On April 17, 2026 Accent Therapeutics, a clinical-stage biopharmaceutical company pioneering novel small molecule precision cancer therapies, reported preclinical data supporting its potentially best-in-class KIF18A inhibitor, ATX-295, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 taking place April 17-22 in San Diego, California.

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"The strength and consistency of the preclinical results supporting our KIF18A program reinforce our confidence in ATX-295 as a novel therapeutic targeting a fundamental vulnerability in cancers with high levels of chromosomal instability," said Serena Silver, Ph.D., Chief Scientific Officer of Accent Therapeutics. "We are further advancing our commitment to maximize ATX-295’s potentially transformative impact for cancer patients by exploring AI-guided tools to assess chromosomal instability."

The company’s presentation includes preclinical data demonstrating the strong anti-tumor activity of ATX-295 across multiple solid tumor indications with high levels of chromosomal instability. The molecule showed potent in vitro activity in high-grade serous ovarian cancer (HGSOC), squamous non-small cell lung cancer (sqNSCLC), and triple-negative breast cancer (TNBC) cell lines, leading to cell cycle arrest and apoptosis. ATX-295 showed robust and durable tumor regression in patient-derived xenograft models of HGSOC, sqNSCLC and TNBC exhibiting whole-genome doubling (WGD), supporting WGD and chromosomal instability as predictive markers of tumor sensitivity to ATX-295. The results also include proof of concept for a novel, artificial intelligence (AI)-based method capable of rapidly detecting WGD in clinical samples, providing the foundation for a clinically feasible biomarker.

ATX-295 is currently under investigation in a first-in-human, Phase 1/2, open-label, dose escalation and expansion study, designed to evaluate the molecule’s safety, tolerability, and preliminary efficacy in patients with locally advanced or metastatic solid tumors, including HGSOC and sqNSCLC (NCT06799065).

Details for the presentation are as follows:

Poster Title: Robust anti-tumor activity of the novel KIF18A inhibitor, ATX-295, in preclinical models of chromosomally instable tumors
Abstract Number: 6641
Session Title: Multi-Axis Antineoplastic Agents
Session Date and Time: Tuesday, April 21: 2:00 PM – 5:00 PM PT
Location: Poster Section 14
Poster Board Number: 2
Presenter: Laura Ghisolfi, Ph.D.
About ATX-295
Accent’s lead program, ATX-295, is a potential best-in-class inhibitor for KIF18A, a mitotic kinesin motor protein critical for cell division in select tumors with chromosomal instability. KIF18A inhibitor treatment results in rapid cell death for cancers with an abnormal number of chromosomes (aneuploid) in vitro and in vivo, while cells with normal numbers of chromosomes (euploid) are unaffected. ATX-295 may address a large patient population across several cancer indications, including ovarian and squamous non-small cell lung cancer. Accent retains full worldwide rights to the KIF18A program, currently being evaluated in an ongoing Phase 1/2 clinical study (NCT06799065) enrolling patients with locally advanced or metastatic solid tumors, including high-grade serous ovarian cancer and squamous non-small cell lung cancer.

(Press release, Accent Therapeutics, APR 17, 2026, View Source [SID1234664483])

On April 17, 2026 OncoNano Medicine, Inc. ("OncoNano"), a clinical-stage biotechnology company developing precision therapies using its proprietary nanotechnology platform, reported it will present new preclinical data at the AACR (Free AACR Whitepaper) Annual Meeting 2026. The presentations highlight the breadth of its ON-BOARD platform and its ability to enable effective, tumor-targeted delivery of therapeutic payloads through clinically validated ultra pH-sensitive micelle technology designed to activate within the tumor microenvironment.

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"Our ON-BOARD platform is designed to overcome key limitations of existing delivery approaches, including reliance on tumor-associated antigens and off-tumor toxicities," said Kartik Krishnan, MD, PhD, Chief Executive Officer of OncoNano. "These data demonstrate the versatility of our platform across multiple payloads and reinforce its potential to deliver profound efficacy with an improved therapeutic index."

