Cogent Biosciences Announces KRAS Poster Presentation at the 2025 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics

On October 24, 2025 Cogent Biosciences, Inc. (Nasdaq: COGT), a biotechnology company focused on developing precision therapies for genetically defined diseases, reported updated preclinical data from the company’s potent and selective pan KRAS(ON) inhibitor in a poster presentation at the 2025 AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper) taking place in Boston, MA, October 22-26, 2025.

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"We are excited today to share updated data from our pan KRAS(ON) program which demonstrates a potential best-in-class profile for our lead molecule," said Andrew Robbins, Cogent’s President and Chief Executive Officer. "We look forward to advancing this program with the goal of filing an Investigational New Drug (IND) application to the U.S. Food and Drug Administration (FDA) in 2026."

Poster Details
The poster will be accessible on the ‘Posters and Publications’ page of Cogent’s website.

Title: Identification of CGT1263, a Potent KRAS Inhibitor with Selectivity for Mutant KRAS over HRAS and NRAS
Session Date and Time: Poster Session B, Friday, October 24, 2025 – 12:30 p.m. – 4:00 p.m. ET
Poster Number: B024
Abstract Number: B024

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 poster presented today describes Cogent’s internally developed KRAS(ON/OFF) inhibitor CGT1263, showing clear selectivity over HRAS and NRAS, with picomolar (pM) activity across a broad panel of KRAS mutant cell lines. In addition, the poster also characterizes CGT1815 (the prodrug of CGT1263), which is designed to optimize human pharmacokinetic performance, supported by pharmacokinetics data from both CGT1815 and CGT1263 across multiple species. Finally, the poster highlights that CGT1815 demonstrates superior efficacy in KRASG12D and KRASG12V tumor growth inhibition studies when compared to RMC-6236.

(Press release, Cogent Biosciences, OCT 24, 2025, View Source [SID1234656987])

Cogent Biosciences Announces KRAS Poster Presentation at the 2025 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics

On October 24, 2025 Cogent Biosciences, Inc. (Nasdaq: COGT), a biotechnology company focused on developing precision therapies for genetically defined diseases, reported updated preclinical data from the company’s potent and selective pan KRAS(ON) inhibitor in a poster presentation at the 2025 AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper) taking place in Boston, MA, October 22-26, 2025.

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"We are excited today to share updated data from our pan KRAS(ON) program which demonstrates a potential best-in-class profile for our lead molecule," said Andrew Robbins, Cogent’s President and Chief Executive Officer. "We look forward to advancing this program with the goal of filing an Investigational New Drug (IND) application to the U.S. Food and Drug Administration (FDA) in 2026."

Poster Details
The poster will be accessible on the ‘Posters and Publications’ page of Cogent’s website.

Title: Identification of CGT1263, a Potent KRAS Inhibitor with Selectivity for Mutant KRAS over HRAS and NRAS
Session Date and Time: Poster Session B, Friday, October 24, 2025 – 12:30 p.m. – 4:00 p.m. ET
Poster Number: B024
Abstract Number: B024

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 poster presented today describes Cogent’s internally developed KRAS(ON/OFF) inhibitor CGT1263, showing clear selectivity over HRAS and NRAS, with picomolar (pM) activity across a broad panel of KRAS mutant cell lines. In addition, the poster also characterizes CGT1815 (the prodrug of CGT1263), which is designed to optimize human pharmacokinetic performance, supported by pharmacokinetics data from both CGT1815 and CGT1263 across multiple species. Finally, the poster highlights that CGT1815 demonstrates superior efficacy in KRASG12D and KRASG12V tumor growth inhibition studies when compared to RMC-6236.

(Press release, Cogent Biosciences, OCT 24, 2025, View Source [SID1234657021])

Aprea Therapeutics Provides Clinical Update from ACESOT-1051 Trial Showing Early Signals of Activity for WEE1 Kinase Inhibitor APR-1051

On October 24, 2025 Aprea Therapeutics, Inc. (Nasdaq: APRE) ("Aprea", or the "Company"), a clinical-stage biopharmaceutical company developing innovative treatments that exploit specific cancer cell vulnerabilities while minimizing damage to healthy cells, reported an update on the ongoing Phase 1 ACESOT-1051 (A Multi-Center Evaluation of WEE1 Inhibitor in Patients with Advanced Solid Tumors, APR-1051) study. The latest results show that, at the 100 mg APR-1051 dose level, 3 out of 4 patients achieved stable disease, as measured using RECIST v1.1 criteria.

