On April 17, 2026 Xilio Therapeutics, Inc. (Nasdaq: XLO), a clinical-stage biotechnology company discovering and developing masked immuno-oncology therapies for people living with cancer, reported new preclinical data for XTX601, a masked T cell engager targeting claudin 18.2 (CLDN18.2), at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place from April 17–22, 2026 at the San Diego Convention Center in San Diego, California.

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"The data to be presented at AACR (Free AACR Whitepaper) underscore the significant potential of our clinically-validated masking technology to address the central challenge that has limited the advancement of T cell engagers in solid tumors – namely, the inability to achieve meaningful anti-tumor activity without inducing severe systemic toxicities," said Uli Bialucha, Ph.D., chief scientific officer of Xilio Therapeutics. "XTX601 has demonstrated a promising preclinical profile, including potent tumor cell killing across multiple CLDN18.2-expressing tumor models and a favorable tolerability profile in non-human primates, supporting its potential to achieve a wide therapeutic index. Importantly, our modular architecture for masked T cell engagers provides flexibility to rapidly evaluate multiple designs in parallel, including masking of the CLDN18.2 binding domain and/or the addition of a co-stimulatory domain, which enables us to seek to optimize the molecule for the best possible clinical profile."

Masked T Cell Engager Design

XTX601 is a potentially first-in-class masked T cell engager designed to selectively target CLDN18.2, a tumor-associated antigen expressed in gastric, pancreatic and esophageal cancers. XTX601 incorporates Xilio’s clinically-validated masking technology and advanced tumor-activated cell engager (ATACR) format, which consists of a T cell engager with a masked CD3 targeting domain, with the goal of minimizing systemic T cell engagement in healthy tissue and overcoming the significant systemic toxicities that have limited non-masked T cell engagers targeting CLDN18.2. In addition, XTX601 is designed with a conditional half-life modulation element for antibody-like pharmacokinetics in its masked state and a short half-life upon activation in the tumor microenvironment to further limit peripheral exposure.

Preclinical Data Highlights Presented at AACR (Free AACR Whitepaper)

In preclinical studies, XTX601 demonstrated the potential to achieve a wide therapeutic index.

XTX601 demonstrated protease-dependent activation and tumor cell killing in high- and low-expression settings for CLDN18.2, with effective masking of the anti-CD3 domain.
XTX601 exhibited robust, dose-dependent anti-tumor activity in multiple murine cell line-derived xenograft models, including GSU gastric carcinoma and OE19 esophageal adenocarcinoma models engrafted with human T cells.
Consistent with its masked design, XTX601 was well tolerated in non-human primates (NHP) with no evidence of cytokine release syndrome and no changes in liver enzymes.
Integration of drug exposure data from murine tumor models and NHP studies indicated a favorable, positive therapeutic index for XTX601 and supports the potential for XTX601 to achieve meaningful anti-tumor activity at doses that are well-tolerated systemically.

Xilio plans to advance its masked T cell engager program targeting CLDN18.2 into investigational new drug (IND)-enabling studies and submit an IND application for this program in 2027.

Presentation Details

Xilio’s poster presentation at AACR (Free AACR Whitepaper) is listed below, and a copy of the presentation will be available under the "Our Approach—Presentations & Publications" section of the company’s website at www.xiliotx.com.

Title: Discovery and Optimization of XTX601, a Masked Claudin 18.2-Targeting T Cell Engager
Session Category: Immunology
Session Title: T Cell Engagers 1
Session Date and Time: Monday, Apr. 20, 2026, from 9:00 a.m. to 12:00 p.m. PST
Location: Poster Section 10, Poster Board 11
Abstract Number: 1619

(Press release, Xilio Therapeutics, APR 17, 2026, View Source [SID1234664510])

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])