On April 17, 2026 Cardiff Oncology, Inc. (Nasdaq: CRDF), a clinical-stage biotechnology company leveraging PLK1 inhibition to develop novel therapies across a range of cancers, reported it will present new preclinical data in a poster at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22 in San Diego, California. These data highlight the potential of Cardiff’s highly specific oral PLK1 inhibitor, onvansertib, in combination with the HER2-targeted antibody-drug conjugate (ADC), trastuzumab deruxtecan (T-DXd), demonstrating robust antitumor activity and the ability to overcome resistance in HER2-low breast cancer models.

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"These preclinical findings highlight a potential new opportunity for onvansertib, demonstrating its ability to enhance the activity of ADCs, which are becoming mainstays in oncology across multiple indications," said Tod Smeal, Ph.D., Chief Scientific Officer of Cardiff Oncology. "By enhancing and prolonging DNA damage, this combination appears to drive greater apoptosis than either agent alone, offering a promising new approach for patients whose cancers have become resistant to standard-of-care treatments."

Poster Presentation Highlights:

Onvansertib + T-DXd synergistically inhibited the viability of HER2-low breast cancer cell lines, including fulvestrant- and CDK4/6i-resistant cells
In the resistant triple-negative breast cancer model and two hormone receptor-positive models, the combination drove tumor regression in nearly all mice, with complete response rates up to 62%
Increased tumor regression, improved tumor growth inhibition, and extended event-free survival across models
Combination showed favorable tolerability in vivo
Following the presentation on April 19, 2026 from 2:00–5:00 PM PT, the poster titled "PLK1 inhibitor onvansertib potentiates the antitumor efficacy of trastuzumab deruxtecan (T-DXd) and reverses its resistance in therapy-resistant HER2-low breast cancer models" will be available on the Scientific Publications page of the Company’s website.

About Onvansertib
Onvansertib is a highly specific, oral PLK1 inhibitor currently in mid-stage clinical development for RAS-mutated metastatic colorectal cancer. It is also being evaluated in multiple other cancers through investigator-initiated studies, including metastatic pancreatic ductal adenocarcinoma (mPDAC), small cell lung cancer (SCLC), triple-negative breast cancer (TNBC), and chronic myelomonocytic leukemia (CMML).

(Press release, Cardiff Oncology, APR 17, 2026, View Source [SID1234664509])

On April 17, 2026 Olema Pharmaceuticals, Inc. ("Olema" or "Olema Oncology", Nasdaq: OLMA), a clinical-stage biopharmaceutical company focused on the discovery, development, and commercialization of targeted therapies for breast cancer and beyond, reported new preclinical data for palazestrant, a complete estrogen receptor antagonist (CERAN) and selective estrogen receptor degrader (SERD), alone and in combination with OP-3136, a novel small molecule that potently and selectively inhibits acetyltransferase 6 (KAT6) inhibitor. The data will be presented in two poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting taking place April 17-22 in San Diego, California.

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"We are very excited to share, for the first time ever, data that confirm the mechanism by which palazestrant completely blocks estrogen receptor transcription and signaling by recruiting the corepressor protein NCoR1," said David C. Myles, Ph.D., Chief Scientific Officer of Olema Oncology. "Further, the synergistic anti-tumor activity of OP-3136 combined with palazestrant in preclinical models highlights the role that both complete ER antagonism and KAT6 inhibition play in addressing acquired resistance associated with metastatic disease. We are pleased to continue to explore the potential of this combination in our ongoing Phase 1 study of OP-3136 and look forward to announcing top-line data from our Phase 3 OPERA-01 trial of palazestrant monotherapy, which is anticipated this fall."

Poster Presentation Details
Title: Palazestrant directly recruits the corepressor protein NCoR1 in vitro leading to complete antagonism of estrogen receptor alpha
Poster/Abstract: 2950
Session: Experimental and Molecular Therapeutics: Cellular Responses to Anticancer Drugs
Date/Time: April 20, 2026, from 2:00pm-5:00pm PT / 5:00pm-8:00pm ET

Key findings:

Palazestrant completely blocks estrogen-driven transcription and demonstrates robust anti-tumor activity in vitro.
In a split-luciferase assay, palazestrant was shown to fully recruit the corepressor, NCoR1, enabling complete estrogen receptor (ER) antagonism.
In both ESR1 wild-type and mutant models, palazestrant more potently suppressed ER-regulated and cell-cycle genes, including PGR and GREB1, than selective estrogen receptor modulators (SERMs), delivering complete inhibition of tumor cell proliferation without partial agonist effects.

These findings position palazestrant as a differentiated endocrine therapy designed to achieve deeper, more consistent ER pathway suppression in estrogen receptor-positive, human epidermal growth factor receptor 2-negative (ER+/HER2-) breast cancer.

