On April 17, 2026 Kura Oncology, Inc. (Nasdaq: KURA), a biopharmaceutical company focused on precision medicines for the treatment of cancer, reported new preliminary data from a subset analysis of patients with clear cell renal cell carcinoma (ccRCC) previously treated with cabozantinib in the ongoing FIT-001 clinical trial (NCT06026410) of darlifarnib (KO-2806) in combination with cabozantinib. Results were presented at the 2026 International Kidney Cancer Symposium (IKCS): Europe in Paris, France.

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The analysis specifically evaluated patients with ccRCC who had previously received cabozantinib, a population that typically derives limited benefit from subsequent therapy. In this setting, the combination of darlifarnib and cabozantinib demonstrated robust antitumor activity along with a manageable safety profile as demonstrated in all RCC patients across multiple dose levels, including full dose cabozantinib. These findings are consistent with clinical and preclinical data presented at the 2025 European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) and in earlier data disclosures supporting the potential of darlifarnib to enhance the activity of VEGFR-targeted therapies and to address mechanisms of resistance.

Clinical Activity in Cabozantinib-Pretreated Patients (N=16):

Objective response rate (ORR) was 44%, with a disease control rate (DCR) of 94% across all doses tested in this population

Tumor shrinkage observed in 75% of patients, with reductions ranging from 32% to 47% among responders

Antitumor activity observed in a heavily pre-treated, cabozantinib-exposed population, including patients whose best response to prior cabozantinib was stable disease

Responses observed in patients previously treated with cabozantinib in the immediate prior line as well as those who had received other TKIs in addition to cabozantinib

Treatment durations ranged from 8 to 56 weeks, with six patients remaining on therapy at the time of data cutoff

These findings are notable given that patients who progress on cabozantinib are generally considered unlikely to respond to subsequent cabozantinib therapy.

"Patients with advanced ccRCC whose disease progresses on cabozantinib have limited treatment options," said Adanma Ayanambakkam, M.D., M.S., Assistant Professor of Hematology Oncology Director of Genitourinary Medical Oncology Research, Stephenson Cancer Center, University of Oklahoma Health Sciences Center. "The tumor shrinkage and high disease control rate observed with darlifarnib in combination with cabozantinib suggest this approach may offer meaningful clinical benefit in a refractory setting or in patients with disease progression after therapy."

The FIT-001 study is evaluating darlifarnib in patients with RCC at once-daily doses of 3 mg, 5 mg or 8 mg alternating 7 days on and off in combination with cabozantinib at once-daily doses of 60 mg or 40 mg. All patients must have received prior immunotherapy. The study has advanced into Phase 1b dose expansion to assess an optimal biologically active dose for the combination.

"These data highlight the potential of darlifarnib to overcome resistance to prior cabozantinib and enhance the activity of VEGF TKIs in patients with advanced RCC," said Mollie Leoni, M.D., Chief Medical Officer of Kura Oncology. "We are highly encouraged by these results and are committed to advancing this combination to evaluate further its potential to deliver meaningful benefit for RCC patients."

2026 IKCS: Europe Presentation
The presentation from 2026 IKCS: Europe is available on Kura’s website at www.kuraoncology.com under the Posters and Presentations tab in the Farnesyl Transferase Inhibition section.

Virtual Investor Event
Kura will host a webcast and conference call today, April 17, 2026, at 7:30 a.m. PT / 10:30 a.m. ET / 4:30 p.m. CEST featuring management and Adanma Ayanambakkam, M.D., M.S., Assistant Professor of Hematology Oncology and Director of Genitourinary Medical Oncology Research, Stephenson Cancer Center, University of Oklahoma Health Sciences Center. The live webcast and replay will be available on the Company’s website at www.kuraoncology.com under the Investors tab in the Events and Presentations section.

(Press release, Kura Oncology, APR 17, 2026, View Source [SID1234664472])

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])