Olema Oncology to Present Preclinical Data for OP-3136, a Potent KAT6 Inhibitor, Demonstrating Anti-Tumor Activity in Multiple Solid Tumor Models at the 2025 AACR Annual Meeting

On March 25, 2025 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 it will present a poster highlighting preclinical anti-tumor activity of OP-3136, a novel small molecule that potently and selectively inhibits lysine acetyltransferase 6 (KAT6), in prostate, ovarian, and non-small cell lung cancer models in a late-breaking session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting taking place April 25-30 in Chicago, Illinois (Press release, Olema Oncology, MAR 25, 2025, View Source [SID1234651465]).

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Poster Presentation Details
Title: OP-3136, a selective KAT6 inhibitor, demonstrates anti-tumor activity in prostate, ovarian, and non-small cell lung cancer preclinical models
Poster/Abstract: LB166
Session: Late-Breaking Research: Tumor Biology 2
Date/Time: April 28, 2025, from 9:00am-12:00pm CT / 10:00am-1:00pm ET
Presenter: Dr. Gopinath S. Palanisamy, DVM, PhD

Additional information can be found on the AACR (Free AACR Whitepaper) Annual Meeting website.

About OP-3136
OP-3136 is a novel, orally available small molecule that potently and selectively inhibits lysine acetyltransferase 6 (KAT6), an epigenetic target that is dysregulated in breast and other cancers. In preclinical studies, OP-3136 has demonstrated significant anti-proliferative activity in ER+ breast cancer models and is combinable and synergistic with endocrine therapies, including palazestrant and cyclin-dependent kinase 4/6 (CDK4/6) inhibitors. The Investigational New Drug (IND) application for OP-3136 was cleared by the U.S. Food and Drug Administration (FDA) in December 2024 and patients are currently enrolling in the Phase 1 clinical trial.

Nurix Therapeutics Announces Multiple Presentations at the American Association for Cancer Research (AACR) 2025 Annual Meeting

On March 25, 2025 Nurix Therapeutics, Inc. (Nasdaq: NRIX), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of targeted protein degradation medicines, reported that company scientists will present preclinical data from its proprietary DEL-AI platform and several degrader programs in two oral presentations and two poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2025 Annual Meeting, which will be held from April 25-30, 2025, in Chicago, IL (Press release, Nurix Therapeutics, MAR 25, 2025, View Source [SID1234651409]).

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Oral Presentation Details:

Title: DEL-AI: Proteome-wide in silico screening of multi-billion compound libraries using machine learning foundation models
Presenting author: Paul Novick, Ph.D.
Session title: Innovative Approaches in Drug Discovery: Novel Leads, Degraders, and AI-Driven Solutions
Session date and time: Monday, April 28, 2025, 2:30 PM – 4:30 PM CST
Abstract ID: 3762

Title: Identification of selective, orally bioavailable Aurora A degraders for treatment of pediatric and adult cancers
Presenting author: Ryan Rountree, Ph.D.
Session title: Degraders and Glues
Session date and time: Tuesday, April 29, 2025, 2:30 PM – 4:30 PM CST
Abstract ID: 6379

Poster Presentation Details:

Title: NRX-0305: a pan-mutant BRAF degrader with broad preclinical efficacy, brain penetrance, and synergistic potential with MEKi across class 1/2/3 BRAF-mutant cancers
Presenting authors: Alexandra ‘Sasha’ Borodovsky, Ph.D.
Session title: Degraders and Glues 2
Session date and time: Monday, April 28, 2025, 9:00 AM – 12:00 PM CST
Abstract ID: 1651

Title: NX-5948 is a CNS-penetrant catalytic Bruton’s tyrosine kinase (BTK) degrader that breaks established design rules for CNS drugs
Presenting authors: Wylie Palmer, Ph.D.
Session title: Targeted Protein Degradation
Session date and time: Wednesday, April 30, 2025, 9:00 AM – 12:00 PM CST
Abstract ID: 7003

About DEL-AI
DEL-AI is Nurix’s discovery platform which employs advanced machine learning to enable all aspects of Nurix’s discovery engine, starting with DNA encoded library (DEL) hit-finding and degrader design, followed by automated chemistry synthesis and direct-to-biology screening and optimization, to rapidly generate degraders and degrader antibody conjugates (DACs) as new chemical entity drug candidates. By leveraging hundreds of billions of DEL compound binding signatures derived from thousands of DEL affinity screens collected from a diverse set of highly validated protein targets, our DEL-AI platform can prospectively identify binders as starting points for drug discovery for virtually any pharmaceutically relevant target.

About Bexobrutideg (NX-5948)
Bexobrutideg is an investigational, orally bioavailable, brain penetrant, small molecule degrader of BTK. Bexobrutideg is currently being evaluated in a Phase 1 clinical trial in patients with relapsed or refractory B cell malignancies. Additional information on the ongoing clinical trial can be accessed at clinicaltrials.gov (NCT05131022).

