太好，然后就是第二类，和韩国biotech ABL bio共同开发出来的管线，例如后来惊世骇俗的Givastomig，这也是分到的家产中最为核心的部分，License进来的管线肯定带不到国外。然后，我们可以看到，再往后面数，更为早期的管线（8-17），I-MAB一条都没有带走。算下来，真正有价值的管线，就是从与ABL bio共同开发的TJ-CD4B和TJ-L14B，也就是后来的Givastomig和Ragistomig。这就是公司新董事长傅唯当时面临的现状，管线虽然还剩三条的海外权益，但其实主要在推进的只有Giva（cldn18.2×4-1BB）一条管线，裁员也裁了三分之一。公司股价是几乎要崩盘的，以至于到2025年3月19日，I-MAB方面收到纳斯达克的通知，称I-MAB不符合纳斯达克上市规则5450(a)(1)的规定，因为ADS（美国存托股份）的最低买入价已连续30个交易日低于每股1.00美元。不过好在该通知不会立即影响I-MAB股票在纳斯达克全球市场的上市或交易，而是会给180天的期限，来重新达到美股1美元的最低竞价要求。财务方面，2024年底现金也只剩下6800万美元。而其此前每年的研发费用都维持在2000万美元左右。无论怎么看，该公司当时都像是已经陷入了绝境。不过我们之前也多次写文章，美股biotech上市了之后如果实在走到绝境了，无路可退了，还有最后一条路走：聘请财务顾问，把手头的早期管线打包称重算价格，license出去，股东分钱，然后公司就作为一个干净的壳子存在啦。卖壳子，是绝境的不错选择。说实话，当时I-MAB不是没这么想过，也确实有人来询价，但是I-MAB的投资人觉得太便宜就没卖（市值1.65亿美元的时候）。一切路都走不通了吗？恰逢这种绝境之下，I-MAB原CEO Raj Kannan辞职，上来的人CEO，则是力挽狂澜的关键人物——傅希涌，康桥资本系下面的一位偏研发风格的职业管理人。根据深蓝观媒体的采访，一位曾在I-Mab工作的人士回忆，傅希涌在七月到任后，首要工作便是与团队逐一审视每个研发项目，梳理所有可用数据与研发思路。当时是看到了Giva的单药初步数据，然后傅希涌迅速启动了联合用药探索，看到了还算不错的初步疗效。这时候，就面临了有限资源推哪条管线选择：CD73单抗Uliledlimab还是Giva？在看到赛诺菲买了Ulil的中国权益后，I-MAB迅速决定all in Giva而放弃Ulil，傅希涌在投资人会议上解释了这个策略的逻辑：公司可以不需要花任何钱，就看到CD73这款药的后续数据。在资源有限，赌不起的情况下，让大户先去冲，自己跟在后面，是最为明智的选择。从2025年4月份开始，I-MAB的基本面开始好转，Giva的初步数据4月底被ESMO GI会议接收，6月26日公布，而公司的股价也从4月的不到1美元涨到了2.5美元左右。数据也十分明艳动人：主要体现在CLDN18.2低表达上，CLDN18.2表达低于75%（CLDN-Low）的患者中，80%（4/5）达到部分缓解。在选定的扩展剂量组（8和12 mg/kg）中，CLDN-Low患者的缓解率提高至100%（3/3）。好起来了，不用退市了，公司至少有一条比较优质的管线撑门面了。I-Mab就开始考虑玩点大的了，例如，收一条管线。2026年10月16日，I-MAB向SEC递交了一份6-K文件，让Affamed往新成立的子公司Visara里注入管线，这就是我们文章一开始要探讨的那条眼科管线——VIS-101的由来。VIS-101一开始是一条中国管线，是奥赛康子公司AskGene研发的。奥赛康在2022年把它大中华区之外的权益授权给了AffaMed。现在，I-MAB直接大手一挥，把该管线的全球权益都收了过来。VIS-101放在Visara下，该公司I-MAB占比65%，Affamed占30%。而之后，VIS-101的海外权益便交给Visara这个合资公司共同开发，国内权益则授权给了云顶新耀——I-MAB的第一大股东。I-MAB自己也改名为新桥生物，计划在港股上市，目前已经能看到招股书。 I-MAB分家后的编年史与VIS-101这条管线资产的来龙去脉，大抵如此。 02 靶点市场扫描 VEGF这个靶点用在眼科上算是老药了。自2006年雷珠单抗获批以来，VEGF单抗在眼科疾病中开疆拓土非常迅速，Elyea（阿柏西普销售额一度接近100亿美元），但是现在第一代VEGF眼科药物普遍面临专利悬崖，第二代药物呼之欲出。但第二代药物往什么地方去脱胎换骨呢？其中一条路是改良自身的用药周期。再生元的方式是退出阿柏西普的Eylea高浓度版本——Eylea HD，其核心价值在于通过提高药物浓度（114.3 mg/mL）和注射体积（0.07mL），将给药间隔从每8周延长至最长16周（欧盟甚至批准24周）。从临床三期数据主要终点来看，可以说Eylea HD非劣效于原版本，并且Eylea HD组无视网膜液（IRF/SRF）患者比例更高（71.1% vs 59.4%），算是一个潜在的长期优势。（视网膜液的存在会导致视力下降，眼内胀痛等）另一条路就是双靶点了，典型的就是罗氏的VEGF-A/Ang-2双抗法瑞西单抗（Vabysmo），其销售额2025年达到了53.6亿美元，是目前全球销售额第二的双抗药物，是两个Fab臂的二价抗体。核心问题，为什么是加Ang-2这个靶点？这个从机制上来说，是因为二者有协同效应，Ang-2通过破坏血管稳定性，使血管内皮细胞对VEGF刺激更加敏感，形成"渗漏-新生血管-炎症"恶性循环。此外，就算用VEGF单抗抑制住了VEGF因子，Ang-2还可通过激活NF-κB等通路，维持一定的血管渗漏和炎症形态。因此，单纯阻断VEGF-A虽能抑制新生血管，但对已存在的病理性血管（如DME中脆弱的毛细血管、RVO中缺血的视网膜血管）无稳定作用，血管仍处于渗漏状态。而Ang-2通路被抑制后，Tie2信号通路回复，从而促进周细胞覆盖和内皮细胞连接重建。从解剖学证据也可以看到，法瑞西单抗组与阿柏西普租相比，患者中央亚区厚度（CST）下降更显著，无视网膜液（IRF/SRF）比例更高（71.1% vs 59.4%）。此外，在给药上，法瑞西给药的间隔也很长，约60-63%患者可实现每16周（Q16W）给药，80%可实现每12周（Q12W）以上给药。现在同靶点双抗竞争格局如下图所示，其实这个赛道真的不算很拥挤的赛道，主要与VIS--101会形成竞争的就是信达的IBI-324，后者马上要开全球三期临床。 03 VIS-101与临床数据双抗本身如下图所示，结构上和罗氏的二价抗体不同，它是四价融合蛋白，相比基准产品，VIS-101对VEGF和Ang-2结合活性分别增加2倍和6倍，抑制活性增加2倍和16倍。我们前面提到，不管是阿柏西普高浓度版本还是法瑞西双抗，二者想做的都是减少给药频率，并且它们已经把给药周期打到12-16周了。而VIS-101更进一步，有希望把这个频率打到20-24周。