On April 21, 2026 Avenzo Therapeutics, Inc. ("Avenzo"), a clinical-stage biotechnology company developing next-generation oncology therapies, reported the acceptance of an abstract for poster presentation at the 2026 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting taking place in Chicago, Illinois from May 29 – June 2, 2026.

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Avenzo will present updated safety and efficacy results from the Phase 1 portion of its ongoing Phase 1/2 clinical study of AVZO-021, its potential best-in-class cyclin-dependent kinase 2 (CDK2) selective inhibitor.

Details of the poster presentation are as follows:

Abstract: 1094

Title: A phase 1/2, first-in-human study of AVZO-021, a selective cyclin-dependent kinase 2 inhibitor (CDK2i), as monotherapy and in combination for patients with advanced solid tumors, including hormone receptor–positive (HR+)/human epidermal growth factor receptor 2–negative (HER2−) breast cancer (BC) and cyclin E1 (CCNE1)–amplified solid tumors: Updated safety and efficacy results.

Session Title: Breast Cancer—Metastatic

Poster Board: 208

Date and Time: June 1, 2026, 1:30 to 4:30 p.m. CT

(Press release, Avenzo Therapeutics, APR 21, 2026, View Source [SID1234664599])

On April 21, 2026 AulosTM Bioscience, an immuno-oncology company working to revolutionize cancer care through development of its lead immune-activating antibody therapeutic imneskibart (AU-007), reported that new Phase 1/2 data from its ongoing study of imneskibart will be presented at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) 2026 Annual Meeting. The presentation will focus on promising results for imneskibart with and without nivolumab in checkpoint inhibitor (CPI)-refractory cutaneous melanoma. The ASCO (Free ASCO Whitepaper) Annual Meeting is being held online and in Chicago, Illinois, from May 29–June 2, 2026.

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Details of the poster presentation are as follows:

Poster Title: Imneskibart + low-dose subcutaneous IL-2 ± nivolumab in patients with CPI-refractory cutaneous melanoma: Promising results from an ongoing phase 1/2 study
Abstract: 9526
Session Type/Title: Poster Session – Melanoma/Skin Cancers
Session Date and Time: Sunday, May 31, 2026, 9:00 a.m.-12:00 p.m. CDT

The poster will be presented in the Exhibit Hall at McCormick Place. An electronic version will also be available on the ASCO (Free ASCO Whitepaper) 2026 online meeting platform.

About Imneskibart
Imneskibart (AU-007) is a human IgG1 monoclonal antibody designed by leveraging artificial intelligence that is highly selective to the CD25-binding portion of IL-2. With a mechanism of action unlike any other IL-2 therapeutic in development, imneskibart redirects IL-2 to reinforce anti-tumor immune effects. This is achieved by preventing IL-2, either exogenous or secreted by effector T cells, from binding to trimeric receptors on regulatory T cells while still allowing IL-2 to bind and expand effector T cells and NK cells. This prevents the negative feedback loop caused by other IL-2-based treatments and biases the immune system toward activation over suppression. Imneskibart also prevents IL-2 from binding to CD25-containing receptors on eosinophils, as well as vasculature and pulmonary endothelium, which may significantly reduce the vascular leak syndrome and pulmonary edema associated with high-dose IL-2 therapy.

To learn more about the imneskibart Phase 1/2 clinical trial program, including study locations in the United States and Australia, please visit ClinicalTrials.gov (identifier: NCT05267626), www.solidtumorstudy.com (U.S.) and www.solidtumourstudy.com (Australia).

(Press release, Aulos Bioscience, APR 21, 2026, View Source [SID1234664598])

On April 21, 2026 Aprea Therapeutics, Inc. (Nasdaq: APRE) ("Aprea", or the "Company"), a clinical-stage precision medicine oncology company focused on the discovery and development of targeted therapies for patients with biomarker-defined cancers, reported the acceptance of an abstract "Early results from the first-in-human phase 1 study of WEE1 inhibitor APR-1051 in patients with advanced solid tumors (ACESOT-1051)" at the 2026 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting, to take place May 29 – June 2, 2026, in Chicago, IL.

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Presentation Details:
Title: Early results from the first-in-human phase 1 study of WEE1 inhibitor APR-1051 in patients with advanced solid tumors (ACESOT-1051)
Presenting author: Shiraj Sen, MD. PhD., NEXT Oncology Dallas, TX
Session: Poster Session – Developmental Therapeutics—Molecularly Targeted Agents and Tumor Biology
Date and Time: May 30, 2026, 1:30 PM-4:30 PM CDT
Poster Board: 244


For more information on the ACESOT-1051 trial, refer to ClinicalTrials.gov NCT06260514.

(Press release, Aprea, APR 21, 2026, View Source [SID1234664597])

On April 21, 2026 Amphista Therapeutics ("the Company" or "Amphista"), a leader in the discovery and development of non-cereblon/non-VHL Targeted Glue degraders, reported the first public disclosure of the chemical structure of its lead Targeted Glue AMX-883, a novel DCAF16-dependent protein degrader of BRD9, during the New Drugs on the Horizon session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 in San Diego, California yesterday.

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The oral presentation titled "Discovery of AMX-883: an orally bioavailable, novel degrader of BRD9 as a karyotype-independent pro-differentiation agent for the potential treatment of acute myeloid leukaemia", detailed the discovery and optimisation of a series of DCAF16-recruiting BRD9 degraders which yielded AMX-883, an orally bioavailable clinical candidate with picomolar potency and exquisite selectivity over the related bromodomain proteins BRD4 and BRD7. The DCAF16-dependent mechanism of action of AMX-883 was structurally confirmed by high-resolution cryo-EM of the ternary complex, revealing true glue-like interactions that stabilize the complex.

