SHANGHAI and HONG KONG, April 18, 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 disease, solid tumors and hematological malignancies indications, today announced that it has released present results from three novel programs in poster presentations at the 2026 American Association for Cancer Research Annual Meeting (AACR 2026). The presentations will feature ATG-125 (B7-H3 x PD-L1 bispecific antibody-drug conjugate [ADC]), an IO + ADC dual-function molecule being developed for the treatment of solid tumors, as well as two investigational T cell engagers (TCEs) developed using the company’s proprietary AnTenGager® TCE platform, including ATG-106 (CDH6 x CD3 TCE) for ovarian and kidney cancers, and ATG-112 (ALPPL2 x CD3 TCE) for gynecological tumors, digestive system malignancies, bladder cancer and NSCLC.
Details of the Poster Presentation:
ATG-125 (B7-H3 x PD-L1 bispecific ADC)
Title: ATG-125, a novel B7H3 x PD-L1 bispecific antibody-drug conjugate, demonstrates potent antitumor efficacy by dual targeting of immune evasion and direct tumor killing
Abstract Number: 5599
Session Category: Immunology
Session Title: T Cell Engagers 2 / Antibody-Drug Conjugates 1
Date: April 21, 2026
Time: 02:00 PM – 05:00 PM (Pacific Time)
05:00 AM, April 22, 2026 – 08:00 AM, April 22, 2026 (Beijing Time)
Location: Poster Section 8
- Introduction: B7-H3 and PD-L1 are immune checkpoint molecules broadly overexpressed across multiple solid tumors and are associated with immune evasion and poor prognosis. Although PD-1/PD-L1-directed therapies have demonstrated clinical benefit, treatment resistance remains a significant challenge. B7-H3 is also emerging as a promising ADC target due to its broad tumor expression and rapid internalization. ATG-125 is a novel B7-H3 x PD-L1 bispecific ADC designed to combine direct tumor killing with immune activation by co-targeting two complementary tumor-associated pathways in a single molecule.
- Results: ATG-125 bound to both B7-H3 and PD-L1 with high specificity and nanomolar affinity and demonstrated robust antigen-dependent internalization in dual-positive tumor cells, enabling efficient intracellular payload release. The molecule induced tumor cell apoptosis, while its parental naked antibody blocked PD-1/PD-L1 interaction and elicited IL-2 and IFN-γ production in mixed lymphocyte reaction assays. ATG-125 also enhanced T-cell activation, as reflected by an increased ratio of CD69+/CD3+ T cells in co-cultures of tumor cells and human PBMCs. In vivo, ATG-125 demonstrated sustained antitumor activity in HCC827 xenograft models, increased tumor infiltration of CD4+ and CD8+ T cells in PBMC-humanized models, and inhibited tumor growth in a dose-dependent manner in MC38-hB7H3 syngeneic models, accompanied by elevated intratumoral CD8+ T-cell infiltration.
- Conclusion: ATG-125 demonstrated synergistic IO+ADC antitumor activity through a differentiated mechanism combining enhanced internalization for payload delivery with the potential to restore anti-tumor immunity. Its compelling preclinical profile supports further development for patients with solid tumors.
ATG-106 (CDH6 x CD3 TCE)
Title: ATG-106, a novel “2+1” format CDH6-targeted T-cell Engager (TCE), shows potent T cell dependent cytotoxicity and in vivo anti-tumor efficacy
Abstract Number: 1621
Session Category: Immunology
Session Title: T Cell Engagers 1
Date: April 20, 2026
Time: 09:00 AM – 12:00 PM (Pacific Time)
00:00 AM, April 21, 2026 – 03:00 AM, April 21, 2026 (Beijing Time)
Location: Poster Section 10
- Introduction: CDH6 plays an important role in embryonic kidney development but has negligible expression in adult kidney tissue. Its overexpression in ovarian and renal cancers, together with limited normal tissue expression, makes CDH6 an attractive therapeutic target. However, T cell engagers in solid tumors have often been limited by insufficient efficacy and the risk of cytokine release syndrome. To address these challenges, Antengene developed ATG-106, a novel “2+1”, sterically masked CDH6 x CD3 bispecific TCE designed to deliver potent antitumor activity with the potential for a reduced CRS risk profile.