为什么要减少给药频次？最直观的好处，节约患者的医疗费用。这一点在今天数据解读会上提到了这个问题，根据公司的说法，疗效持久性提高和销售额提高呈正相关，如下图所示，从四周给药一次到8周给药一次再到8-16周给药一次，产品发布后第二年收入随着上涨。这背后深层次原因应该是和用户偏好显著相关，降低给药频次可以使得单品渗透市场的速度加快。而VIS-101在这个方向确实卷到了极致：不仅是后期维持治疗上，在前期上负荷剂量上，法瑞西需要打4针，而VIS101仅需3针。有意思的是，管理层给出的VIS-101上市第二年收入还是很谦虚的（10亿美金）。基线情况如下图所示，我们可以看到基线的BCVA上，3mg和6mg组差距是不大的。并且有意思的是，6mg组入组的患者一半以上接受过抗VEGF疗法治疗，而3mg这部分占比只有30%。最后疗效上要看的指标也很简单：和法瑞西双抗相比是否有优势，我们可以看到，无论是在初治还是后线治疗的患者中，其疗效都比法瑞西单抗在STAIRWAY二期临床结果中好。值得注意的是，后面的QA当中，有一个问题问得很好： FDA宣布注册临床可只做一个三期，VS101在开展三期临床时能否享受该待遇？如果能够实现那真的是省了不少钱和时间。但公司还只是说根据临床2b期进展的情况边走边看和FDA沟通，目前基本计划仍按保守方案做两次全球注册。该药的价值如果真的能得到兑现的话，至少是50亿美元级别销售峰值的大单品。结语：新桥生物真的可以说是浴火重生了一次，这一次它不仅带着cldn18.2×4-1BB双抗，更带着这款有50亿美元峰值潜力的单品走向二级市场。新桥生物，长夜已尽，高天正熹。识别微信二维码，添加抗体圈小编，符合条件者即可加入抗体微信群！请注明：姓名+研究方向！版权声明本公众号所有转载文章系出于传递更多信息之目的，且明确注明来源和作者，不希望被转载的媒体或个人可与我们联系(cbplib@163.com)，我们将立即进行删除处理。所有文章仅代表作者观不本站。

引进/卖出临床2期

2026-03-09

·BioSpace

NovaBridge and Visara Announce Positive Results from VIS-101 Phase 2a Wet AMD Study

VIS-101, purpose-designed to be best-in-class for retinal vascular diseases, is a tetravalent, dual VEGF-A X ANG-2 inhibitor Topline Phase 2a data show VIS-101 provides rapid, robust and durable treatment responses in wet AMD VIS-101 demonstrated mean BVCA improvements of >10 ETDRS letters and median CST reductions of 100-150 mm Potentially best-in-class durability with a favorable safety pro no dose-limiting toxicity Phase 2b dose-determining study expected to begin in H2 2026; global Phase 3 program expected to begin in 2027 Conference Call and Webcast today, March 09 at 9:00 AM ET ROCKVILLE, Md., March 09, 2026 (GLOBE NEWSWIRE) -- NovaBridge Biosciences (Nasdaq: NBP) (NovaBridge or the Company) a global biotechnology platform company committed to accelerating access to innovative medicines, and its subsidiary, Visara, Inc. (Visara), today announced positive topline results from the Phase 2a study of VIS-101, a purpose-designed tetravalent, dual VEGF-A X ANG-2 inhibitor in development for retinal vascular diseases including wet age-related macular degeneration (wet AMD), diabetic macular edema (DME), and retinal vein occlusion (RVO). Topline results show that VIS-101 produced rapid, robust and durable treatment responses in wet AMD, with potential best-in-class durability and a favorable safety profile. Wet AMD affects more than 20 million people globally 1 . Topline Data: VIS-101 produced rapid and robust efficacy, and durable treatment responses with both 3 mg and 6 mg dose cohorts: Mean improvement in Best Corrected Visual Acuity (BCVA) of >10 Early Treatment of Diabetic Retinopathy Study (ETDRS) letters Median central subfield thickness (CST) reduction of 100-150 mm Potential best-in-class durability with: ~two thirds of patients retreatment-free at 4 months ~half of patients retreatment-free at 6 months Favorable safety and no dose limited toxicity “I am encouraged by the positive Phase 2a