Antengene Presents Latest Preclinical Results of ATG-207 (αCD3-TGF-β Bifunctional Fusion Protein) at ACR 2026

SHANGHAI and HONG KONG, Nov. 12, 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 latest preclinical results of ATG-207 (αCD3-TGF-β Bifunctional Fusion Protein) in a Poster Presentation at the 2026 American College of Rheumatology (ACR) Annual Meeting. ATG-207 is our proprietary, globally first-in-class αCD3-TGF-β bifunctional fusion protein being developed for the treatment of T cell–mediated autoimmune diseases.

Details of the Poster Presentation

Title: Preclinical Characterization of ATG-207, a Masked and TGFβRIII-Biased αCD3-TGF-β Fusion Protein, for the Treatment of T Cell-Related Autoimmune Diseases
Poster: #0974
Session: Poster Session B, (0965-0976) T Cell Biology & Targets in Autoimmune & Inflammatory Disease Poster B

Study Overview:

• T cell–mediated autoimmune diseases are characterized by persistent pathogenic effector T-cell activity and inadequate regulatory T-cell (Treg) function, resulting in loss of durable immune tolerance. Therapies that restore immune balance through Treg induction are therefore of significant interest. Transforming growth factor-beta (TGF-β) is a pivotal cytokine for Treg differentiation and maintenance, yet its systemic delivery is clinically restricted by broad receptor engagement that raises significant safety concerns.
• ATG-207 was developed by introducing a peptide-masked and TGFβRIII-biased TGF-β domain to an anti-CD3 antibody. ATG-207 achieves precision T cell targeting through CD3 engagement, which localizes the molecule to the T cell surface and enables spatially restricted signaling. It controls TGF-β activity via dynamic masking, as a conformationally dynamic mask reduces systemic receptor engagement and minimizes off-target TGF-β activity. ATG-207 drives TGFβRIII-biased signaling with preferential engagement of TGFβRIII to enhance TGF-β responsiveness in T cells while potentially limiting activity in non-T cell compartments. Collectively, these features support coordinated immune tolerance induction, since ATG-207 promotes regulatory T cell (Treg) induction and controlled attenuation of pathogenic T cell activity.

Results:

• Binding affinity of ATG-207 to different TGF-β receptors was assessed using surface plasmon resonance (SPR). The results showed that ATG-207 exhibited a preference for binding to TGFβRIII compared to TGFβRII.
• SPR assay showed that ATG-207 exhibited 100-fold reduced TGFβR binding compared with unmasked TGF-β. In contrast, relative to masked TGF-β (M-TGF-β), the CD3-targeting moiety enhanced ATG-207-mediated TGF-β downstream signaling in CD3⁺ T cells. These findings demonstrate that ATG-207 induces CD3-dependent TGF-β signaling.
• ATG-207 induced functional iTreg in vitro. CD4⁺ T cells isolated from the indicated donors were stimulated with the indicated agents for 5 days. FOXP3 expression was determined by flow cytometry, and surface functional markers of iTreg were characterized to verify phenotypic features. Functional assays further confirmed that ATG-207-induced iTregs potently suppressed T cell proliferation and possessed immune-suppressive activity.
• TCR expression on T cell surface. Flow cytometric analysis of TCR membrane expression on primary T cells after 1-hour incubation with the indicated agents at 37°C. The results showed that ATG-207 significantly reduced the expression of TCR on the surface of primary T cells.
• Mouse surrogate-ATG-207 demonstrated potent efficacy in both mouse experimental autoimmune encephalomyelitis (EAE) and inflammatory bowel disease (IBD) in vivo models.
• ATG-207 showed robust therapeutic efficacy in both CD3-humanized EAE model and B16F10 melanoma-induced vitiligo model using CD3 humanized mice.
• ATG-207 and mATG-207 were well tolerated in mouse toxicology studies.

Conclusion: ATG-207 combines CD3-mediated T cell modulation with TGFβRIII-biased TGF-β signaling to suppress pathogenic T cells while promoting regulatory T cell differentiation. These preclinical findings support receptor-biased, context-restricted TGF-β delivery as a potential strategy for durable immune tolerance restoration in T cell–mediated autoimmune 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 diseases, 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; partnered with K2 Therapeutics established by MPM BioImpact), 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 35 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:

PR / IR Contacts: 
Peter Qian
E-mail: [email protected]

BD Contacts:
Ariel Guo
E-mail: [email protected]

SOURCE Antengene Corporation Limited