On April 17, 2026 Boundless Bio (Nasdaq: BOLD), a clinical-stage oncology company interrogating extrachromosomal DNA (ecDNA) biology to deliver transformative therapies to patients with previously intractable oncogene amplified cancers, reported preclinical data supporting its lead ecDNA-directed therapy (ecDTx), BBI-940, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026. Boundless has identified a novel kinesin target ("Kinesin") essential to ecDNA segregation and inheritance in cancer cells, but non-essential in healthy cells. BBI-940, a potentially first-in-class, oral, and selective Kinesin degrader, is currently being evaluated in the Phase 1 KOMODO-1 trial (NCT07408089) in patients with advanced or metastatic ER+/HER2- breast cancer and TNBC-LAR.

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"Extrachromosomal DNA is well established as a distinct enabler of chromosomal instability associated with oncogene amplification, therapeutic resistance, and poor outcomes for patients," said Chris Hassig, Ph.D., Chief Scientific Officer of Boundless Bio. "We have discovered and validated a novel kinesin target that plays a critical role in ecDNA segregation during cell division, thereby affording tumors with a high degree of genomic plasticity. Our data demonstrate that selective degradation of this target delivered potent antitumor activity in validated breast cancer models, particularly those with ecDNA. Our genetic, in vitro, in vivo, and toxicity profile of BBI-940 supports our recently initiated, first-in-human KOMODO-1 clinical trial evaluating BBI-940 in ER+/HER2- and TNBC-LAR breast cancer patients."

Details of the presentation are as follows:

Title: Selective degradation of a novel kinesin as a potential therapeutic strategy addressing high-risk extrachromosomal DNA (ecDNA) positive cancers, including breast cancer
Abstract Number: LB361
Session Title: Late-Breaking Research: Experimental and Molecular Therapeutics 3
Session Date and Time: Tuesday April 21, 2026, 2:00 PM – 5:00 PM PT
Location: Poster Section 53
Poster Board Number: 18

Genetic and pharmacologic degradation of Kinesin caused ecDNA mis-segregation, ecDNA depletion, and reduced viability of ecDNA+ cancer cells. Selective degradation of Kinesin in a panel of tumor cell lines demonstrated sensitivity across multiple tumor types and 32% sensitivity in breast cancer cell lines, including those positive for ecDNA and FGFR1 gain. This molecularly defined subgroup for Kinesin degradation was further validated in vivo with demonstrated monotherapy tumor regressions in an ecDNA+ TNBC-LAR model, and significant antitumor activity as monotherapy and combination in an ecDNA+/FGFR1+ ER+ breast cancer model.

About BBI-940
Our lead ecDTx, BBI-940, is a novel, oral, and selective kinesin degrader being evaluated in the ongoing, first-in-human Phase 1 KOMODO-1 (Kinesin Oral Molecular Degrader for Oncology) clinical trial (NCT07408089) in patients with advanced or metastatic estrogen receptor-positive, HER2-negative (ER+/HER2-) breast cancer or triple-negative breast cancer of the luminal androgen receptor subtype (TNBC-LAR). BBI-940 targets a specific kinesin protein, "Kinesin", essential for ecDNA segregation and inheritance in cancer cells, but non-essential in healthy cells. BBI-940 is designed to exploit the heightened dependence of ecDNA-positive tumors on mitotic machinery by degrading Kinesin to induce mitotic catastrophe and cell death.

(Press release, Boundless Bio, APR 17, 2026, View Source [SID1234664506])

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])

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 SAGA Diagnostics, a pioneer in blood-based cancer detection and precision medicine redefining the standard for early molecular residual disease (MRD) detection, reported that the company and its collaborators will present data from two abstracts at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 17–22 in San Diego, California. These abstracts showcase the ultrasensitive structural variant (SV)-based detection of circulating tumor DNA (ctDNA) in metastatic breast cancer (mBC) and high-grade serous ovarian cancer (HGSOC).