safety and efficacy data as it provides important proof-of-concept for VIS-101 as a potential treatment for wet AMD. The data validates VIS-101’s purpose-engineered design and gives us added confidence in its potential to deliver best-in-class durability while maximizing visual gains in the treatment of wet AMD,” said Emmett T. Cunningham, Jr., MD, PhD, MPH, Founder and Executive Chairman of Visara and Vice-Chairman of the NovaBridge Board of Directors . “The data clearly show that VIS-101 produced rapid, robust and durable treatment responses, with favorable tolerability, after three loading doses. Importantly, VIS-101 also demonstrated potential best-in-class durability, with nearly half of treatment naïve patients remaining retreatment free for more than six months following induction. Such strong clinical results provide a meaningful foundation to advance our development program, including plans to initiate a dose-determining Phase 2b study in the second half of this year, followed by a global Phase 3 program in 2027.” “This study is an important milestone for VIS-101. As a retina specialist and drug developer, I am truly encouraged by VIS-101’s emerging product profile. The combination of robust visual and anatomic improvements, with potentially best-in-class durability and a favorable safety pro to date by VIS-101, has the potential to offer tangible benefits to people living with wet AMD and other retinal vascular diseases where the high treatment burden required by current therapies impacts their visual outcomes. I am energized to continue to partner with the Visara team and the retina and patient community worldwide as we work to bring this innovative potential therapy to patients in need,” said Carlos Quezada-Ruiz, MD, FASRS, Chairman of the Scientific Advisory Board of Visara . Nikolas JS London, MD, FACS, Managing Partner and President, Retina Consultants San Diego added, “It’s an exciting time in our field. The widespread adoption of faricimab has firmly established dual VEGF-A/ANG-2 inhibition as the pathway forward for retinal vascular disease. Durability remains the greatest unmet need, and the Phase 2a data for VIS-101 — with nearly half of treatment-naïve patients retreatment-free at six months after just three loading doses — is among the most encouraging I’ve seen at this stage. If Phase 3 data bear out, I would expect widespread adoption and meaningful benefit for the millions of patients living with these conditions.” “The positive data reported today for VIS-101 is an important inflection point for Visara, NovaBridge, and our investors. It further de-risks the development of VIS-101 and provides greater visibility to the value-creation potential of NovaBridge’s global biotech platform and our unique “hub-and-spoke” business strategy of partnering with world-class industry leaders to identify and accelerate the development