On April 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 has released present results from three novel programs in poster presentations at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) 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.

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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 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.

(Press release, Antengene, APR 17, 2026, View Source [SID1234664488])

On April 17, 2026 intoDNA, a global precision medicine company that provides biopharma and clinicians with decision-grade insights into DNA damage and repair biology to reduce risk, accelerate timelines, and enable truly precise patient care, reported it will present two posters at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, being held April 17-22, 2026 in San Diego, California.

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AACR poster presentation details are below:

Title: Direct measurement of NER activity using sSTRIDE-NER
Date: April 20, 2026, 9:00 a.m. – 12:00 p.m.
Track: Experimental and Molecular Therapeutics
Session: DNA Damage and Repair 2
Section: 14

Title: In situ measurement of PARP1 activity and trapping at single-strand DNA breaks
Date: April 22, 2026, 9:00 a.m. – 12:00 p.m.
Track: Experimental and Molecular Therapeutics
Session: Late-Breaking Research: Experimental and Molecular Therapeutics 4
Section: 53

intoDNA’s poster presentation titled, Direct measurement of NER activity using sSTRIDE-NER, demonstrates that a new assay based on the STRIDE (SensiTive Recognition of Individual DNA Ends) platform, showed:

High specificity: multiple negative technical controls yielded minimal background signal.
A time-dependent increase in nuclear signal intensity, consistent with accumulation of NER-associated SSBs.
Potential to investigate mechanisms of resistance to platinum drugs, to evaluate DNA repair-targeting agents, and to support the development of functional biomarkers predictive of therapy response.
New opportunities to functionally and spatially profile NER capacity in cancer cell models and patient-derived tissue samples.
intoDNA’s poster presentation titled, In situ measurement of PARP1 activity and trapping at single-strand DNA breaks, demonstrates that sSTRIDE-PARP1, a novel in situ assay:

Directly detects PARP1 localized at single-strand DNA breaks at single-cell resolution.
Enables direct, quantitative and functional measurement of PARP1 engagement at damaged DNA within intact cells.
Distinguishes cell lines with different basal levels of PARylation and PARP1 activity.
Provides a translational platform for mechanistic characterization of PARP inhibitors, comparative profiling of PARPi trapping capacity, and development of functional biomarkers to support patient stratification, drug development, and resistance studies in DNA damage response-targeted therapies.
"Current precision medicine approaches fall short and intoDNA envisions a future where the right therapies reach the right patients, at the right time. With our panel of novel assays, biopharma and clinicians gain decision-grade insights into DNA damage and repair biology to reduce risk, accelerate timelines, and enable truly precise patient care," said Magda Kordon-Kiszala, PhD, Founder and CEO of intoDNA.

Posters are available on the intoDNA website.

(Press release, intoDNA, APR 17, 2026, View Source [SID1234664504])

On April 17, 2026 ORIC Pharmaceuticals, Inc. (Nasdaq: ORIC), a clinical stage oncology company focused on developing treatments that address mechanisms of therapeutic resistance, reported the presentation of multiple poster presentations at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting highlighting the potential of rinzimetostat (ORIC-944), a potent and selective allosteric inhibitor of PRC2 to treat prostate cancer. The posters can be found in the publication section of ORIC’s website here.

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"Our research continues to show the therapeutic potential of PRC2 inhibition across the prostate cancer disease spectrum, by reducing tumor adaptability and sustaining the benefit derived from androgen-receptor targeted therapies," said Lori Friedman, PhD, chief scientific officer. "Additionally, our preclinical studies reveal that targeting PRC2 via EED has potential advantages over targeting EZH2, which, together with the clinical data generated to date, furthers our conviction that rinzimetostat is a potential best-in-class PRC2 inhibitor."

Poster presentations:

Rinzimetostat blockade of PRC2 activity, a key mechanism of treatment resistance, improves response of androgen receptor pathway inhibition across a spectrum of prostate cancer models

Key findings of the presentation:

In a transcriptomics analysis of >1,100 prostate samples spanning normal prostate, primary prostate cancer, and metastatic disease, PRC2 activity was observed early in the development of prostate cancer and was sustained during disease progression and treatment resistance, highlighting it as a critical therapeutic target.
More than half of localized primary tumors demonstrated elevated PRC2 activity vs. normal prostate tissue, and an elevated PRC2 activity in locally advanced tumors associates with poor survival, indicative of a key role early in the disease.
Elevated PRC2 activity was observed in the vast majority of both metastatic CSPC and metastatic CRPC tumors relative to normal prostate tissue.
Rinzimetostat in combination with darolutamide demonstrated antitumor activity across a breadth of in vivo models representing the prostate cancer continuum, including CSPC and CRPC.