Poster Presentation Details

A Polymer-Drug Conjugate Platform for Tumor Specific Drug Delivery: Advancement of a Clinically Validated Ultra pH-Sensitive Micelle Technology
Presenter: Qingtai Su, PhD, Senior Scientist
Session Date/Time: April 20, 2026 | 2:00–5:00 PM PT
Location: Poster Section 14 | Board #17 | Poster #3026

This presentation highlights the breadth and tunability of the ON-BOARD platform, demonstrating tumor-specific delivery of multiple cytotoxic compounds through targeting the acidic tumor microenvironment. Preclinical data show strong in vitro and in vivo anti-tumor activity across a range of payload-linker combinations, including superior tumor growth inhibition and robust responses compared to standard-of-care agents. Findings further illustrate the ability to modulate payload release through linker design, supporting a differentiated, antigen-independent approach to drug delivery.

ONM-421, a pH-Responsive Polymer-Drug Conjugate Nanoparticle, Delivers MMAE to Solid Tumors and Shows Antigen-Independent Antitumor Efficacy in Mice
Presenter: Jason Miller, PhD, Associate Director
Session Date/Time: April 20, 2026 | 2:00–5:00 PM PT
Location: Poster Section 14 | Board #12 | Poster #3021

Building on the platform’s versatility, this presentation features ONM-421 as a lead example of ON-BOARD–enabled delivery. Preclinical findings demonstrate potent, antigen-independent anti-tumor efficacy across multiple xenograft models, including strong tumor growth inhibition and survival benefit. ONM-421 showed broader activity compared to an MMAE-based antibody-drug conjugate, including efficacy in tumors with low target expression where the ADC was less active. In these models, ONM-421 also demonstrated improved tolerability relative to a standard chemotherapy when given at an efficacious dose. These data highlight enhanced payload stability and protection during circulation, reinforcing the platform’s ability to enable targeted tumor delivery while reducing off-target toxicity.

(Press release, OncoNano Medicine, APR 17, 2026, View Source [SID1234664499])

On April 17, 2026 Acrivon Therapeutics, Inc. ("Acrivon" or "Acrivon Therapeutics") (Nasdaq: ACRV), a clinical stage biotechnology company discovering and developing precision medicines utilizing its proprietary Generative Phosphoproteomics AP3 (Acrivon Predictive Precision Proteomics) platform deployed for rational drug design and predictive clinical development, reported preclinical data that showed powerful synergies between its two lead assets and emerging and foundational standard-of-care anti-cancer agents. Both ACR-368, a CHK1/2 inhibitor currently in a registrational-intent Phase 2b study, and ACR-2316, a WEE1/PKMYT1 inhibitor currently in a Phase 1/2 study, showed strong synergy in combination with anti-PD-L1 checkpoint inhibition. Additionally, ACR-368 synergized with a Topo 1 inhibitor, a payload commonly used in ADCs. The data will be presented at the AACR (Free AACR Whitepaper) 2026 Annual Meeting being held in San Diego, CA.

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"We are excited to be presenting these highly actionable data, mechanistically derived from our AP3 platform, at AACR (Free AACR Whitepaper)," said Peter Blume-Jensen, M.D., Ph.D., chief executive officer, president, and co-founder of Acrivon. "Our findings highlight attractive opportunities for future frontline development of ACR-368 and ACR-2316 in combination with immune checkpoint inhibitors and ADCs."

The posters can be found on the Acrivon website under "Posters and Presentations" or by using this LINK.

Poster Presentation Details:

Title Potent synergy between CHK1/2 inhibitor ACR-368 and the ADC payload topoisomerase 1 inhibitor: Rationale for ADC + ACR-368 combination therapy
Date and Time Sunday, April 19, 2026; 2:00 p.m. – 5:00 p.m. PT
Session Experimental and Molecular Therapeutics: DNA Damage and Repair 1
Poster Number 239

Title ACR-368 synergizes with PD-L1 blockade by coordinated activation of adaptive and innate immunity pathways to achieve robust anti-tumor efficacy
Date and Time Monday, April 20, 2026; 9:00 a.m. – 12:00 p.m. PT
Session Late-Breaking Research: Immunology 2
Poster Number LB152

