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 Volastra Therapeutics, a clinical-stage oncology company pioneering therapies targeting chromosomal instability (CIN), reported multiple scientific disclosures coinciding with the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22 in San Diego, California. The data define an Rb pathway–driven pan-cancer development framework for KIF18A inhibitors and highlight a proprietary p16 IHC biomarker approach designed to translate that strategy clinically, reinforcing Volastra’s leadership in advancing CIN biology into therapeutic opportunity.

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Separate from its AACR (Free AACR Whitepaper) 2026 presentation, Volastra has posted "KIF18A Inhibition as a Therapeutic Strategy in Cancers with Rb Pathway Inactivation" (Andreu et al. DOI: View Source – preprint publication). Drawing on what is believed to be one of the largest datasets of its kind, the work identifies Rb pathway inactivation as the mechanistic basis of response to KIF18A inhibition and establishes a development path that extends well beyond high-grade serous ovarian cancer.

The study includes clinical data from a substantial cohort of 79 heavily pretreated patients with high-grade serous ovarian cancer treated with either of two distinct KIF18A inhibitors, sovilnesib and VLS-1488. The concordance of the biomarker-defined signal across both agents is particularly compelling and argues against a drug-specific observation. Biomarker-positive tumors were distinguished by marked enrichment for objective responses, durable disease control, and longer progression-free survival, yielding a sharp clinical separation from biomarker-negative disease and strongly supporting both the biomarker strategy and prospective clinical development.

These findings reposition KIF18A inhibition from a histology-defined opportunity into a pan-cancer synthetic lethal strategy centered on one of the most commonly disrupted tumor suppressor pathways in human cancer. This creates a credible path across what is estimated to represent approximately 15% of human cancers. Within that biology, Volastra has identified a proprietary p16 IHC biomarker strategy that enriches for response to its KIF18A inhibitors and provides a practical route to clinical translation.

"The data provide a strong scientific rationale for using p16 status to identify patients most likely to benefit from KIF18A inhibition," said David Southwell, Chief Executive Officer of Volastra Therapeutics. "Importantly, this work reframes KIF18A inhibition from a narrow single cancer-type opportunity into a broader pan-cancer strategy grounded in Rb pathway biology. This p16 biomarker approach provides a practical way to translate that insight into clinical development and patient selection."

AACR Poster Highlights Clear Synergy with Taxanes and Other Microtubule-Targeting Agents

Volastra will also present an official AACR (Free AACR Whitepaper) poster titled "Combination of VLS-1488 and taxanes induces anti-tumor synergistic effect in cancer cells" in the Experimental and Molecular Therapeutics, Novel Antitumor Agents 1 Session on April 19 from 2-5PM Pacific Time (PT) (Poster section 17, poster 18). The presentation will highlight preclinical combination data showing clear synergistic activity between KIF18A inhibition and taxanes and other microtubule-targeting agents. These findings support a development strategy that could extend KIF18A inhibitors into earlier lines of therapy, including combination approaches in frontline settings.

"The totality of these data help define both the monotherapy and combination development paths for KIF18A inhibitors," said Samuel F. Bakhoum, M.D., Ph.D., Co-Founder and Chief Scientific Officer of Volastra Therapeutics. "With this new mechanistic understanding of KIF18A inhibitor sensitivity, it is evident that the biomarker data will help us identify patients most likely to benefit from monotherapy, while the combination findings point to a precision-based approach to identify the most rational therapeutic partners for development in earlier line settings."

Separately, Dr. Bakhoum, also an adjunct faculty member at the Geisel School of Medicine at Dartmouth, will chair an AACR (Free AACR Whitepaper) educational session "Chromosomal Instability in Cancer: From Mechanism to Therapy and Clinical Translation" on Saturday, April 18, 2026, in his academic capacity. The session reflects the field’s growing appreciation of CIN as both a driver of aggressive disease and a source of therapeutic vulnerability.

"This momentum underscores the growing recognition of CIN biology and the increasing importance of CIN-directed therapeutic strategies across oncology," Dr. Bakhoum said.

(Press release, Volastra Therapeutics, APR 17, 2026, View Source [SID1234664476])

On April 17, 2026 Agenus Inc. (Nasdaq: AGEN), a leader in immuno-oncology innovation, reported data from an investigator-initiated Phase II trial at Memorial Sloan Kettering Cancer Center, investigating botensilimab (BOT) and balstilimab (BAL) in combination with agenT-797, MiNK’s allo-iNKT cell therapy, ramucirumab and paclitaxel in patients with advanced PD-1 refractory gastroesophageal adenocarcinoma. The data are being presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 17-22, 2026, in San Diego, CA.