of highly differentiated innovative programs,” said Sean Fu, PhD, MBA, Chief Executive Officer of NovaBridge . “These results provide a helpful blueprint and offer an encouraging sign that we are well placed for success as we continue to build our portfolio.” About the Randomized Phase 2a Study of VIS-101 in Wet AMD Patient Characteristics: The study enrolled 38 patients in China, aged 50-80 years of age with wet AMD (both treatment naïve and pre-treated). Patients were randomized 2:1 between 6mg dose (n=25) and 3 mg (n=13). Baseline characteristics were similar between both dose groups (noting a slightly higher proportion of pre-treated patients in the 6 mg dosing group). Baseline Patient Demographics: Similar between dosing groups Topline Phase 2a Data Based on patients in the 6mg and 3mg dosing groups Dose level 6 mg (n=25) 3 mg (n=13) Total (n=38) Patients Age (years of age) • Average 69.5 71.5 Gender (%) • Male/Female 68%/32% 61.5%/38.5% 65.8%/34.2% Mean Baseline BCVA (Letters) 54.7 52.3 53.9 Median Baseline CST ( m m) 417.2 407.6 413.9 Prior Anti-VEGF Therapy (%) • Yes/No 52%/48% 30.8%/69.2% 44.7%/55.3% Safety: VIS-101 Demonstrated a Favorable Safety Pro No Dose-Limiting Toxicity The total treatment-related treatment emergent adverse events (TEAEs) were 0% (n=0) in the 3 mg dose and 8% (n=2) in the 6 mg dose, with 1 event each in two separate patients. Conference Call and Webcast NovaBridge will host an Investor Update call today, March 09, 2026, at 9:00 AM ET Registration link: Click here A replay of the webcast will be available on the News & Events page of the Investors section of the NovaBridge website for 90 days at: . About the Randomized Phase 2a Study of VIS-101 in Wet AMD The Phase 2a randomized study (NCT05456828) evaluated the safety and efficacy of VIS-101 (aka AM712 or ASKG712) in patients with wet AMD, including patients who were naïve to treatment or VEGF-experienced. The study enrolled a total of 38 wet AMD patients in China. Patients were randomized 2:1 to 6mg VIS-101 (n=25) or 3 mg VIS-101 (n=13). The primary endpoint was safety and pharmacokinetics and the secondary endpoint was efficacy, measured by best corrected visual acuity (BCVA) change from baseline (assessed by early treatment diabetic retinopathy scale (ETDRS Letters), change in central subfield thickness (CST, measured in mm), and retreatment rate. Subjects were given three loading doses at weeks 0, 4 and 8, with monthly follow-up to week 36 or retreatment (based on protocol-defined Disease Activity Criteria based on BCVA, CST and wet AMD activity). Safety and efficacy endpoints were assessed at each visit including 24 weeks (6 months) after the last loading dose. About VIS-101 VIS-101 (also known as ASKG712 or AM712), purpose-designed to be best-in-class, is a dual VEGF-A X ANG-2 inhibitor in development for the treatment of retinal vascular diseases, such