Evidence map›Paper›PMID 41969434›Full record

ArticleTranslational cancer research2026

The claudin-18.2-CD3 bispecific antibody IBI389 exerts an antitumor effect on malignant tumors with positive claudin-18.2 expression by promoting T-cell infiltration and remodeling the tumor immune microenvironment.

Yajie Zhu, Xiaorong Liu, Chenliang Zhang, Shuang Zhou, Di Ye, Qiulin Tang, Hengyi Xiao, Feng Bi

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PubMed Full text at PMC Publisher
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Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Yajie Zhu *Laboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Xiaorong Liu *School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Chenliang ZhangLaboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Shuang ZhouLaboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Di YeLaboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Qiulin TangLaboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Hengyi XiaoThe Lab of Aging Research, National Clinical Research Center for Geriatrics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Feng BiLaboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Gastric cancer is one of the most lethal malignancies in the world, but effective therapeutic options for patients with this disease remain limited. Claudin-18.2 (CLDN18.2) has emerged as a promising therapeutic target, yet the functional role of CLDN18.2 and the mechanisms of CLDN18.2-directed immunotherapy remain poorly understood. This study aims to explore the antitumor effects and related mechanisms of the CLDN18.2-CD3 bispecific antibody. Methods: The antitumor efficacy and immunological mechanisms of the CLDN18.2-CD3 bispecific antibody IBI389 were evaluated through two preclinical models: a human peripheral blood mononuclear cell (PBMC)-reconstituted AGS xenograft and a B-hCD3EDG murine KPC pancreatic cancer model. Stable CLDN18.2-overexpressing cell lines were established for Results: CLDN18.2 overexpression enhanced the proliferation and migration of gastric and pancreatic cancer cells Conclusions: In this study, we demonstrated that IBI389 effectively redirects T cells to CLDN18.2-expressing tumors, suppresses tumor growth, and synergizes with PD-1 blockade and has a favorable safety profile. By virtue of its ability to enhance immune infiltration, remodel cytokine responses, and reduce tumor-immune spatial separation, IBI389 may have considerable potential as a novel therapeutic strategy for CLDN18.2-positive gastric cancer and related malignancies.

Indexed as

bispecific antibodyClaudin-18.2 (CLDN18.2)gastric cancerprogrammed death-1 blockade (PD-1 blockade)tumor immune microenvironment (TIME)

Identifiers

PMID41969434
PMCPMC13067181

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