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])

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])

Initial results from ongoing dose-escalation study of XmAb819 & oncology pipeline update

On October 24, 2025 Xencor presented its corporate presentation.

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(Presentation, Xencor, OCT 24, 2025, View Source [SID1234656985])

Xencor Presents Initial Data for XmAb819, a First-in-class ENPP3 x CD3 Bispecific T-Cell Engager, in Development for Clear Cell Renal Cell Carcinoma

On October 24, 2025 Xencor, Inc. (NASDAQ:XNCR), a clinical-stage biopharmaceutical company developing engineered antibodies for the treatment of cancer and autoimmune diseases, reported initial results from the ongoing Phase 1 dose-escalation study of XmAb819, a ENPP3 x CD3 T-cell engaging bispecific antibody, in patients with advanced clear cell renal cell carcinoma (ccRCC). The results were presented in a poster at the AACR (Free AACR Whitepaper)-NCI-EORTC Conference on Molecular Targets and Cancer Therapeutics in Boston, Massachusetts.

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"We are excited to be developing XmAb819 as a novel first-in-class ENPP3 T-cell engager that could potentially offer a much-needed new therapeutic modality for patients with advanced clear cell renal cell carcinoma and clinicians. In our first clinical presentation of dose-escalation data, XmAb819 demonstrated compelling anti-tumor activity and a well-tolerated safety profile in very heavily pre-treated patients," said Bassil Dahiyat, Ph.D., president and chief executive officer at Xencor. "We are on-track with our first dose-expansion cohort now selected and are enrolling patients as we continue to dose escalate. We are confident that we will be able to select a recommended Phase 3 dose during 2026 to support the initiation of our first pivotal study in advanced ccRCC during 2027."

The poster will be archived under "Events & Presentations" in the Investors section of the Company’s website located at www.xencor.com.

Phase 1 Study of XmAb819 in Advanced ccRCC

The Phase 1 clinical trial is a multicenter, open-label, dose-escalation and dose-expansion study designed to evaluate XmAb819 as monotherapy in patients with advanced ccRCC. As of the September 19, 2025 data cut-off, 69 patients received XmAb819 across 10 intravenous (IV) dose cohorts and 5 subcutaneous (SC) dose cohorts. Patients received a median of 4 prior lines of therapy (range 1-8). All patients received prior anti-PD1 therapy and prior VEGF-TKI therapy, and 36% of patients were previously treated with a HIF2α inhibitor. Efficacy was assessed by investigators using RECIST v1.1.

XmAb819 demonstrated evidence of anti-tumor activity and an acceptable safety profile that was generally well tolerated across dose levels. Of the 20 efficacy-evaluable patients treated at the dose levels that were preclinically predicted to be within the target dose range, 25% achieved a partial response (PR) as best response (n=5, 4 confirmed PRs and 1 unconfirmed PR), with a 70% disease control rate (DCR, 14/20). All five responders remain on treatment, and 50% (10/20) of all efficacy-evaluable patients within the target dose range remain on treatment. For one patient with a first-scan assessment of progressive disease, a subsequent 47% reduction in target lesions was reported, and the patient remains on-treatment as of the data cut-off (treatment week 30). All 6 patients within the target dose range with greater than 30% reduction in lesion size remain on treatment as of the data cut-off.

The most common treatment-emergent adverse events (TEAE) were cytokine release syndrome (CRS), rash and gastrointestinal-related toxicities that were primarily Grade 1 or 2 in severity and predominantly associated with prime-step dosing in the first four weeks of treatment. Grade 3 TEAEs related to treatment were rash (16%), liver enzyme elevations (7%) and CRS1 (4%). One dose-limiting toxicity of Grade 4 elevated liver enzymes was deemed related to treatment. No cases of treatment-related immune effector cell-associated neurotoxicity syndrome (ICANS) were observed. No Grade 5 events were reported. Four patients (6%) were dose-reduced due to treatment-related AEs, and three patients (4%) discontinued treatment due to treatment-related AEs, which includes two patients who experienced elevated liver enzymes and one patient who experienced a non-fatal myocardial infarction in the presence of hypotension and CRS.

1 While 51 patients received the correct priming dose of XmAb819, higher than expected serum levels of XmAb819 were observed in 18 patients, which was investigated during early 2025 and linked to priming dose preparation errors that resulted from use of certain ports and syringes during drug dilution. Of the 51 patients receiving the correct priming dose, 2 (4%) experienced Grade 3 CRS. Of the 18 patients that were found to have a 3- to 8-fold higher than expected concentration of study drug post-priming dose, 5 (28%) experienced Grade 3 CRS. Mitigation of dosing errors through site retraining is complete, and the root cause of these errors will be eliminated through the introduction of a low concentration formulation to be implemented during the first half of 2026.