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This Phase II trial, which is the first to combine BOT and BAL with agenT-797 in patients with gastroesophageal cancer who progressed after frontline therapy, was designed to explore the role of immune priming and treatment sequencing. Patients received induction with agenT-797 (alone or plus BOT/BAL) followed by the full combination regimen, or initiated the combination without induction, with longitudinal biomarker sampling throughout. In this study (n=17), the regimen delivered a 77% DCR with long-term survival beyond 20 months in a subset, and the induction arm showed meaningful gains in PFS (6.9 vs. 3.5 months; HR 0.19; p=0.015) and OS (9.5 vs. 5.2 months), with 43% of induction-treated patients alive at both 12 and 18 months—underscoring that durability and survival may be the most clinically relevant endpoints in this PD-1 refractory population.

"These findings illustrate the mechanistic synergy of agenT-797 with botensilimab and balstilimab in this PD-1 refractory setting," said Dhan Chand, Ph.D., Vice President of Research at Agenus. "The induction approach promoted significant intratumoral infiltration of T cells and dendritic cells, the formation of organized tertiary lymphoid structures in on-treatment biopsy tissue from a patient with durable benefit, and activation of peripheral CD4 and CD8 T-cell populations. These changes are consistent with immune priming and tumor immune reprogramming, providing a biological rationale for the improved progression-free survival observed with the induction strategy."

Efficacy findings from the Phase II (n=17) study included:

DCR was observed in 77% of all treated patients, and long-term survival beyond 20 months was seen in a subset
Patients who received induction cycle had longer progression-free survival (PFS) than those treated without induction, with median PFS of 6.9 months versus 3.5 months (HR 0.19; p=0.015), supporting the potential importance of immune priming and treatment sequencing.
Median overall survival (OS) was 9.5 months in the induction cohort versus 5.2 months without induction, with 43% of induction-treated patients alive at both 12 and 18 months, compared with 20% and 0%, respectively, in the non-induction cohort.
The study did not meet its primary endpoint of ORR; however, disease control and longer-term survival observed in a subset of patients support further study of this approach.
Correlative analyses showed that treatment with BOT, BAL, and agenT-797 was associated with significant intratumoral T cell and dendritic cell infiltration, the formation of organized tertiary lymphoid structures in on-treatment biopsies from a patient with prolonged benefit, and activation of peripheral CD4 and CD8 T cells.

The safety profile was consistent with the component agents. The most common treatment-emergent adverse events among all patients included fatigue, fever, diarrhea, anorexia, nausea and mucositis. Immune-related adverse events included dermatitis, colitis, gastritis, enteritis, hepatitis and hypothyroidism.

Additional analysis of the full biospecimen dataset is ongoing and is expected to provide further insight into immune mechanisms, optimal sequencing, and potential biomarkers that could help identify patients most likely to benefit.

Presentation Details:

Abstract Title: A phase II study of agenT-797, botensilimab (BOT) and balstilimab (BAL) in PD-1 refractory gastroesophageal cancer (GEC)
Presenter: Samuel L. Cytryn M.D.; Gastrointestinal Medical Oncologist, Memorial Sloan Kettering Cancer Center
Session Name: Phase II and Phase III Clinical Trials
Date/Time: April 20, 2026 | 2:00–5:00 PM PT; 5:00-8:00 PM EDT
Poster Section: 52
Abstract No.: CT166

(Press release, Agenus, APR 17, 2026, View Source [SID1234664492])

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 Zentalis Pharmaceuticals, Inc. (Nasdaq: ZNTL), a clinical oncology innovator advancing late-stage development of investigational first-in-class WEE1 inhibitor azenosertib as a biomarker-driven treatment approach for ovarian cancer, reported data from two posters being presented at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 17-22, 2026, in San Diego, CA. The data show encouraging preclinical activity of azenosertib in triple-negative breast cancer (TNBC) and highlight the poor prognosis of Cyclin E1-positive ovarian cancer patients with currently available treatments in a real-world data analysis.

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Compelling Preclinical Activity in Triple-Negative Breast Cancer with Azenosertib

"The preclinical data in triple-negative breast cancer being presented at AACR (Free AACR Whitepaper) showed that azenosertib combinations can induce complete tumor responses in a model resistant to emerging ADC therapies, supporting the potential to broaden the impact of azenosertib beyond ovarian cancer," said Julie Eastland, Chief Executive Officer of Zentalis. "This includes potential development of azenosertib through differentiated combination strategies with antibody-drug conjugates (ADCs) and chemotherapy. As ADCs advance toward first-line use in TNBC, effective post-ADC treatment strategies represent a growing unmet need that azenosertib combinations may be uniquely positioned to fill. Our data suggest azenosertib may achieve this through multiple mechanisms – possibly resensitizing tumors to chemotherapy, enhancing the responses to ADC, and extending the duration of response – which is an exciting potential future direction for our pipeline."

