Antengene presents first ATG-207 preclinical data on immune tolerance at EULAR 2026

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.