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A poster titled Early safety and efficacy of APR-1051, a novel WEE1 inhibitor, in patients with cancer-associated gene alterations: Updated data from ACESOT-1051 Phase 1 trial will be presented today at the AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper). The poster, to be presented by Drs. Timothy Yap MBBS, PhD, FRCP, University of Texas MD Anderson Cancer Center and lead investigator of the study, and Philippe Pultar, MD, Senior Medical Advisor at Aprea, summarizes preliminary results from the trial with a cutoff date of September 17, 2025. A copy of the poster will be available on Investors page of the Aprea corporate website under "Investor Presentations & Resources."

"We continue to be encouraged by these early clinical findings, which demonstrate signals of anti-tumor activity with APR-1051 in a heavily pre-treated patient population," said Dr. Pultar. "We believe the observation of disease control in tumors harboring FBXW7, CCNE1, and KRAS mutations align with our mechanistic understanding of WEE1 inhibition and reinforces the scientific rationale for APR-1051 development. We believe these promising data provide an important foundation as we continue with dose escalation in the ongoing study and we look forward to providing further updates as we advance to higher dose level in the ongoing study."

ACESOT-1051 Clinical Update (data cutoff October 19, 2025)

The primary objective of the trial is to characterize the safety profile, dose-limiting toxicity, maximum tolerated dose or maximum administered dose, and recommended Phase 2 dose of APR-1051. Secondary objectives are to 1) to characterize the pharmacokinetics of APR-1051 and the major metabolites and active metabolites of APR-1051, and 2) to assess preliminary efficacy of APR-1051
Results from Dose Level 6 (100 mg), show 3 out of 4 patients achieved stable disease, per RECIST v1.1 in heavily pretreated gastrointestinal and gynecologic malignancies
Disease stabilization was observed in patients with FBXW7, CCNE1, and KRASG12V + TP53 alterations
Favorable tolerability: No dose limiting toxicities (DLTs) or unexpected safety issues reported to date.
Following successful clearance of the 100 mg cohort, dose escalation has progressed to Dose Level 7 (150 mg)
For more information on ACESOT-1051, refer to ClinicalTrials.gov NCT06260514.

Individual Patient Results

86-year-old female with rectal cancer: Treated at a 100 mg dose after five prior lines, the patient achieved stable disease (-13% reduction). Tumor harbored FBXW7 mutation which is a mechanistically relevant biomarker for WEE1 inhibition. 145 days on treatment and ongoing
55-year-old male with rectal cancer: Treated at a 100 mg dose after four prior lines, the patient achieved stable disease (+1%). Tumor harbored KRASG12V + TP53-mutant patient supports mechanistic activity in this genotype. 63 days on treatment and ongoing
73-year-old female with endometrial cancer: Treated at a 100mg after five prior lines, patient achieved stable disease by RECIST v1.1 criteria (+15%) at the first evaluation before voluntarily withdrawing consent after approximately two months of treatment. Tumor harbored CCNE1 and TP53 mutations supports mechanistic activity in this genotype.
50-year-old female with colon cancer: Treated at 100mg after two prior lines. This patient had disease progression at first assessment (8 weeks).

(Press release, Aprea, OCT 24, 2025, View Source [SID1234656973])

Actinium Pharmaceuticals Presents New Data Demonstrating Potent and Durable Efficacy of ATNM-400, a First-in-Class Multi-Tumor Actinium-225 Radiotherapy, at the 32nd Annual Prostate Cancer Foundation Scientific Retreat

On October 24, 2025 Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of differentiated targeted radiotherapies, reported new preclinical data for ATNM-400, its novel, first-in-class antibody radioconjugate armed with the potent alpha-emitter Actinium-225 (Ac-225) at the 32nd Annual Prostate Cancer Foundation (PCF) Scientific Retreat being held October 23 – 25, 2025 in Carlsbad, CA.