Preclinical evidence supports azenosertib as a therapeutic strategy in TNBC:
•TNBC cell lines showed higher Cyclin E1 expression and greater sensitivity to WEE1 inhibition compared to other breast cancer cell lines
oAzenosertib monotherapy demonstrated meaningful antitumor activity across a diverse panel of 12 TNBC in vivo xenograft models (42-99% tumor growth inhibition)
•In a patient-derived xenograft model of TNBC with clinical resistance to sacituzumab govitecan, an approved topoisomerase 1 inhibitor (TOPO1i) ADC, azenosertib + enfortumab vedotin (EV):
oInduced complete responses in 7 of 8 mice (87.5%); 5 mice did not progress after treatment discontinuation
oPrevented tumor progression in 8 of 8 mice for more than 52 days compared to 100% progression observed within 30 days with EV alone
oDrove deep tumor regression in mice models refractory to sacituzumab govitecan or trastuzumab deruxtecan with large tumor volumes (average ~900mm3)

•Combinations of azenosertib with TOPO1i-payload ADCs (sacituzumab govitecan, datopotamab deruxtecan, or trastuzumab deruxtecan) enhanced both depth and duration of response compared to ADC monotherapy in ADC-naïve models
•Azenosertib + paclitaxel restored substantial sensitivity to paclitaxel in a model resistant to both paclitaxel and TOPO1i ADCs (51% tumor growth inhibition vs. 16% with paclitaxel alone)

Cyclin E1 Protein Overexpression Characterizes Ovarian Cancer Patients with Poor Prognosis

"The real-world data being presented at AACR (Free AACR Whitepaper) provide important validation that Cyclin E1-positive ovarian cancer patients face a particularly challenging disease trajectory with standard-of-care therapies," said Ingmar Bruns, M.D., Chief Medical Officer of Zentalis. "The consistency of worse outcomes across independent cohorts and multiple treatment settings underscores the significant unmet need in this population. These findings provide important context for Zentalis’ registration-intended DENALI and ASPENOVA studies, which are evaluating WEE1 inhibition with azenosertib monotherapy as a targeted approach for the Cyclin E1-positive population that currently has limited effective treatment options."

Real-world data from two independent cohorts (Tempus Lens Ovarian cancer dataset and Zentalis’ historical clinical trials) consistently demonstrated that Cyclin E1-positive ovarian cancer patients experience worse clinical outcomes:
•After first-line treatment, Cyclin E1-positive patients, with or without CCNE1 gene amplification, had shorter time to next treatment compared to Cyclin E1-negative patients (13.2 months and 14.9 months, respectively, compared to 19.5 months, p=0.002)
•Cyclin E1-positivity is associated with a trend toward reduced clinical benefit from standard-of-care PROC treatments

AACR Poster Details

Title: "WEE1 Inhibition as a Therapeutic Strategy in Triple-Negative Breast Cancer: Evaluating Single Agent and Combination Activity of Azenosertib in Preclinical Models"
Abstract Number: 2012
Date/Time: Monday, April 20, 2026, 2:00 p.m. – 5:00 p.m. PDT
Presenting Author: Alexandra Levy, MS

Title: "Real-World Treatment Patterns and Outcomes Reveal Distinct Clinical Trajectories of Patients with Cyclin E1-Positive Ovarian Cancer"
Abstract Number: 1708
Date/Time: Sunday, April 19, 2026, 2:00 p.m. – 5:00 p.m. PDT
Presenting Author: Jinkil Jeong, PhD

The posters can be accessed on the Supporting Publications page of the Zentalis website.

About Azenosertib
Azenosertib is an investigational, potentially first-in-class, selective, and orally bioavailable inhibitor of WEE1 currently being evaluated in clinical studies in ovarian cancer and additional tumor types. WEE1 acts as a master regulator of the G1-S and G2-M cell cycle checkpoints, through negative regulation of both CDK1 and CDK2, to prevent replication of cells with damaged DNA. By inhibiting WEE1, azenosertib enables cell cycle progression, despite high levels of DNA damage, thereby resulting in the accumulation of DNA damage and leading to mitotic catastrophe and cancer cell death.

Azenosertib is in late-stage development as a potential treatment for Cyclin E1-positive platinum-resistant ovarian cancer (PROC). There is currently no approved treatment option specifically for this biomarker-selected population which comprises approximately 50% of PROC patients. Cyclin E1 protein overexpression has been established as a sensitive and specific predictive biomarker for identifying patients who could potentially derive benefit from azenosertib treatment, based on retrospective analysis of azenosertib studies in PROC. Validation of the Cyclin E1 companion diagnostic assay is ongoing in the DENALI and ASPENOVA trials.

Azenosertib has been granted Fast Track Designation by the U.S. FDA for the treatment of patients with Cyclin E1-positive platinum-resistant ovarian cancer. Fast Track Designation is intended to facilitate the development and expedite the review of therapies that have the potential to treat serious conditions and address unmet medical needs.

(Press release, Zentalis Pharmaceuticals, APR 17, 2026, View Source [SID1234664477])