Rinzimetostat, an allosteric EED inhibitor with best-in-class properties for the treatment of prostate cancer, is effective in PRC2 methyltransferase-resistant settings in preclinical studies

Key findings of the presentation:

PRC2 inhibition induces transcriptional and chromatin effects that restrain tumor plasticity and enhance antitumor activity of androgen receptor inhibitors in prostate cancer models.
Differential potency of PRC2 inhibitors on EZH1- vs. EZH2-containing complexes impacts activity in resistance contexts, providing potential advantages for EED targeting.
Rinzimetostat retained antitumor activity in prostate cancer cells with overexpressed EZH1 in vitro, while potency was diminished for mevrometostat or tazemetostat.
Preclinical studies show that rinzimetostat overcomes acquired resistance mechanisms observed in the clinic for tazemetostat and valemetostat.
Rinzimetostat demonstrates improved solubility, oral bioavailability, CYP profile, and clinical half-life versus comparator compounds.

(Press release, ORIC Pharmaceuticals, APR 17, 2026, View Source [SID1234664473])

On April 17, 2026 Immunitas Therapeutics ("Immunitas"), a clinical stage precision immunotherapy company committed to discovering and developing novel, antibody-based therapeutics for patients with autoimmune diseases and cancer, reported Phase 1/2a clinical data for IMT-009, its first-in-class anti-CD161 antibody, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17-22 in San Diego, California.

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The presentation, titled "A first-in-human, dose escalation (DE) and biomarker cohort expansion (BCE) of IMT-009 (IMT) in advanced cancer and Phase 1b (Ph1b) combination with fruquintinib (F) in microsatellite stable colorectal cancer (MSS CRC)," highlights Phase 1/2a results supporting continued evaluation of IMT-009 as both a monotherapy and combination treatment for patients with solid tumors and hematologic malignancies.

"These data highlight IMT-009’s potential as a novel immunotherapy with a differentiated mechanism designed to address significant unmet needs across difficult-to-treat cancers," said Amanda Wagner, Chief Executive Officer at Immunitas. "We are particularly encouraged by the early signals of clinical activity and the emerging biomarker insights, which may help guide patient selection and inform future development strategies, both as a monotherapy and in combination."

As of January 30, 2026, 22 patients were treated with IMT-009 monotherapy in the dose-escalation portion of the trial, and 26 patients were enrolled in the biomarker cohort expansion across selected tumor types. IMT-009 is a fully human, Fc-attenuated IgG1 monoclonal antibody that targets CD161, a receptor associated with immune suppression and treatment resistance in cancer. By blocking the CD161-CLEC2D pathway, IMT-009 is designed to enhance anti-tumor immune activity. In the Phase 1b combination arm, 19 patients with second- to fourth-line MSS colorectal cancer received IMT-009 in combination with fruquintinib.

Key findings from the presentation include:

Preliminary anti-tumor activity in heavily pretreated patients: Among patients with MSS colorectal cancer treated with IMT-009 monotherapy at 240 mg or higher, one confirmed partial response was observed, and one additional patient remained on treatment for 14 months with stable disease. In the combination arm, one confirmed partial response was observed, with three additional patients remaining on treatment for more than six months.
Favorable tolerability profile: IMT-009 was generally well tolerated as monotherapy and in combination with fruquintinib. In the monotherapy dose-escalation study, the highest treatment-related adverse event observed was Grade 2. In the combination arm, there was one Grade 4 treatment-emergent adverse event that was not considered related to IMT-009 by the investigator.
Biomarker findings supporting patient selection strategies: Translational analyses suggest that the presence and number of CLEC2D-positive/CD161-positive tertiary lymphoid structures (TLS), as well as CXCL13 expression, may be associated with clinical benefit and could help inform future patient selection approaches.
Presentation Details
Title: A first-in-human, dose escalation (DE) and biomarker cohort expansion (BCE) of IMT-009 (IMT) in advanced cancer and Phase 1b (Ph1b) combination with fruquintinib (F) in microsatellite stable colorectal cancer (MSS CRC)
Presenting Author: Susanna V. Ulahannan, M.D., The University of Oklahoma, Stephenson Cancer Center/SCRI
Abstract Number: CT048
Session: First-in-Human Phase I Clinical Trials
Location: Poster Section 50
Date & Time: Monday, April 20, 2026, 9:00 a.m. – 12:00 p.m. PT

About IMT-009
IMT-009 is a fully human, Fc-attenuated IgG1 monoclonal antibody that binds to CD161 and blocks its interaction with its ligand, CLEC2D. Preclinical data confirm that CD161 blockade with IMT-009 results in enhanced anti-tumor activity. IMT-009 is under evaluation in a Phase 1/2a clinical trial for use as a monotherapy and combination treatment for solid tumor and hematological malignancies. The Phase 1 study is designed to evaluate the safety, tolerability, pharmacodynamic biomarkers, and preliminary efficacy of IMT-009 as well as identify the Recommended Phase 2 Dose (RP2D).