- Results: ATG-106 exhibited reduced binding affinity to CD3+ cells before CDH6 crosslinking, while inducing approximately 100- to 400-fold more potent cytotoxicity against CDH6-positive tumor cells compared with a “1+1” CrossMab control TCE. The molecule demonstrated potent T cell-dependent cytotoxicity in ovarian and renal cancer models and showed low immunogenicity risk in vitro. In PBMC-humanized 786-O kidney cancer xenograft models, ATG-106 induced tumor shrinkage in all treated mice, with complete remissions observed in the 0.1 mg/kg and 0.3 mg/kg groups. ATG-106 also induced tumor shrinkage and complete remission in PBMC-humanized OVCAR-3 ovarian cancer models. Notably, pro-inflammatory cytokine levels remained very low in treated animals, suggesting low CRS risk. In non-human primate studies, the surrogate molecule ATG-106-RM was well tolerated at doses up to 10 mg/kg.
- Conclusion: ATG-106 demonstrated limited T cell binding in the absence of target cells, potent cytotoxicity against tumor cells, and encouraging in vivo efficacy in ovarian and kidney cancer models. Favorable safety findings with the surrogate molecule in non-human primates further support continued clinical development of ATG-106 as a CDH6-targeted TCE candidate.
ATG-112 (ALPPL2 x CD3 TCE)
Title: ATG-112, a novel ALPP/G x CD3 bispecific T cell engager, for the treatment of ALPP/G+ solid tumors
Abstract Number: 1620
Session Category: Immunology
Session Title: T Cell Engagers 1
Date: April 20, 2026
Time: 09:00 AM – 12:00 PM (Pacific Time)
00:00 AM, April 21, 2026 – 03:00 AM, April 21, 2026 (Beijing Time)
Location: Poster Section 10
- Introduction: Placental alkaline phosphatase and related placental-like/germ-cell isoforms, including ALPPL2 and ALPG, are aberrantly expressed in a range of solid tumors while being largely absent from normal adult tissues except the placenta, making them highly promising tumor-selective immunotherapy targets. Antengene developed ATG-112, an ALPP/G x CD3 bispecific TCE based on the AnTenGager® platform in a “2+1” format, featuring bivalent antigen binding to improve low-antigen tumor recognition and a sterically masked CD3 binding arm designed to restrict T-cell activation to the tumor microenvironment.
- Results: Tissue microarray IHC analysis showed that ALPP/G expression was restricted to placental tissue among normal organs and was not detected in other normal tissues, while frequent expression was observed in endometrial and ovarian cancers, with lower prevalence in bladder, gastric and pancreatic cancers. ATG-112 demonstrated high binding affinity to both ALPP/G-positive tumor cells and recombinant proteins, with EC50 and KD values in the sub-nanomolar range. It induced robust T cell-dependent cytotoxicity against target-positive cells with picomolar EC50 values, while in vitro cytokine-release assays showed minimal cytokine secretion from human PBMCs. In vitro studies also demonstrated that the spatial masking effect of ATG-112 is reversible. Immunogenicity assessment showed low immunogenic potential, and in vivo ATG-112 delivered potent tumor suppression across multiple dose levels in humanized mouse models, with low cytokine release and controllable CRS risk at efficacious doses. The program also demonstrated strong developability characteristics.
- Conclusion: ATG-112 demonstrated a compelling preclinical profile, with potent in vitro and in vivo antitumor activity and minimal cytokine release. These findings support the continued advancement of ATG-112 toward clinical development for solid tumors.
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 and includes several in-house discovered programs, including ATG-022 (CLDN18.2 ADC), ATG-037 (oral CD73 inhibitor), ATG-101 (PD-L1 x 4-1BB bispecific antibody), and ATG-125 (B7-H3 × PD-L1 bispecific ADC).
Antengene has also developed AnTenGager®, a proprietary T cell engager 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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