About NRX-0305
NRX-0305 is a potent, selective, and orally bioavailable mutant-specific BRAF degrader that Nurix is exploring for use in oncology. Nurix has reported preclinical data demonstrating potent anti-tumor activity in multiple cell line-derived and patient-derived xenograft disease models representing Class I, Class II and Class III B-RAF mutations. Anti-tumor activity was also observed in the setting of CNS disease and treatment-resistance, suggesting the potential for utility across a broad range of solid tumor types

About Aurora A Kinase
Aurora A kinase (AURKA) is an oncogene frequently overexpressed in adult solid tumors, hematologic malignancies, and pediatric cancers. Several AURKA inhibitors are effective in preclinical tumor models, but this activity has failed to translate into clinical efficacy. To address the limitations of inhibitors, Nurix has designed bifunctional targeted protein degraders of AURKA that enable removal of both enzymatic and scaffolding functions.

Elevation Oncology to Present Preclinical Data for EO-1022 at the American Association for Cancer Research (AACR) Annual Meeting 2025

On March 25, 2025 Elevation Oncology, Inc. (Nasdaq: ELEV), an innovative oncology company focused on the discovery and development of selective cancer therapies to treat patients across a range of solid tumors with significant unmet medical needs, reported that it will present preclinical data for its novel HER3 ADC, EO-1022, in a late-breaking poster presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2025, being held April 25-30 in Chicago, Illinois (Press release, Elevation Oncology, MAR 25, 2025, View Source [SID1234651424]).

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EO-1022 is an antibody drug conjugate (ADC) containing seribantumab, a fully human IgG2 anti-HER3 monoclonal antibody (mAb), which is site-specifically conjugated at glycan to the monomethyl auristatin E (MMAE) payload with a drug-to-antibody ratio (DAR) of 4. Elevation Oncology designed EO-1022, leveraging the advanced site-specific conjugation technology platform licensed from Synaffix B.V. Elevation Oncology is developing EO-1022 for the treatment of solid tumors that express HER3, including breast cancer and non-small cell lung cancer, and expects to file an IND application in 2026.

"We are eager to share the first preclinical data for EO-1022 at the AACR (Free AACR Whitepaper) Annual Meeting," said Joseph Ferra, President and Chief Executive Officer of Elevation Oncology. "With EO-1022, we are combining the most advanced site-specific conjugation technology platform with the clinically validated MMAE payload, which is widely used across ADC programs but has yet to be introduced into a HER3-targeting ADC in the clinic. We believe this unique combination will enable us to provide a new treatment option to patients with HER3-expressing solid tumors, including those who are refractory to other HER3-targeting agents in development. We look forward to advancing EO-1022 into clinical development next year."

Details of the poster presentation at AACR (Free AACR Whitepaper) 2025 are as follows:

Title: Preclinical discovery and characterization of EO-1022, a site-specific glycan-conjugated anti-HER3 vc-MMAE ADC for treating solid tumors

Abstract Presentation Number: LB004
Session Title: Late-Breaking Research: Experimental and Molecular Therapeutics 1
Session Date and Time: Sunday, April 27, from 2 p.m. to 5 p.m. CT (3 p.m. to 6 p.m. ET)
Location: Poster Section 50
The late-breaking abstract will become available on the AACR (Free AACR Whitepaper) website beginning at 12:00 noon CT (1:00 p.m. ET) on April 25, 2025, and published in an online-only supplement to Cancer Research.

About EO-1022

Elevation Oncology is developing EO-1022, a potentially differentiated HER3 ADC for the treatment of HER3-expressing solid tumors, including breast cancer and non-small cell lung cancer. EO-1022 consists of seribantumab, a fully human IgG2 anti-HER3 antibody, site-specifically conjugated at glycan to the MMAE payload with a DAR of 4. It leverages seribantumab’s desirable internalization properties and advanced site-specific ADC technology which makes possible the use of the potent cytotoxic MMAE payload. Elevation Oncology expects to file an IND application in 2026.

MAIA Biotechnology Announces Poster Presentation at ESMO’s European Lung Cancer Congress 2025

On March 25, 2025 MAIA Biotechnology, Inc., (NYSE American: MAIA) ("MAIA", the "Company"), a clinical-stage biopharmaceutical company developing targeted immunotherapies for cancer, reported that an abstract detailing a potential predictive biomarker for THIO treatment was selected for poster presentation at the European Lung Cancer Congress 2025 (ELCC 2025) taking place, March 26-29, in Paris, France (Press release, MAIA Biotechnology, MAR 25, 2025, View Source [SID1234651440]). ELCC is a program of the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper).