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SV-based ctDNA Monitoring in Metastatic Breast Cancer (mBC)

In collaboration with Drs. David Cescon and Mitchell Elliott at University Health Network (UHN) Canada, a retrospective analysis was conducted for patients with mBC (all subtypes) undergoing standard systemic therapy, utilizing the Pathlight SV-based MRD test. SAGA was able to successfully generate fingerprints in 66 patients using standard tissue-based Pathlight. Using ultradeep cfDNA-based whole-genome sequencing, SV-based tissue-free fingerprints were generated to rescue additional patients for which tissue was unavailable, enabling these patients to benefit from informed MRD testing.

The study’s SV-based approach achieved a high 77% detection rate (294/380) for ctDNA, with nearly a third of those cases identified in the ultrasensitive range. Additionally, Pathlight proved to be a powerful predictor of patient outcomes: where ctDNA was undetectable, patients showed exceptional responses to therapy, including prolonged disease stability and complete clinical response. Furthermore, Pathlight successfully tracked treatment responses across multiple lines of therapy, with rising ctDNA levels preceding radiologic signs of disease progression.

"Metastatic breast cancer remains a challenge to manage clinically, and the use of an accurate complementary biomarker may help improve the care for our patients," said Mitchell Elliott, MD, FRCPC. "By leveraging structural variants – highly conserved features of the tumor genome – we enable ultrasensitive ctDNA detection in the metastatic setting which closely aligns with standard of care radiographic assessment. This approach supports the potential for more reliable treatment monitoring and unlocks new opportunities for clinical utility in this setting."

Improved Prognostic Assessment in Ovarian Cancer

In collaboration with the Medical University of Vienna and LMU Munich, a retrospective analysis was performed on plasma samples collected prospectively from 84 patients with advanced high-grade serous ovarian cancer (HGSOC). High baseline detection was observed (94%), with MRD remaining in 85% of cases postoperatively. Within the subgroup of patients with pathological complete tumor resection, ctDNA clearance at the first cycle of chemotherapy (C1) (20%) and the sixth cycle (C6) (70%) was associated with significantly lower recurrence risk compared to those with persistent ctDNA. Most notably, ctDNA persistence at C6 was identified as a powerful independent prognostic marker, where ctDNA-positive patients faced a median time to clinical recurrence of just 10.7 months compared to 21.3 months for those who cleared ctDNA. While CA-125 levels failed to significantly predict recurrence at key treatment milestones, ctDNA dynamics offered precise risk stratification even after optimal primary surgery, providing a vital clinical window for personalized maintenance strategies and risk-adjusted treatment interventions.

"The consistent performance of SV-based MRD monitoring by Pathlight across these diverse, late-stage cancers underscores its broad clinical applicability," added Wendy Levin, MD, MS, Chief Clinical Officer of Saga Diagnostics. "This isn’t just about better data-it’s about the potential for clinical utility. By accurately informing on treatment monitoring where traditional tools fail, we are unlocking the ability to tailor therapies in real-time, ultimately improving outcomes through more informed, individualized patient management."

Key SAGA Diagnostics Presentations During AACR (Free AACR Whitepaper) 2026:

Abstract Title

Presentation Details

Tumor-informed circulating tumor DNA identifies high-grade serous ovarian cancer patients at highest risk for recurrence despite optimal first-line treatment with primary macroscopic complete resection

Poster Presentation
Location: Section 42
Date: April 19, 2026
Time: 2:00-5:00 PM
Speaker: Magdalena Postl, MD

Serial ctDNA monitoring in metastatic breast cancer using an ultrasensitive tumor-informed structural variant-based assay

Poster Presentation: #3864
Location: Section 45
Date: April 20, 2026
Time: 2:00-5:00 PM
Speaker: Mitchell Elliott, MD, FRCPC

The full abstracts for SAGA Diagnostics at AACR (Free AACR Whitepaper) 2026 can be found here.