Webcast Details

Xencor will host a webcast today at 1:30 a.m. ET (10:30 a.m. PT) to discuss the initial results outlined in this news release. The live webcast may be accessed through this link and through "Events & Presentations" in the Investors section of the Company’s website, located at investors.xencor.com. A recording will be available for at least 30 days.

About XmAb819

XmAb819 is a first-in-class, tumor-targeted, T-cell engaging XmAb 2+1 bispecific antibody in development for patients with clear cell renal cell carcinoma (ccRCC). XmAb819 engages the immune system and activates T cells for highly potent and targeted lysis of tumor cells expressing ENPP3, an antigen highly expressed on kidney cancers. ENPP3 is a differentially expressed target, with high level expression in renal cell carcinoma (RCC) and low-level expression on normal tissues. With two tumor-antigen binding domains and one T-cell binding domain, Xencor’s XmAb 2+1 format enables antibodies to bind more avidly and selectively kill tumor cells with higher antigen density, potentially sparing normal cells. Xencor is conducting a Phase 1 study to evaluate XmAb819 in patients with advanced ccRCC.

(Press release, Xencor, OCT 24, 2025, View Source [SID1234656984])

Alphamab Oncology Announces the First Patient Dosed in a Phase I Clinical Study of PD-L1/αvβ6 Bispecfic ADC JSKN022

On October 24, 2025 Alphamab Oncology (stock code: 9966.HK) reported that the first patient has been successfully dosed at Sun Yat-sen University Cancer Center in the phase I clinical study (Study ID: JSKN022-101) of JSKN022, an independently developed innovative bispecific antibody-drug conjugate (ADC) targeting PD-L1 and integrin αvβ6, for the treatment of advanced malignant solid tumors (Press release, Alphamab, OCT 24, 2025, View Source [SID1234656982]). JSKN022 is the Company’s fourth ADC candidate entering clinical development, as well as the world’s first PD-L1/αvβ6 bispecific ADC to advance into clinical trials.

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JSKN022 innovatively combines immuno-oncology (IO) mechanisms with ADC approaches, utilizing Alphamab Oncology’s proprietary glycan-specific conjugation platform and linker-payload (Alphatecan) to significantly improve stability and homogeneity. The molecule is designed to bind to PD-L1 and/or integrin αvβ6 on the surface of tumor cells. After binding to either target, JSKN022 enters the lysosome through target-mediated endocytosis. The linker is hydrolyzed by proteolytic enzymes, releasing cytotoxic topoisomerase I inhibitor, which then induces apoptosis of PD-L1 and/or integrin αvβ6 positive tumor cells. In addition, the inhibitor can block TGFβ signaling to modulate immune function, and kill antigen-negative cells through the bystander effect, thereby achieving multiple anti-tumor activity. Preclinical data presented at the 2025 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, demonstrated that JSKN022 effectively inhibited the proliferation of cancer cells and demonstrated greater tumor suppression than single-target ADCs.

JSKN022-101 is an open-label, multi-center, phase I clinical trial of JSKN022, including dose-escalating and dose-optimization phases. This study aims to evaluate the safety, tolerability, pharmacokinetics (PK)/pharmacodynamics (PD), and antitumor activity of JSKN022 in patients with advanced malignant solid tumors, and determine the maximum tolerated dose (MTD) and/or recommended Phase II dose (RP2D).

At present, no ADC targeting integrin αvβ6 or PD-L1 has been approved for marketing worldwide, with all related investigational candidates remaining in clinical development stages. JSKN022 will potentially bring in novelty in the therapeutic approach for cancers that are refractory or resistant to PD-1/PD-L1 inhibitors.

About JSKN022

JSKN022 is a first-in-class ADC targeting both PD-L1 and integrin αvβ6. Based on independently developed Envafolimab, Alphamab integrates immuno-oncology (IO) mechanisms with ADC approaches. This novel drug molecule utilizes proprietary glycan-specific conjugation technology and linker-payload (Alphatecan) to enhance both stability and homogeneity. The molecule is designed to bind to PD-L1 and/or integrin αvβ6 on the surface of tumor cells. After binding to either target, JSKN022 enters the lysosome through target-mediated endocytosis. The linker is hydrolyzed by proteolytic enzymes, releasing cytotoxic topoisomerase I inhibitor, which then induces apoptosis of PD-L1 and/or integrin αvβ6 positive tumor cells. In addition, the inhibitor can block TGFβ signaling to modulate immune function, and kill antigen-negative cells through the bystander effect, thereby achieving multiple anti-tumor activity. JSKN022 is expected to provide a novel therapeutic option for cancers that are refractory or resistant to PD-1/PD-L1 inhibitors. The Phase I clinical study of JSKN022 in patients with advanced malignant solid tumors has been conducted in China.