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

- Link: https://www.thailand-business-news.com/pr-news/antengene-presents-latest-preclinical-results-of-atg-207-%ce%b1cd3-tgf-%ce%b2-bifunctional-fusion-protein-at-acr-2026
- Published: 2026-11-12T10:21:00+07:00
- Author: PR Newswire

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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 QianE-mail: [peter.qian@antengene.com](https://www.thailand-business-news.com/pr-news/peter.qian@antengene.com)

BD Contacts:
Ariel GuoE-mail: [ariel.guo@antengene.com](https://www.thailand-business-news.com/pr-news/ariel.guo@antengene.com)

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