Title Treatment with ACR-2316, a potential first- and best-in-class WEE1/PKMYT1 inhibitor, combined with anti-PD-L1 induces complete tumor regression with durable immune memory
Date and Time Monday, April 20, 2026; 2:00 p.m. – 5:00 p.m. PT
Session Clinical Research: Combination Immunotherapies
Poster Number 3789

(Press release, Acrivon Therapeutics, APR 17, 2026, View Source [SID1234664515])

On April 17, 2026 Orum Therapeutics ("Orum" or the "Company") (KRX: 475830), a biotechnology company pioneering the field of degrader-antibody conjugates (DACs), reported the presentation of new preclinical data for ORM-1153, a CD123-targeting DAC designed to selectively deliver a proprietary GSPT1-degrading payload, in development for the treatment of AML and other CD123-positive hematological malignancies. The data were presented in two posters at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026.

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"These data show strong preclinical activity and the potential for a differentiated safety and tolerability profile, supporting the advancement of ORM-1153 as a next-generation CD123-targeting degrader-antibody conjugate for acute myeloid leukemia," said Chad May, Ph.D., Chief Scientific Officer of Orum. "Our approach combines a proprietary CD123-antibody and novel GSPT1-targeted protein degrader with the goal of achieving greater selectivity than conventional cytotoxic antibody-drug conjugates. We believe this strategy can enable more effective and better-tolerated therapies for patients with AML."

The first poster (Abstract Number: 1824) highlights how ORM-1153 was engineered with a proprietary CD123-antibody designed for enhanced internalization and reduced Fc-gamma receptor interactions, together with a linker optimized for plasma stability, an approach intended to improve delivery, reduce off-target and immune cell engagement, and support favorable pharmacologic properties. Consistent with that design, ORM-1153 showed strong preclinical anti-leukemia activity at low doses, along with prolonged accumulation in tumors, undetectable systemic free payload, and favorable repeat-dose non-human primate findings supporting a manageable safety and tolerability profile.

Data from the second poster (Abstract Number: 1710) extend Orum’s previously presented findings by showing activity across primary AML patient samples and in models with relevant tumor mutations, including TP53. Taken together, the findings support the potential for broad activity in AML, including in patients with TP53 mutations.

"These AACR (Free AACR Whitepaper) data are particularly encouraging in the context of AML, where many patients, especially those with TP53 mutations, continue to have limited treatment options and poor outcomes," said Olaf Christensen, M.D., Chief Medical Officer of Orum. "The activity we are seeing across primary patient samples and TP53-relevant models, together with a consistent pharmacologic and tolerability profile, supports the continued advancement of ORM-1153 toward clinical development."

Both posters are available on Orum’s website and will be presented at AACR (Free AACR Whitepaper) on Monday, April 20, from 9 am to 12 pm PDT.

About ORM-1153

ORM-1153 is a CD123-targeting degrader-antibody conjugate developed using Orum’s Dual-Precision TPD² approach. The molecule is built from two proprietary elements, a GSPT1-degrading payload and an anti-CD123 antibody engineered for high internalization efficiency, conjugated with a cleavable β-glucuronide linker. By combining tumor-selective antibody delivery with targeted protein degradation, ORM-1153 is designed to induce cancer cell death through degradation of GSPT1, a protein implicated in cell survival, including in TP53-mutant AML, while minimizing effects on normal tissues.

About Orum’s TPD² Approach

Orum’s unique Dual-Precision Targeted Protein Degradation (TPD²) approach builds novel targeted protein degraders combined with the precise cell delivery mechanisms of antibodies to generate innovative, first-in-class, cell-selective TPDs for the treatment of cancer and other serious diseases. Orum has developed new targeted protein degrader payloads to specifically degrade an intracellular target protein within cancer cells via the E3 ubiquitin ligase pathway. Conjugated to antibodies, the payloads are designed to be delivered specifically to target cells and precisely degrade the intracellular target protein of interest.

(Press release, Orum Therapeutics, APR 17, 2026, View Source [SID1234664797])

On April 17, 2026 Cogent Biosciences, Inc. (Nasdaq: COGT), a biotechnology company focused on developing precision therapies for genetically defined diseases, reported that preclinical data from the Company’s KRAS and ErbB2 pipeline programs will be presented during poster sessions at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 taking place in April 17-22 in San Diego, CA.

