SHANGHAI and HONG KONG, June 8, 2026 /PRNewswire/ — Antengene Corporation Limited (“Antengene”, SEHK: 6996.HK) , a leading innovative, commercial-stage global biotech company dedicated to discovering, developing and commercializing first-in-class and/or best-in-class medicines for autoimmune diseases, solid tumors and hematological malignancies indications, today announced that it has presented the first preclinical data on ATG-207, α masked and TGFβRIII-biased CD3-TGF-β bifunctional fusion protein in a poster presentation at the 2026 European Congress of Rheumatology (EULAR 2026), held from June 3 to 6 at Excel London in the United Kingdom. The data showed that ATG-207 preferentially binds TGFβRIII, rapidly downregulates T cell receptor expression on the T cell surface, induces regulatory T cells. Proteomic analysis revealed that ATG-207 markedly modulates functional remodeling of primary T cells. ATG-207 demonstrated potent therapeutic activity through a mouse surrogate molecule in experimental autoimmune encephalomyelitis and adoptive T cell transfer colitis mouse models, and was associated with substantially reduced proinflammatory cytokine release compared with an unbiased αCD3-TGF-β fusion protein control.
Details of the Poster
Title: A masked and TGFβRIII-biased αCD3-TGF-β fusion protein promotes regulatory T cell induction and immune tolerance
Poster Number: POS-1110
Track: Basic and Translational
Topic: Across diseases
Sub-Topic: Adult Rheumatology
Introduction: T cell-mediated autoimmune diseases are characterized by sustained activation of pathogenic effector T cells and insufficient or unstable regulatory T cell function, resulting in an inability to establish durable immune tolerance. These diseases remain an area of significant unmet medical need, as existing anti-inflammatory therapies may not sufficiently eliminate persistent pathogenic effector T cells or restore long-term immune balance. ATG-207 is designed to address these challenges through a differentiated dual mechanism that integrates CD3-mediated T cell modulation with localized, TGFβRIII-biased TGF-β activity, with the goal of selectively suppressing pathogenic T cells while promoting regulatory T cell induction and immune tolerance.
Mechanism of Action: ATG-207 is designed to localize activity to T cells through CD3 engagement while delivering controlled, TGFβRIII-biased TGF-β signaling. Its dynamic masking is intended to reduce systemic receptor engagement and limit off-target TGF-β activity. By preferentially engaging TGFβRIII over TGFβRII, ATG-207 promotes TGF-β responsiveness in T cells while potentially minimizing activity in non–T cell compartments. This coordinated mechanism supports regulatory T cell induction and attenuation of pathogenic T cell activity.
Results: ATG-207 showed preferential binding to TGFβRIII compared with TGFβRII and significantly reduced T cell receptor (TCR) expression on the surface of primary T cells. In healthy donor and systemic lupus erythematosus patient donor CD4+ T cells, ATG-207 demonstrated potent induced regulatory T cell activity, as measured by FOXP3 expression. Proteomic profiling of primary T cells treated with ATG-207 showed evidence of T cell functional remodeling, including changes in pathways associated with T cell signaling and immune regulation. In vivo, a mouse surrogate of ATG-207 demonstrated therapeutic activity in both experimental autoimmune encephalomyelitis, a multiple sclerosis model, and adoptive T cell transfer colitis, an inflammatory bowel disease model. In human whole blood assays, ATG-207 induced minimal production of pro-inflammatory cytokines, including IL-2, IL-6, TNF-α, and IFN-γ.
Conclusion: ATG-207 represents a differentiated immune tolerance–restoring strategy that integrates precision T cell targeting, context-restricted TGF-β activity, and TGFβRIII-biased signaling. The preclinical data support its potential as a next-generation therapeutic approach for T cell–mediated autoimmune and inflammatory diseases.
About Antengene
Antengene Corporation Limited (“Antengene”, SEHK: 6996.HK) is a global, R&D-driven, commercial-stage biotech company focused on developing first-in-class/best-in-class therapeutics for diseases with significant unmet medical needs. Its pipeline spans from preclinical to commercial stages, with key investigational candidates including ATG-022 (CLDN18.2 ADC), ATG-037 (oral CD73 inhibitor), ATG-101 (PD-L1 x 4-1BB bispecific antibody), ATG-125 (B7-H3 × PD-L1 bispecific ADC), ATG-207 (αCD3-TGF-β bifunctional fusion protein), as well as T cell engager (TCE) programs developed using Antengene’s proprietary AnTenGager® platform.
AnTenGager® is Antengene’s proprietary TCE 2.0 platform, featuring “2+1” bivalent binding for low expressing targets, steric hindrance masking, and proprietary CD3 sequences with fast on/off kinetics to minimize cytokine release syndrome (CRS) and enhance efficacy. These characteristics support the platform’s broad applicability across autoimmune disease, solid tumors and hematological malignancies, with programs targeting CD19 x CD3 (ATG-201 for B cell-related autoimmune diseases; partnered with UCB), CDH6 x CD3 (ATG-106 for ovarian cancer and kidney cancer), ALPPL2 x CD3 (ATG-112 for gynecological tumors, digestive system malignancies, bladder cancer and NSCLC), LY6G6D x CD3 (ATG-110 for microsatellite-stable colorectal cancer), GPRC5D x CD3 (ATG-021 for multiple myeloma), LILRB4 x CD3 (ATG-102 for acute myeloid leukemia and chronic myelomonocytic leukemia) and FLT3 x CD3 (ATG-107 for acute myeloid leukemia).
To date, Antengene has obtained 32 investigational new drug (IND) approvals in the U.S. and Asia, and obtained new drug application (NDA) approvals in 10 Asia Pacific markets. Its lead commercial asset, XPOVIO® (selinexor), is approved in the Mainland of China, Taiwan China, Hong Kong China, Macau China, South Korea, Singapore, Malaysia, Thailand, Indonesia and Australia, and has been included in the national insurance schemes in five of these markets (Mainland of China, Taiwan China, Australia, South Korea and Singapore).
Forward-looking statements
The forward-looking statements made in this article relate only to the events or information as of the date on which the statements are made in this article. Except as required by law, we undertake no obligation to update or revise publicly any forward-looking statements, whether as a result of new information, future events or otherwise, after the date on which the statements are made or to reflect the occurrence of unanticipated events. You should read this article completely and with the understanding that our actual future results or performance may be materially different from what we expect. In this article, statements of, or references to, our intentions or those of any of our Directors or our Company are made as of the date of this article. Any of these intentions may alter in light of future development. For a further discussion of these and other factors that could cause future results to differ materially from any forward-looking statement, please see the other risks and uncertainties described in the Company’s Annual Report for the year ended December 31, 2025, and the documents subsequently submitted to the Hong Kong Stock Exchange.
For more information, please contact:
Investor Contacts:
Donald Lung
E-mail: [email protected]
BD Contacts:
Ariel Guo
E-mail: [email protected]
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