On March 17, 2026 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, reported that it will present results from three preclinical studies in poster presentations at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting (AACR 2026), taking place from April 17th to 22th, at the San Diego Convention Center, California, the United States. 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 cancers and NSCLC.
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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 overexpressed in a wide range of solid tumors and are associated with immune evasion and poor prognosis. ATG-125 is a novel bispecific ADC designed to simultaneously target B7-H3 and PD-L1, enabling targeted cytotoxic payload delivery while modulating immune checkpoint signaling. Preclinical studies evaluated binding affinity, internalization, cytotoxicity, immune activation, and antitumor efficacy in solid tumor models.
Results: ATG-125 demonstrated strong binding to both B7-H3 and PD-L1 and efficient antigen-dependent internalization, enabling intracellular release of a topoisomerase I inhibitor payload. The molecule showed potent target-dependent cytotoxicity across multiple solid tumor cell lines and enhanced T-cell activation in immune assays. In xenograft models, ATG-125 induced marked tumor regression and demonstrated superior antitumor activity compared with single-target ADC comparators.
Conclusion: ATG-125 represents a differentiated bispecific ADC strategy that integrates targeted cytotoxicity with immune checkpoint modulation, supporting its potential as a next-generation therapy for 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: Cadherin-6 (CDH6) plays a critical role in embryonic kidney development but shows minimal expression in normal adult tissues. However, CDH6 is frequently overexpressed in several cancers including ovarian and renal cancer, making it a promising therapeutic target. ATG-106 is a novel "2+1" CDH6 x CD3 T-cell engager designed with a sterically masked CD3 binding arm to enable tumor-dependent T-cell activation. ATG-106 was evaluated in a series of in vitro and in vivo studies including binding affinity, CD3 signaling pathway activation, T cell dependent cytotoxicity (TDCC), cytokine release, and antitumor activity in PBMC-humanized xenograft models.
Results: ATG-106 demonstrated reduced binding affinity to CD3-positive cells prior to CDH6 engagement while inducing significantly enhanced cytotoxic activity against CDH6-positive tumor cells compared with conventional TCE formats. In PBMC-humanized xenograft models of renal and ovarian cancer, ATG-106 induced robust tumor regression with complete responses observed in multiple treatment groups. Cytokine analysis showed minimal induction of pro-inflammatory cytokines, suggesting a potentially reduced risk of cytokine release syndrome.
Conclusion: ATG-106 demonstrated potent CDH6-dependent T-cell activation and strong antitumor activity with a favorable cytokine profile in preclinical models, supporting further development as a potential therapy for CDH6-expressing solid tumors.
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 (ALPP) and related placental-like/germ-cell isoforms (ALPPL2 / ALPG) are aberrantly expressed in multiple solid tumors including ovarian, endometrial, gastric and pancreatic cancers, while being largely absent in normal adult tissues. ATG-112 is a novel ALPP/G x CD3 bispecific T-cell engager developed using the AnTenGager platform, featuring bivalent binding to tumor antigens and a sterically masked CD3 arm to restrict T-cell activation to the tumor microenvironment. The molecule was evaluated in preclinical studies assessing antigen binding, T cell dependent cytotoxicity, cytokine release and antitumor activity.
Results: ATG-112 demonstrated high binding affinity to ALPP/G-positive tumor cells and induced potent antigen-dependent T cell-mediated cytotoxicity in vitro. In PBMC humanized xenograft tumor models, ATG-112 showed dose-dependent tumor growth inhibition and robust antitumor activity. Cytokine release assays demonstrated minimal cytokine production, indicating a favorable safety profile with potentially reduced risk of excessive immune activation.
Conclusion: ATG-112 demonstrated potent antigen-dependent T cell-mediated cytotoxicity and robust antitumor activity with minimal cytokine release in preclinical models, supporting its advancement toward clinical development for ALPP/G-positive solid tumors.
(Press release, Antengene, MAR 17, 2026, View Source [SID1234663640])