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"We are proud to join ELCC 2025, a premier conference focused directly on the science of thoracic oncology," said Vlad Vitoc, M.D., CEO of MAIA. "Our poster features our latest findings on cytokine Interleukin-6 (IL-6) as a potential predictive immune response biomarker for THIO sequenced with a checkpoint inhibitor. Predictive biomarkers can further illuminate THIO’s unique mechanisms of action which have shown exceptional efficacy in our Phase 2 clinical trial."

Presentation details:

Title:

Phase 2 Study of Telomere-Targeting Agent THIO Sequenced by Cemiplimab in Immune Checkpoint Inhibitor-Resistant Advanced NSCLC: Interleukin-6 as a Potential Predictive Biomarker

Abstract number:

997

Date:

March 28, 2025

Time:

12:00 p.m. CET

Presenter:

Tomasz Jankowski, M.D., Ph.D. – Lead investigator for THIO-101 Phase 2 clinical trial

Poster access:

MAIA’s poster will be available at maiabiotech.com/publications on March 28, 2025

The European Lung Cancer Congress is a collaborative effort of the most important multidisciplinary societies representing thoracic oncology specialists, working together to advance science, disseminate education and improve the practice of lung cancer specialists worldwide.

About Ateganosine

Ateganosine (THIO, 6-thio-dG or 6-thio-2’-deoxyguanosine) is a first-in-class investigational telomere-targeting agent currently in clinical development to evaluate its activity in Non-Small Cell Lung Cancer (NSCLC). Telomeres, along with the enzyme telomerase, play a fundamental role in the survival of cancer cells and their resistance to current therapies. The modified nucleotide 6-thio-2’-deoxyguanosine induces telomerase-dependent telomeric DNA modification, DNA damage responses, and selective cancer cell death. Ateganosine-damaged telomeric fragments accumulate in cytosolic micronuclei and activates both innate (cGAS/STING) and adaptive (T-cell) immune responses. The sequential treatment with ateganosine followed by PD-(L)1 inhibitors resulted in profound and persistent tumor regression in advanced, in vivo cancer models by induction of cancer type–specific immune memory. Ateganosine is presently developed as a second or later line of treatment for NSCLC for patients that have progressed beyond the standard-of-care regimen of existing checkpoint inhibitors.

ORIC® Pharmaceuticals Announces ORIC-944 Preclinical Presentation at the 2025 American Association for Cancer Research (AACR) Annual Meeting

On March 25, 2025 ORIC Pharmaceuticals, Inc. (Nasdaq: ORIC), a clinical stage oncology company focused on developing treatments that address mechanisms of therapeutic resistance, reported that a preclinical abstract highlighting the potential of ORIC-944, a potent and selective allosteric inhibitor of PRC2 to treat prostate cancer, has been accepted for poster presentation at the 2025 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting taking place April 25-30, 2025 in Chicago, IL (Press release, ORIC Pharmaceuticals, MAR 25, 2025, View Source [SID1234651410]).

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Poster presentation details:

Title: ORIC-944, a PRC2 inhibitor with best-in-class properties, restores luminal features and restricts adaptation in prostate cancer models, conferring synergy with AR pathway inhibitors
Abstract Number: 452
Date & Time: Sunday, April 27, 2025, 2:00 – 5:00 p.m. CT
Session Category: Experimental and Molecular Therapeutics
Session Title: Epigenetic Targets
Location: Poster Section 20

Abstract Highlights
ORIC-944 is a potent, highly selective, orally bioavailable, allosteric inhibitor of PRC2 that demonstrates best-in-class drug properties, including potency, solubility, and pharmacokinetics, with half-life supporting once daily dosing. In preclinical prostate cancer models, ORIC-944 demonstrated robust inhibition of PRC2, enhanced luminal cell state, and increased androgen receptor (AR) signaling. Analysis of chromatin revealed that ORIC-944 specifically restricts accessibility to lineage-associated transcription factors known to impart cellular plasticity in prostate cancer. This plasticity-restricted luminal state conferred by PRC2 inhibition is dependent on AR, leading to antitumor activity either in the hormone-depleted context or in the combination setting with an AR pathway inhibitor (ARPI). Together these data indicate that ORIC-944 reinforces a luminal cell state and, notably, restricts access to plasticity genes leading to a highly AR-dependent state in prostate models. This mechanism supports the observed preclinical synergy between PRC2 inhibition and ARPIs in both ARPI-sensitive and ARPI-resistant settings. These results position ORIC-944 as a potential best-in-class PRC2 inhibitor that blocks prostate tumor adaptation, restores luminal features, and sensitizes tumors to ARPIs. A phase 1b trial of ORIC-944 in combination with ARPIs is ongoing in metastatic prostate cancer (NCT05413421).