(Press release, SAGA Diagnostics, APR 17, 2026, View Source [SID1234664503])

On April 17, 2026 Ensem Therapeutics, Inc. (ENSEM), a clinical-stage, oncology-focused biopharmaceutical company, reported presentations of preclinical data at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, being held April 17–22 in San Diego, CA. The data support the differentiated preclinical profiles of ETX-929, a pan-KRAS inhibitor for the treatment of KRAS-altered solid tumors, and ETX-880, a covalent WRN inhibitor for the treatment of microsatellite instability-high (MSI-H) solid tumors.

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"These AACR (Free AACR Whitepaper) presentations underscore the breadth and depth of ENSEM’s oncology pipeline, fueled by our proprietary Kinetic Ensemble platform," said Shengfang Jin, PhD, Co-Founder, President, and Chief Executive Officer of ENSEM. "With ETX-929 and ETX-880, we are advancing potential best-in-class small molecule inhibitors against two of the most compelling targets in oncology today—KRAS and WRN. These programs, alongside our clinical-stage PI3Kα program ETX-636, demonstrate the power of our platform to systematically tackle high-value, difficult-to-drug targets with differentiated molecules."

AACR Presentation Details

Details of the presentations are as follows:

ETX-929 (Pan-KRAS Inhibitor)

Title: ETX-929, a potential best-In-class, oral, highly potent and selective dual ON / OFF state Pan-KRAS small molecule inhibitor for the treatment of KRAS mutant and wild-type amplified cancers
Poster ID: 418
Session: Novel Antitumor Agents 1
Date/Time: 4/19/2026 2PM – 5PM PT
Location: Poster Section 17, Poster Board Number: 21
ETX-880 (Covalent WRN Inhibitor)

Title: ETX-880, a potential best-in-class, oral, highly potent and selective covalent inhibitor of Werner helicase for the treatment of microsatellite instability-high (MSI-H) cancers
Poster ID: 423
Session: Novel Antitumor Agents 1
Date/Time: 4/19/2026 2PM – 5PM PT
Location: Poster Section 17, Poster Board Number: 26
About ETX-929

ETX-929 is a potent and selective oral pan-KRAS inhibitor designed leveraging ENSEM’s proprietary Kinetic Ensemble platform. ETX-929 inhibits multiple KRAS-mutant variants, including KRASG12D, KRASG12V, KRASG12C, and other clinically relevant mutations, in both the active (GTP-bound/ON) and inactive (GDP-bound/OFF) states. KRAS is the most frequently mutated oncogene in human cancers, driving approximately 25% of all solid tumors, including pancreatic, colorectal, and non-small cell lung cancers. Despite recent advances in allele-specific KRAS inhibitors, there remains a significant unmet need for pan-KRAS therapeutics that can address the full spectrum of KRAS-driven cancers. ETX-929 has demonstrated potent anti-tumor activity in preclinical models and has completed IND-enabling studies with anticipated IND clearance in Q2 2026.

About ETX-880

ETX-880 is a covalent, potent, oral inhibitor of Werner syndrome ATP-dependent helicase (WRN) designed leveraging ENSEM’s Kinetic Ensemble platform. WRN helicase has emerged as a compelling synthetic lethal target in microsatellite instability-high (MSI-H) cancers. MSI-H tumors arise from defects in the DNA mismatch repair pathway and are found across multiple tumor types, including colorectal, endometrial, gastric, and ovarian cancers. While immune checkpoint inhibitors have demonstrated clinical benefit in MSI-H cancers, 40–70% of patients either do not respond or eventually develop resistance, underscoring the need for novel therapeutic approaches. ETX-880’s covalent binding mechanism is designed to deliver deep and sustained WRN inhibition, and the compound has demonstrated selective anti-proliferative activity against MSI-H cancers in preclinical studies. ETX-880 is currently at the IND-enabling stage.

(Press release, ENSEM Therapeutics, APR 17, 2026, View Source [SID1234664502])