as wet AMD, diabetic macular edema (DME) and retinal vein occlusion (RVO), which affect more than 57 million people globally 1 . VIS-101’s bispecific, tetravalent design format provides more binding sites and increased VEGF-A and ANG-2 affinity, for rapid, robust and class-leading durable responses. VIS-101 has completed initial safety and dose-escalation studies in both the US and China and a randomized, dose-ranging 2a study in China (NCT05456828). VIS-101 is expected to advance to a dose-determining Phase 2b study in 2026, with initiation of the global Phase 3 program in 2027. Source information: Invest Ophthalmol Vis Sci. 2021 Nov 24; 62 (14): 26. doi: 10.1167/iovs.62.14.26 About Visara, Inc. Visara is a clinical-stage biopharmaceutical company focusing on the development of best-in-class ophthalmic therapeutics. The Company is led by Co-Founder and Executive Chairman Emmett T. Cunningham, Jr., MD, PhD, MPH, a physician, innovator, entrepreneur, and investor and internationally recognized specialist in infectious and inflammatory eye disease, and Chief Medical Officer Cadmus Rich, MD, MBA, a serial entrepreneur and seasoned ophthalmic drug developer. NovaBridge is the majority shareholder of Visara, and Visara controls global rights to VIS-101, outside of Greater China and certain countries in Asia. About NovaBridge NovaBridge is a global biotechnology platform company committed to accelerating access to innovative medicines. The Company combines deep business development expertise with agile translational clinical development to identify, accelerate, and advance breakthrough assets. By bridging science, strategy, and execution, NovaBridge enables transformative therapies to progress rapidly from discovery toward patients in need. The Company’s differentiated pipeline is led by givastomig, a potential best-in-class, Claudin 18.2 X 4-1BB bispecific antibody, and VIS-101, purpose-designed to be a best-in-class dual VEGF-A X ANG-2 inhibitor. Givastomig conditionally activates T cells via the 4-1BB signaling pathway in the tumor microenvironment where Claudin 18.2 is expressed. Givastomig is being developed to treat Claudin 18.2-positive gastric cancer and other gastrointestinal malignancies. The product candidate is being evaluated in a global, randomized Phase 2 study, following the recent announcement of positive topline results from a Phase 1b, multi-center, open label study in first line gastric cancer. The Company is also collaborating with its partner, ABL Bio, for the development of ragistomig, a bispecific antibody integrating PD-L1 as a tumor engager and 4-1BB as a conditional T cell activator, in solid tumors. Additionally, NovaBridge owns worldwide rights outside of China to uliledlimab, an anti-CD73 antibody that targets adenosine-driven immunosuppression in cancer. VIS-101 targets VEGF-A and ANG-2 to provide more rapid, robust and