Title: Palazestrant, a CERAN, in combination with OP-3136, a KAT6 inhibitor, synergistically downregulates cell proliferation and metastasis related gene signatures
Poster/Abstract: 2949
Session: Experimental and Molecular Therapeutics: Cellular Responses to Anticancer Drugs
Date/Time: April 20, 2026, from 2:00pm-5:00pm PT / 5:00pm-8:00pm ET

Key findings:

Combining OP-3136 with palazestrant drives synergistic anti-tumor activity in in vivo ER+/HER2- breast cancer models, which is mediated by suppression of cell-cycle and estrogen receptor-driven oncogenic signaling processes.
The combination of OP-3136 plus palazestrant downregulates genes associated with MYC, E2F, and G2M more effectively than either agent alone or OP-3136 in combination with fulvestrant.
Combining OP-3136 with palazestrant or fulvestrant suppresses expression of genes associated with MTORC1 signaling, indicating that targeting KAT6 and ER-alpha can suppress mechanisms of acquired resistance.

These findings provide a strong biological rationale for advancing palazestrant in combination with OP-3136 for the treatment of ER+ metastatic breast cancer.

Copies of these posters will be available on the Publications page of Olema’s website in alignment with the AACR (Free AACR Whitepaper) embargo. Additional information, including abstracts, is available on the AACR (Free AACR Whitepaper) Annual Meeting website.

(Press release, Olema Oncology, APR 17, 2026, View Source [SID1234664508])

On April 17, 2026 Pyxis Oncology, Inc. (Nasdaq: PYXS), a clinical-stage company developing next-generation therapeutics for difficult-to-treat cancers, reported that it will present new preclinical data highlighting that a mouse analogue of MICVO (maMICVO) demonstrates anti-tumor activity in a preclinical head and neck squamous cell carcinoma (HNSCC) model as monotherapy, and synergistic anti-tumor activity in combination with anti-mouse PD-1. These data will be presented in a poster session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 in San Diego, California, held April 17 – April 22, 2026.

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"These new preclinical data are particularly compelling as they further reinforce MICVO’s clinical development in HNSCC, both as a novel monotherapy treatment and in combination with anti-PD-1," said Tom Civik, Interim Chief Executive Officer and Director of Pyxis Oncology. "An important finding from the data is that combination treatment with maMICVO and anti-mouse PD-1 demonstrated synergistic anti-tumor activity and greater tumor control than either treatment alone in an immunotherapy-refractory preclinical HNSCC model, highlighting MICVO’s novel three-pronged mechanism of action and its potential to meaningfully enhance response to immunotherapy. Following our mid-year 2026 MICVO Phase 1 monotherapy update in 2L+ R/M HNSCC, we look forward to sharing updated data from the ongoing Phase 1/2 combination dose escalation study of MICVO in combination with pembrolizumab for 1L/2L+ R/M HNSCC patients in the second half of 2026."

Micvotabart pelidotin (MICVO), is a first-in-concept antibody drug conjugate (ADC) that targets extradomain-B of fibronectin (EDB+FN), a non-cellular structural component of the tumor extracellular matrix (ECM). MICVO is designed to treat solid tumors through a three-pronged mechanism of action: direct cancer cell killing, bystander effect and immunogenic cell death. MICVO is currently being evaluated as monotherapy in a Phase 1 clinical study in patients with recurrent and metastatic head and neck squamous cell carcinoma (R/M HNSCC) and in combination with Merck’s anti-PD-1 therapy, KEYTRUDA (pembrolizumab), in a Phase 1/2 clinical study in patients with R/M HNSCC and other solid tumors.

Poster Key Highlights:

Monotherapy with maMICVO inhibited tumor outgrowth in MOC2, a syngeneic preclinical model of HNSCC
maMICVO produced dose-dependent inhibition of EDB+FN-expressing MOC2 tumor outgrowth, with 6 mg/kg showing the strongest tumor growth inhibition
Treatment with maMICVO modulated the immune compartment of MOC2 tumors toward a more favorable immune-permissive environment for immunotherapy
Treatment with maMICVO reduced the overall abundance of immune-suppressive regulatory T cells (Tregs) in MOC2 tumors
maMICVO also increased the CD8 T cell-to-Treg ratio and enhanced the abundance of a progenitor exhausted T cell subset that is highly responsive to anti-PD-1 therapy

Combination treatment with maMICVO and anti-mouse PD-1 acted synergistically to produce greater tumor control than either treatment alone
The combination of maMICVO and anti-mouse PD-1 resulted in greater tumor control and tumor growth inhibition than monotherapy with either maMICVO or anti-mouse PD-1
Bliss independence analysis confirmed that maMICVO acted synergistically with anti-mouse PD-1 in a preclinical model unresponsive to anti-mouse PD-1 monotherapy
Poster Information:

Title: Mouse analog of micvotabart pelidotin, an antibody-drug conjugate targeting extradomain-B of fibronectin, demonstrates anti-tumor efficacy in an immunotherapy-refractory syngeneic head and neck squamous cell carcinoma model
Session Title: Antibody Technologies and Platforms 2
Date/Time: April 21, 2026 | 9:00 AM – 12:00 PM PT
Location: Poster Section 11
Poster Board Number: 14
Presentation Number: 4406

This poster presentation will also be available on the Pyxis Oncology website on the Scientific publications page following the event.

(Press release, Pyxis Oncology, APR 17, 2026, View Source [SID1234664507])

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])