(Press release, Immunitas Therapeutics, APR 17, 2026, View Source [SID1234664489])

On April 17, 2026 Byondis B.V., an independent biopharmaceutical company creating innovative targeted medicines for patients with cancer, reported it will profile the Company’s first-in-class antifolate and phosphonate antibody-drug conjugate (ADC) technology platforms in poster sessions at the American Society for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 in San Diego, CA, from today through to 22 April.

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Wim Dokter, PhD, Chief Scientific Officer at Byondis, said: "The research we are presenting at AACR (Free AACR Whitepaper) highlights the potential of two of our state-of-the-art ADC technology platforms to address significant limitations with current therapeutic approaches in cancer treatment. Our first-in-class antifolate linker-drug platform features an orthogonal mechanism of action based on clinically validated biology. This approach is engineered to address acquired resistance that can develop with current ADC treatments, positioning it for use across treatment lines. Our phosphonate linker-drug platform offers a complementary mechanism that can provide new treatment options for patients, including those who may not respond to immune therapy. Both platforms underscore our mission to deliver breakthrough solutions and enable a new generation of cancer therapeutics for patients."

Antifolate ADCs, a novel linker-drug platform for targeted therapy with a clearly differentiated mechanism of action (abstract #: 3178/13)
Session Category: Experimental and Molecular Therapeutics
Session Title: Targeting Cell Surface Vulnerabilities to Overcome Therapeutic Resistance
Time: 20 April, 2:00 PM – 5:00 PM

Resistance to widely used ADC payloads, such as topoisomerase-I and tubulin inhibitors, is increasing, underscoring the need for differentiated approaches. Byondis has revisited the clinically validated antifolates class and developed a proprietary antifolate linker-drug platform that provides a differentiated and validated mechanism of action with a payload designed to overcome systemic side effects.

The optimized payload demonstrates low- to sub-nanomolar potency, strong inhibition of dihydrofolate reductase (DHFR), and broad in vitro cytotoxicity cell lines. It also shows no interaction with key resistance-associated transporters (BCRP, PGP) and favorable physicochemical properties, supporting GMP-scale manufacturing and ADC compatibility. A glucuronide-based linker enhances therapeutic index while maintaining favorable physicochemical properties, preserving ADC stability and enabling potential dual-payload strategies.

Byondis’ lead antifolate ADC, targeting an undisclosed tumor antigen, has shown strong in vitro activity and achieved robust tumor regressions in non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC) patient-derived xenograft models, with no significant toxicity at active doses. This differentiated profile supports broad tumor applicability, positioning it for use from first-line therapy through to combination approaches.

Phosphonate antibody-drug conjugates, an innovative, immunostimulatory class of ADCs that drive inside-out activation of Vγ9Vδ2 T cells, enabling selective tumor cell killing (abstract #: 6921/2)
Session Category: Immunology
Session Title: Antibody-Drug Conjugates 2
Time: 22 April, 9:00 AM – 12:00 PM

Addressing a critical need for patients who do not respond to immune therapy, Byondis’ linker-drug platform, ByonBoost, is engineered to activate Vγ9Vδ2 (γδ) T cells in the tumor microenvironment, enabling targeted delivery with an immunologic antitumor effect and compatibility with single and dual-payload concepts.

Gamma delta (γδ) T cells are potent cytotoxic effectors that eliminate tumor cells independently of MHC presentation and are associated with improved clinical outcomes. However, prior approaches to activate Vγ9Vδ2 T cells have been limited by lack of tumor specificity and short half-life.

To address these limitations, Byondis has developed tumor-targeting phosphonate ADCs that selectively deliver payloads to tumor cells, enabling inside-out activation of Vγ9Vδ2 T cells. These ADCs combine a tumor-associated antigen (TAA)-targeting antibody with a cleavable phosphonate payload and have been successfully applied across multiple targets, including CD123, CD20, TROP2, and HER2. They drive robust and targeted immune activation, inducing cytokine release, degranulation and tumor cell killing in vitro, including in studies where primary patient material was used. In non-human primate models, the lead candidate displayed excellent tolerability with no clinical signs of cytokine release syndrome (CRS), even at high doses.

This modular platform enables the dual mechanisms of action of direct tumor targeting and immune activation while preserving antibody effector function. With broad applicability across tumor types and compatibility with multiple antibodies, it represents a differentiated and scalable approach to targeted immunotherapy.

(Press release, Byondis, APR 17, 2026, View Source [SID1234664505])