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ATNM-400, which targets a non-PSMA antigen associated with prostate cancer progression and treatment resistance, demonstrated superior tumor control and improved overall survival compared with the active agents in key standard-of-care therapies including enzalutamide (the active agent in Xtandi, Astellas/Pfizer) and 177Lu-PSMA-617 (the active agent in Pluvicto, Novartis), as well as 225Ac-PSMA-617 across multiple preclinical prostate cancer models.

These data further reinforce ATNM-400’s potential as a paradigm changing, PSMA-independent Ac-225 alpha radiotherapy, offering opportunities for use as a monotherapy, in combination regimens, and in patients relapsing after ARPI or PSMA-directed treatments. ATNM-400 data has now been presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper), Society for Nuclear Medicine and Molecular Imaging (SNMMI) and PCF annual conferences in 2025 demonstrating its growing potential in various treatment settings in prostate cancer. In addition, data highlighting its potential in non-small cell lung cancer will be presented at the AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper) on Saturday, October 25, 2025.

Key Findings in Prostate Cancer Treatment Settings:

Potent and Durable Tumor Control, Increased Overall Survival and Synergistic Activity in Enzalutamide Resistant Prostate Cancer

Studies were performed in 22Rv1 prostate cancer models, which are known to be resistant to enzalutamide

ATNM-400 demonstrated superior and 5-times more durable anti-tumor efficacy extending to 100 days compared to approximately 20 days with enzalutamide alone

Given that ARPI therapies like enzalutamide are known to increase the ATNM-400 target antigen expression, combination treatment with ATNM-400 and enzalutamide was synergistic, resulting in complete tumor eradication in 40% of treated animals and significantly prolonged survival, whereas enzalutamide alone provided no durable disease control
Potent and Durable Tumor Control, Increased Overall Survival and Synergistic Activity in Enzalutamide Resistant Prostate Cancer

In models that progressed on enzalutamide, subsequent treatment with ATNM-400 achieved robust tumor control and extended survival, highlighting its potential in post-enzalutamide settings
Subsequent treatment with ATNM-400 achieved robust tumor control and extended survival, highlighting its potential in post-enzalutamide settings

Highly Effective and Increased Overall Survival in 177Lu-PSMA-617 Resistant Prostate Cancer

22Rv1 prostate cancer models are also resistant to 177Lu-PSMA-617

ATNM-400 overcame 177Lu-PSMA-617 resistance with approximately 5-times long tumor control and 2-times longer overall survival in tumor bearing animals
Highly Effective and Increased Overall Survival in 177Lu-PSMA-617 Resistant Prostate Cancer

Potent Therapeutic Activity Independent of PSMA Expression Levels

ATNM-400 targets a highly differentiated, non-PSMA antigen associated with the development and progression of prostate cancer, exhibiting potent therapeutic activity independent of PSMA expression levels

The expression of the ATNM-400 antigen target was not altered post-177Lu-PSMA-617
Potent Therapeutic Activity Independent of PSMA Expression Levels

22Rv1 cell lines are low-PSMA expressing and LNCaP cell lines are high-PSMA expressing
Addressing Critical Unmet Needs in mCRPC

Prostate cancer patients who progress to mCRPC face limited treatment options. While ARPI therapies like enzalutamide and PSMA-targeted radiotherapies like Pluvicto have extended survival, resistance and disease progression remain major challenges. In addition, a significant number of patients do not respond to PSMA-targeted radiotherapy as approximately 25%-30% of patients with mCRPC have low or no detectable PSMA and approximately 60% of patients have at least one PSMA-negative prostate cancer lesion.

By targeting a distinct, non-PSMA antigen associated with treatment resistance and poor outcomes, ATNM-400 represents a mechanistically differentiated alpha-radiotherapy approach that has potential in various treatment settings in prostate cancer. Its combination of a high-affinity antibody and potent alpha-emitting Ac-225 payload provides a path to overcome therapeutic resistance and extend patient survival beyond current standards of care.

Differentiation and Potential Clinical Impact

Sandesh Seth, Chairman and Chief Executive Officer, Actinium Pharmaceuticals, Inc., stated, "Since unveiling ATNM-400 earlier this year at AACR (Free AACR Whitepaper), our enthusiasm for this program only continues to grow commensurate with the promising results generated supporting its potential in various treatment settings in prostate cancer. ATNM-400 combines the precision of antibody targeting with the unparalleled potency of Ac-225 alpha particles, and importantly, it does so through a biologically distinct, PSMA-independent mechanism. These new preclinical data presented at PCF provide further validation for ATNM-400 and positions it as a candidate capable of transforming the treatment paradigm for patients with mCRPC. We are thrilled by the positive reactions to our ATNM-400 data and its differentiated non-PSMA approach."