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"As we prepare for the potential launch of bezuclastinib later this year, we are excited to share updates from two of our pipeline programs this weekend at the 2026 annual AACR (Free AACR Whitepaper) meeting," said Andrew Robbins, Cogent’s President and Chief Executive Officer. "First, we are presenting data on CGT1263, our novel pan-KRAS(ON) inhibitor, which shows best-in-class cellular potency along with evidence that its kinase selectivity advantage over multi-RAS inhibitors could drive clinical differentiation with regards to skin toxicity, a current liability of advanced clinical programs. Separately, we provide an update on CGT4255, our novel, selective ErbB2 inhibitor that was specifically designed for its best-in-class CNS penetrant properties to address a significant unmet need for HER2+ patients with brain metastases. This presentation also includes preclinical data in combination with a HER2 ADC suggesting potential synergistic activity leading to improved duration of therapy as well as re-sensitization of patients following HER2 ADC resistance. With multiple potential blockbuster programs advancing in our pipeline, we believe these new data underscore the long-term potential of Cogent Biosciences."

Poster Details

Title: Characterization of CGT1263, a KRAS (ON/OFF) inhibitor clinical candidate with selectivity for mutant KRAS over HRAS and NRAS
Session Category: Experimental and Molecular Therapeutics
Session Title: Novel Antitumor Agents 1
Session Date and Time: April 19, 2026 – 2:00 PM – 5:00 PM PT (5:00 PM – 8:00 PM ET)
Location: Poster Section 17
Poster Board Number: 13
Poster Number: 410

Mutations in KRAS are among the most prevalent mutations found in cancer, occurring most often in colorectal cancer, non-small cell lung cancer and pancreatic cancer. The preclinical poster highlights Cogent’s internally developed pan-KRAS(ON) inhibitor with >500x selectivity for KRAS over HRAS and NRAS. Plasma exposure following oral administration across species resulted in sustained pERK inhibition and robust antitumor activity. Tumor pERK inhibition was also achieved with limited skin suppression, supporting the potential of a larger therapeutic window for CGT1263 when compared to multi-RAS inhibitors currently in clinical development. This aligns with historical data implicating the RAS-MAPK-ERK pathway as essential for skin development given its role in regulation of keratinocyte proliferation, differentiation, and survival; combined suppression of multiple targets within this pathway is thought to be the driver of frequent rash observed in patients treated with multi-RAS inhibitors. Overall, these findings suggest CGT1263 could provide an advantage for patients, enabling higher dosing designed to elicit a more profound molecular response. Investigational New Drug (IND) enabling studies are ongoing with an IND submission expected later this year.

Title: Preclinical characterization of CGT4255, an EGFR sparing, pan-mutant HER2 clinical development candidate with potential best-in-class brain penetration
Session Category: Experimental and Molecular Therapeutics
Session Title: Tyrosine Kinase, Phosphatase, and Other Inhibitors
Session Date and Time: April 21, 2026 – 2:00 PM – 5:00 PM PT (5:00 PM – 8:00 PM ET)
Location: Poster Section 18
Poster Board Number: 7
Poster Number: 5869

Cogent’s EGFR-sparing, brain-penetrant ErbB2 inhibitor includes potent coverage of key mutations (YVMA, S310F, V842I, L755S) inadequately addressed by currently approved therapies. Activating mutations in the ErbB2 gene have been identified in multiple cancers and demonstrate a tumorigenic role similar to that of ErbB2 amplification. New data presented describe CGT4255’s >100-fold selectivity over EGFR while robustly engaging HER2 amplification, insertion and mutant lines in addition to reinforcing best-in-class potential CNS performance relative to other agents in development. Additional mechanistic studies presented suggest CGT4255 may have synergistic effects on efficacy and durability when combined with HER2 targeted ADCs. Preclinical evidence demonstrates that concurrent treatment of CGT4255 and T-DXd enhances receptor internalization and cancer cell apoptosis, suggesting the potential for a synergistic combination that could improve patient outcomes. The Phase 1 study of CGT4255 is ongoing.

Posters will be available on the ‘Posters and Publications’ page of Cogent’s website.

(Press release, Cogent Biosciences, APR 17, 2026, View Source [SID1234664468])