Amphista nominated AMX-883 as its first clinical development candidate in October 2025, based on a preclinical data package which expands the growing evidence base defining a critical role for BRD9 in maintaining acute myeloid leukaemia (AML) blast stemness and survival.

Martin Pass, Chief Development Officer at Amphista Therapeutics, said: "I’m delighted to be able to share the preclinical characterization data for AMX-883, our BRD9 Targeted Glue degrader, for the first time at AACR (Free AACR Whitepaper). Not only does it showcase the ability of our Eclipsys platform to deliver truly differentiated and high-quality molecules, but it also brings new insight and mechanistic understanding to BRD9’s role in AML and the hope that targeted removal from AML blasts may bring profound benefit to patients".

The data presented demonstrate that by degrading BRD9, AMX-883 relieves the differentiation block characteristic of AML, inducing expression of myeloid differentiation genes and repressing pro-proliferative programmes. AMX-883 increases markers of myeloid maturation across a range of AML cell lines representing diverse cytogenetic backgrounds, including TP53-mutant disease. This underlines its potential as a broad-acting, pro-differentiation agent and karyotype-independent therapeutic with the potential to benefit a wider population of AML patients than current treatments.

Critically, through BRD9 degradation, AMX-883 blocks patient-derived tumour growth in vivo as a monotherapy and demonstrated synergistic efficacy while in combination with venetoclax and prevented the emergence of resistance to venetoclax in vitro, addressing a major clinical challenge in AML.

Patrick Kelly, Chief Medical Officer at Amphista Therapeutics, added: "AML is a devastating disease with a poor prognosis, and most patients will relapse or become refractory to current treatments within a matter of months. As a karyotype-independent, pro-differentiation agent, AMX-883 has the potential to address a critical unmet need in AML by offering a broadly applicable treatment option. We are excited to advance this highly differentiated molecule into clinical trials in the second half of this year bringing new hope to patients facing this serious disease."

The Company is advancing AMX-883 into a Phase I clinical trial for AML in H2 2026.

(Press release, Amphista Therapeutics, APR 21, 2026, View Source [SID1234664596])

On April 21, 2026 Allogene Therapeutics, Inc. (Nasdaq: ALLO), a clinical-stage biotechnology company pioneering the development of allogeneic CAR T (AlloCAR T) products for cancer and autoimmune disease, reported that regulatory authorities in South Korea and Australia have cleared the Company to expand its pivotal Phase 2 ALPHA3 study evaluating cemacabtagene ansegedleucel (cema-cel) in first-line (1L) consolidation treatment for patients with large B-cell lymphoma (LBCL).

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The study, currently enrolling across more than 60 sites in North America, will expand to over 80 global sites with the addition of South Korea and Australia. This growing trial footprint reflects strong interest in ALPHA3 from clinical trial sites.

"Expanding into South Korea and Australia allows us to leverage regions with established clinical research infrastructure and experienced investigators," said David Chang, M.D., Ph.D., President, Chief Executive Officer and Co-Founder of Allogene. "These countries provide high-quality trial environments and efficient healthcare delivery systems. These regulatory approvals, follow our recent interim futility analysis, and we expect this expansion to support the continued enrollment and global development of cema-cel."

The Company recently announced findings from a planned interim futility analysis of the ALPHA3 trial from the first 24 patients enrolled. In this analysis, cema-cel demonstrated a 58.3% (7/12) minimal residual disease (MRD) clearance versus 16.7% (2/12) in the standard-of-care (SOC) observation arm in the 1L consolidation setting. Cema-cel was generally well-tolerated, with no serious treatment-related adverse events and no cytokine release syndrome (CRS) or immune effector cell-associated neurotoxicity syndrome (ICANS). There were no hospitalizations for treatment-related adverse events, suggesting consolidation of MRD+ remission with cema-cel may be suitable for a fully outpatient regimen. The ALPHA3 study is expected to enroll approximately 220 patients by the end of 2027. An interim analysis of event-free survival (EFS) is anticipated in mid-2027, followed by the primary EFS analysis in mid-2028. If positive, results could support a Biologics License Application (BLA) submission.

About Cemacabtagene Ansegedleucel (cema-cel)
Cemacabtagene ansegedleucel, or cema-cel, is a next generation anti-CD19 AlloCAR T investigational product for the treatment of large B cell lymphoma (LBCL). In June 2022, the U.S. Food and Drug Administration granted Regenerative Medicine Advanced Therapy (RMAT) designation to cema-cel in r/r LBCL. Allogene has oncology rights to cema-cel in the US, EU and UK with options for rights in China and Japan.

About the ALPHA3 Trial
Over 60,000 patients are expected to be treated for LBCL annually in the US, the EU and the UK. While first line (1L) R-CHOP or other chemoimmunotherapy is effective for most patients, approximately 30% will relapse and require subsequent treatment. The current standard of care after 1L treatment has been simply to "watch and wait" to see if the disease relapses. The pivotal Phase 2 ALPHA3 study takes advantage of cema-cel as a one-time, off-the-shelf treatment that can be administered immediately upon discovery of MRD following six cycles of R-CHOP or other chemoimmunotherapy, positioning it to become the standard "7th cycle" of frontline treatment available to all eligible patients with MRD.

(Press release, Allogene, APR 21, 2026, View Source [SID1234664595])