Mr. Seth added, "As we have recently announced, beyond prostate cancer, we are also advancing ATNM-400 into non-small cell lung cancer (NSCLC), where it has shown the ability to overcome resistance to osimertinib (TAGRISSO, AstraZeneca) an EGFR-TKI therapy in preclinical models. Together, these data highlight Actinium’s innovate approach to R&D that leverages our radiochemistry expertise and strong translational biology capabilities to create first-in-class, multi-indication radiotherapeutics."

Actinium Pharmaceuticals envisions multiple clinical applications for ATNM-400 in prostate cancer, including:

Monotherapy in earlier disease settings prior to PSMA-directed radiotherapy.

Combination therapy with ARPI’s to enhance and prolong treatment responses.

Sequential therapy for patients relapsing after ARPI or PSMA-targeted radioligand treatments.
Summary of Preclinical Highlights of ATNM-400

Novel Mechanism: First-in-class Ac-225-based antibody radioconjugate against a non-PSMA target, overexpressed in advanced and resistant prostate cancer.

Superior Efficacy: Outperformed 177Lu-PSMA-617, Ac225-PSMA-617 and enzalutamide in direct head-to-head preclinical comparisons.

Durable Responses: A single 40 µCi/kg dose produced strong tumor inhibition; multi-dose regimens yielded long-term tumor control exceeding both enzalutamide and 177Lu-PSMA-617.

Overcomes Resistance: ATNM-400 maintained potent anti-tumor activity in models resistant to both enzalutamide and 177Lu-PSMA-617.

Combination Synergy: Synergized with enzalutamide, achieving complete tumor regressions in 40% of treated animals and markedly extending survival.

Favorable Biodistribution: Demonstrated selective and durable tumor uptake and rapid clearance from normal tissues, supporting a strong therapeutic index.
About ATNM-400

ATNM-400 is a highly innovative, first-in-class, and multi-indication Actinium-225 (Ac-225) targeted radiotherapy candidate in development for prostate cancer and non-small cell lung cancer (NSCLC). ATNM-400 is highly differentiated in prostate cancer as it targets a distinct non-PSMA antigen strongly implicated in prostate cancer progression and treatment resistance. Unlike 177Lu-PSMA-617, the active agent in Pluvicto and the majority of radiotherapies under development, which rely on PSMA targeting, ATNM-400 is designed to maintain efficacy in low-PSMA or PSMA-resistant disease, a major unmet clinical need. Ac-225 delivers high-linear-energy-transfer alpha particles that induce irreparable double-strand DNA breaks, offering superior potency over beta emitters like Lutetium-177 (177Lu), and has a shorter tissue path length that may reduce off-target toxicity. The receptor specifically targeted by ATNM-400 continues to be expressed at a high level even after androgen receptor inhibitor (ARPI) and ATNM-400 has shown to overcome resistance to the ARPI therapy enzalutamide and work synergistically in combination with enhanced tumor control including complete tumor regression. In NSCLC, ATNM-400 has shown to overcome resistance to osimertinib, an EGFR tyrosine kinase inhibitor (TKI) that is a standard of care therapy.

Prostate cancer is the most commonly diagnosed cancer in men, with ~1.5 million new cases globally and over 313,000 cases expected in the U.S. in 2025. While early-stage disease is typically managed with surgery, radiation, and ARPI therapy, up to 20% of cases progress to mCRPC – a lethal stage with limited treatment options. Targeted radiotherapy is a growing field in prostate cancer, dominated by PSMA-targeting agents like Pluvicto, which had sales of over $1.3 billion in 2024, yet many patients either lack PSMA expression or develop resistance to Pluvicto. In the U.S., 40,000 to 60,000 mCRPC patients annually progress after ARPI therapy that as a class generated sales of over $10.0 billion in 2024 including enzalutamide (Xtandi), which led the ARPI class with sales of over $5.9 billion in 2024, highlighting a significant unmet need. Lung cancer is the leading cause of cancer deaths and there are there are over 200,000 new cases expected in the U.S. in 2025. NSCLC accounts for approximately 85% of all lung cancer cases. The EGFR TKI Osimertinib (TAGRISSO, AstraZeneca) generated sales of $6.6 billion in 2024. Across prostate cancer and NSCLC, there are approximately 500,000 new cases in the U.S. alone.

