en.Wedoany.com Reported - Antengene Corporation Limited (HKEX: 6996.HK) presented preclinical data for ATG-207, an alpha-masked, TGFβRIII-preferring CD3-TGF-β bifunctional fusion protein, for the first time in a poster presentation at the 2026 European Congress of Rheumatology (EULAR 2026). The data showed that ATG-207 preferentially binds to TGFβRIII over TGFβRII, rapidly downregulating T cell receptor expression and inducing regulatory T cells.
The congress was held from June 3 to 6 at the ExCeL London in the United Kingdom. Antengene is an innovative biotechnology company focused on autoimmune diseases, solid tumors, and hematological malignancies. The disclosed preclinical data demonstrated that ATG-207 preferentially binds to TGFβRIII over TGFβRII, significantly reducing T cell receptor (TCR) expression on the surface of primary T cells, and exhibiting potent induction of regulatory T cell activity in CD4+ T cells from both healthy donors and donors with systemic lupus erythematosus. Proteomics analysis revealed that ATG-207 significantly modulates functional remodeling of primary T cells. In mouse models, a surrogate molecule of ATG-207 showed potent therapeutic activity in experimental autoimmune encephalomyelitis (a multiple sclerosis model) and adoptive T cell transfer colitis (an inflammatory bowel disease model), and was associated with significantly reduced pro-inflammatory cytokine release compared to a non-preferential αCD3-TGF-β fusion protein control.
ATG-207 is designed to localize activity to T cells by binding to CD3, while delivering controlled, TGFβRIII-preferring TGF-β signaling. Its dynamic masking mechanism aims to reduce systemic receptor binding and limit off-target TGF-β activity. In human whole blood assays, ATG-207 induced minimal production of pro-inflammatory cytokines such as IL-2, IL-6, TNF-α, and IFN-γ. Antengene believes that ATG-207 represents a differentiated immune tolerance restoration strategy, integrating precise T cell targeting, context-restricted TGF-β activity, and TGFβRIII-preferring signaling. These preclinical data support its potential as a next-generation therapeutic for T cell-mediated autoimmune and inflammatory diseases.
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