durable treatment responses for patients with retinal vascular diseases including wet age-related macular degeneration, diabetic macular edema, and retinal vein occlusion. VIS-101 has completed a randomized, dose-ranging Phase 2a study for wet AMD and expects to initiate a Phase 2b study in H2 2026. NovaBridge is the majority shareholder of Visara, Inc., and Visara controls global rights to VIS-101, outside of Greater China and certain countries in Asia. For more information, please visit and follow us on LinkedIn. Forward Looking Statements This announcement contains forward-looking statements. These statements are made under the “safe harbor” provisions of the U.S. Private Securities Litigation Reform Act of 1995. These forward-looking statements can be identified by terminology such as “will”, “expects”, “believes”, “designed to”, “anticipates”, “future”, “intends”, “plans”, “potential”, “estimates”, “confident”, and similar terms or the negative thereof. NovaBridge may also make written or oral forward-looking statements in its periodic reports to the U.S. Securities and Exchange Commission (the SEC), in its annual report to shareholders, in press releases and other written materials and in oral statements made by its officers, directors or employees to third parties. Statements that are not historical facts, including statements about the Company’s beliefs and expectations, are forward-looking statements. Forward-looking statements in this press release include, without limitation, statements regarding: the strategy, clinical development, plans, results, safety and efficacy givastomig, VIS-101 and its other drug candidates; the strategic and clinical development of NovaBridge’s drug candidates, including givastomig, ragistomig, uliledlimab, and VIS-101; the impact of independent evaluations of our clinical trial results; anticipated clinical milestones and results, and related timing. Forward-looking statements involve inherent risks and uncertainties that may cause actual results to differ materially from those contained in these forward-looking statements, including but not limited to the following: the Company’s ability to demonstrate the safety and efficacy of its drug candidates; the clinical results for its drug candidates, which may or may not support further development or New Drug Application/Biologics License Application (NDA/BLA) approval; the content and timing of decisions made by the relevant regulatory authorities regarding regulatory approval of the Company’s drug candidates; the Company’s ability to achieve commercial success for its drug candidates, if approved; the Company’s ability to obtain and maintain protection of intellectual property for its technology and drugs; the Company’s reliance on third parties to conduct drug development, manufacturing and other services; the Company’s limited operating history and the