(Press release, Actinium Pharmaceuticals, OCT 24, 2025, View Source [SID1234656990])

Arvinas Presents Preclinical Data for ARV-806 Demonstrating Robust and Differentiated Activity in Models of KRAS G12D-mutated Cancer at the 2025 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics

On October 24, 2025 Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company creating a new class of drugs based on targeted protein degradation, reported preclinical data for ARV-806, a PROTAC KRAS G12D degrader, at the 2025 AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper) in Boston, Massachusetts. The ARV-806 data presented show a differentiated profile based on degradation potency, antiproliferative activity, and induction of cancer cell death. ARV-806 is designed to target both the ON and OFF forms of KRAS G12D, which is the most common mutation of the KRAS protein. ARV-806 has the potential to address high unmet need in solid tumors, such as pancreatic, colorectal and non-small cell lung cancer.

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"These data suggest the potential of targeted protein degradation to overcome historical limitations in addressing undruggable KRAS mutations," said Angela Cacace, Ph.D., Chief Scientific Officer of Arvinas. "ARV-806’s ability to eliminate both ON and OFF forms of KRAS G12D, combined with its potency and durability shown in preclinical models, supports our confidence in its clinical potential to deliver meaningful benefit for patients with KRAS G12D-mutated cancers."

Key highlights from the presentation include:

In vitro, ARV-806 degraded KRAS G12D with picomolar potency across pancreatic, colorectal, and lung cancer cell lines but did not induce degradation of wild-type and other mutant RAS isoforms.
ARV-806 is differentiated from other KRAS G12D targeting agents in development and has potential to be a best-in-class therapy for KRAS G12D mutated cancers due to:
Catalytic activity, which allows it to overcome upregulation, a common mechanism of resistance to inhibitor treatment
Compared with clinical-stage KRAS G12D ON and OFF inhibitors and another clinical-stage G12D degrader, ARV-806 demonstrated:
>25-fold greater potency in reducing cancer cell proliferation,
>40-fold higher potency in degrading KRAS G12D protein (versus the comparable clinical-stage G12D degrader), and
>10-fold lower concentrations required to induce pro-apoptotic BIM expression.
Following a single intravenous dose in a colorectal tumor xenograft model, ARV-806 degraded >90% of KRAS G12D for seven days, with parallel suppression of c-MYC (a key driver of cancer cell proliferation) and induction of BIM (Bcl-2-interacting mediator of cell death, a pro-apoptotic factor) for ≥5 days.
ARV-806 demonstrated robust efficacy responses at low doses in tumor models including: ≥30% tumor volume reductions in pancreatic and colorectal cell line-derived xenograft (CDX) models and a patient-derived xenograft (PDX) model of lung cancer.

These data demonstrate sustained pharmacodynamic activity consistent with long-lasting target degradation, which we believe supports intermittent clinical dosing. Arvinas is currently evaluating ARV-806 in a Phase 1 clinical trial in patients with KRAS G12D–mutated advanced solid tumors (NCT07023731).

Also shown in the poster, orally bioavailable pan-KRAS degraders have been identified that potently degrade multiple variants of KRAS and spare other RAS isoforms. A tool pan-KRAS PROTAC demonstrated robust single-agent activity and superior combination efficacy with immune checkpoint blockade compared with a pan-RAS ON inhibitor (7 complete responses compared with 2 complete responses).

About ARV-806
ARV‑806 is a novel, investigational PROTAC degrader designed to selectively target and degrade mutant Kirsten rat sarcoma (KRAS) G12D which is the most common mutation of the KRAS protein. Therefore, ARV-806 has the potential to address high unmet need in solid tumors, such as pancreatic, colorectal and lung cancer. ARV‑806 is currently being evaluated in a Phase 1 clinical trial in patients with advanced solid tumors harboring KRAS G12D mutations.

(Press release, Arvinas, OCT 24, 2025, View Source [SID1234656974])