Company’s ability to obtain additional funding for operations and to complete the development and commercialization of its drug candidates; and those risks more fully discussed in the “Risk Factors” section in the Company’s annual report on Form 20-F filed with the SEC on April 3, 2025 as well as the discussions of potential risks, uncertainties, and other important factors in the Company’s subsequent filings with the SEC. All forward-looking statements are based on information currently available to the Company. The Company undertakes no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events, or otherwise, except as may be required by law. NovaBridge Investor & Media Contacts PJ Kelleher LifeSci Advisors +1-617-430-7579 pkelleher@lifesciadvisors.com NovaBridge Biosciences +1-240-745-6330 IR@novabridge.com

临床2期临床结果临床1期临床3期

100 项与 Givastomig 相关的药物交易

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研发状态

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适应症	最高研发状态	国家/地区	公司	日期
CLDN18.2阳性胃腺癌	临床2期	美国	天境生物科技（上海）有限公司	2026-03-03
CLDN18.2阳性胃腺癌	临床2期	中国	天境生物科技（上海）有限公司	2026-03-03
CLDN18.2阳性胃腺癌	临床2期	日本	天境生物科技（上海）有限公司	2026-03-03
CLDN18.2阳性胃腺癌	临床2期	韩国	天境生物科技（上海）有限公司	2026-03-03
PD-L1阳性胃食管交界处腺癌	临床2期	美国	天境生物科技（上海）有限公司	2026-03-03
PD-L1阳性胃食管交界处腺癌	临床2期	中国	天境生物科技（上海）有限公司	2026-03-03
PD-L1阳性胃食管交界处腺癌	临床2期	日本	天境生物科技（上海）有限公司	2026-03-03
PD-L1阳性胃食管交界处腺癌	临床2期	韩国	天境生物科技（上海）有限公司	2026-03-03
PD-L1阳性胃腺癌	临床2期	美国	天境生物科技（上海）有限公司	2026-03-03
PD-L1阳性胃腺癌	临床2期	中国	天境生物科技（上海）有限公司	2026-03-03

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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


NCT04900818 (Company_Website) 人工标引	临床1期	CLDN18.2阳性胃癌 \| HER2阴性胃癌一线 HER2 Negative \| CLDN18.2 Positive	54	Givastomig 8 mg/kg	網選鏇網糧願積顧憲繭(獵衊廠網鬱鹽廠廠齋獵) = 壓壓襯憲蓋鹹築選鹽壓齋膚憲蓋廠簾窪淵簾齋 (鑰鑰艱艱廠鑰夢鑰蓋夢 ) 更多	积极	2026-01-06
				Givastomig 12 mg/kg	網選鏇網糧願積顧憲繭(獵衊廠網鬱鹽廠廠齋獵) = 衊淵遞壓獵鬱獵獵壓顧齋膚憲蓋廠簾窪淵簾齋 (鑰鑰艱艱廠鑰夢鑰蓋夢 ) 更多
Pubmed 人工标引	N/A	CLDN18.2阳性实体瘤 \| CLDN18.2阳性胃食管交界处癌 CLDN18.2 Positive	75	Givastomig	壓構淵廠遞齋網糧積鑰(鹽觸餘鏇餘夢廠構蓋積) = No DLT were reported up to 18 mg/kg 壓蓋遞繭簾製艱鬱艱鏇 (鹹獵構艱衊範壓願餘窪 ) 更多	积极	2025-06-30
NCT04900818 (ESMO_GI2025 \| GlobeNewswire) 人工标引	临床1期	PD-L1阳性胃癌一线	17	Givastomig	糧壓遞獵襯鑰窪遞築願(積構衊餘齋獵糧艱鏇餘) = No dose limiting toxicities (DLT) were observed 艱遞襯憲積築襯獵構構 (窪餘繭壓夢選觸廠鹽憲 ) 更多	积极	2025-06-26
				Givastomig 8 and 12 mg/kg
NCT04900818 (SITC2024) 人工标引	临床1期	晚期胃食管交界处腺癌 CLDN18.2 Positive	-	givastomig	壓壓構衊願廠製選製顧(鏇夢鹹艱餘顧鹹繭簾構) = 鹽鹹觸糧廠網築構齋繭鏇憲鏇膚製襯淵鏇艱襯 (憲襯窪膚鏇艱鏇願襯壓 )	积极	2024-11-05
NCT04900818 (ESMO2024 \| Company_Website) 人工标引	临床1期	食管癌 \| CLDN18.2阳性胃癌 CLDN18.2 positive	39	givastomig/kg	憲繭築窪蓋壓願醖醖鬱(繭遞構壓齋膚觸遞齋鑰) = 糧餘築構選鹽繭選餘製鏇鬱獵鑰壓膚網繭膚淵 (觸築蓋鑰鏇構範網鹹鹽 ) 更多	积极	2024-09-14
NCT04900818 (ESMO 12023 \| ESMO 22023) 人工标引	临床1期	实体瘤 CLDN18.2 Positive	50	Givastomig	壓願壓顧簾鬱窪構廠鏇(築齋憲選鹽膚構鏇糧廠) = 窪壓壓廠憲顧製淵積獵襯鏇積顧窪簾顧鑰鹹顧 (製簾選膚衊餘窪淵觸壓 ) 更多	积极	2023-10-23
				Givastomig (CLDN18.2+ gastroesophageal cancer)	餘壓願願鬱鏇夢鏇選鑰(範選鑰繭簾憲構選製夢) = 餘膚廠網範鹽繭鬱齋製鏇繭蓋壓範網憲積廠獵 (範壓壓簾繭鹹膚淵積選 ) 更多