Cerenome Announces New Dual Mechanism of Action Featuring Lethal DNA Damage and Beneficial Immunomodulation Supporting Lead Investigational Drug REYOBIQ™ 

The mouse-model findings support a potential combination approach, with median survival longer than control or either treatment alone.

Rhea-AI Summary

Cerenome (CNSY) announced preclinical findings suggesting its investigational drug REYOBIQ combines tumor DNA damage with immune-system effects in ovarian cancer models. In two mouse models, its active agent, rhenium Re186 obisbemeda, was associated with tumor injury and changes in the tumor environment. DNA-damage and cell-death programs activated within 24 hours; immune activation increased and immune-suppressing programs decreased by Day 28.

Combining the agent with anti-PD-1, a treatment that blocks an immune checkpoint, extended median survival to 65 days, longer than control or either agent alone. The combination reduced tumor burden, with brief weight loss and no evidence of substantial added toxicity.

Positive

• Minor pointCombination treatment extended median survival to 65 days in mice, longer than control or either agent alone.
• Minor point186RNL improved mouse survival dose-dependently across 0.075 to 1.257 mCi doses (p = 0.0003).
• Minor pointCombination treatment reduced tumor burden; tissue samples showed minimal remaining tumor in the omentum.
• Minor pointDNA-damage and cell-death programs activated within 24 hours of treatment in mouse models.
• Minor pointImmune activation programs increased and macrophage-associated immune suppression decreased by Day 28.

6 minor points

• Minor point186RNL lowered IL-10, an immune-suppressing signaling protein, compared with untreated controls.
• Minor pointCombination treatment increased T cells and natural killer cells, while monocytes fell in mouse models.
• Minor pointCombination-driven immune response peaked at 24 hours and lasted through Day 28, dominated by CD8+ T cells.
• Minor pointCD8+ T-cell activation markers CD25 and CD69 were higher with combination treatment than anti-PD-1 alone.
• Minor pointCombination treatment showed no evidence of substantial added toxicity in the mouse models.
• Minor point. Forward-looking: it has not happened yet and may not happen.Cerenome and academic collaborators are further characterizing REYOBIQ's immune-system activity across a range of tumors.

Negative

• Minor pointCombination treatment was associated with brief weight loss in the mouse models.

Key Figures

Dose-dependent survival result: 0.075 to 1.257 mCi; p = 0.0003 Median survival: 65 days Immune response timing: Peaked at 24 hours and lasted through Day 28

Dose-dependent survival result

0.075 to 1.257 mCi; p = 0.0003

ID8agg mouse model

Median survival

65 days

186RNL plus anti-PD-1 in preclinical ovarian cancer models

Immune response timing

Peaked at 24 hours and lasted through Day 28

Preclinical ovarian cancer models

Key Terms

checkpoint blockade, apoptosis, interferon signaling, il-10

4 terms

checkpoint blockade medical

"Combination treatment with anti-PD-1 checkpoint blockade"

A type of cancer immunotherapy that uses drugs—most often monoclonal antibodies—to block proteins (immune checkpoints) that restrain T cells, such as PD-1, PD-L1 or CTLA-4. By preventing these checkpoint proteins from sending inhibitory signals, checkpoint blockade increases the immune system’s ability to recognize and attack tumor cells; it can also cause inflammatory side effects because the same mechanism reduces immune tolerance to healthy tissues.

apoptosis medical

"DNA-damage, p53 and apoptosis (cell-death) programs switched on"

Apoptosis is a controlled, built‑in process where cells deliberately shut down and are safely removed, like a person retiring and clearing out their belongings so the house stays orderly. Investors care because many drugs and diagnostics target or measure this process: how well a therapy triggers or avoids apoptosis can determine clinical trial success, safety profiles, regulatory approval, and ultimately a company’s valuation.

interferon signaling medical

"interferon signaling, innate immunity, and antigen-presentation programs"

A cell communication system in which interferon proteins, released by cells in response to viruses, bacteria, or immune triggers, bind to specific receptors on nearby or the same cells and activate intracellular pathways (most commonly the JAK–STAT cascade) that turn on interferon-stimulated genes. Those genes produce proteins that limit pathogen replication, change how cells present antigens, and alter immune-cell behavior; the exact effects depend on the interferon type (type I, II, or III), the receptor distribution on target cells, and the tissue context.

il-10 medical

"186RNL substantially lowered IL-10, an immunosuppressive cytokine"

IL-10 is a small signaling protein the immune system uses to dial down inflammation, acting like a thermostat that tells immune cells to calm down to prevent excessive damage. For investors, IL-10 matters because therapies that boost, mimic, or block its activity can change how well treatments work, affect safety profiles, guide clinical trial design, and influence regulatory and commercial prospects for drugs targeting inflammatory and immune-related diseases.

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Findings suggest a dual mechanism of action for REYOBIQ against cancer cells

New findings revealed potential dual mechanism as combinations with checkpoint blockade further enhanced REYOBIQ therapeutic action in multiple cancers

HOUSTON, Oct. 21, 2026 (GLOBE NEWSWIRE) -- Cerenome, Inc. (Nasdaq: CNSY) ("Cerenome" or the "Company") today announced that new preclinical data presented at the 16^th Biennial Rivkin Ovarian Cancer Research Symposium illustrate the emerging immunomodulatory properties of REYOBIQ™ (rhenium Re186 obisbemeda), its lead investigational targeted radiotherapeutic. The Ovarian Cancer Research Alliance sponsored the symposium, held October 16–18, 2026, in Philadelphia. In two mouse models of aggressive epithelial ovarian cancer, treatment with rhenium (186Re) obisbemeda (rhenium-186 nanoliposome, 186RNL), the active agent in REYOBIQ, was associated with tumor injury and changes in the tumor microenvironment. Combination treatment with anti-PD-1 checkpoint blockade also showed improved antitumor activity.

"Turning ‘cold’ or immunologically resistant tumors into ‘hot’ or immunologically responsive tumors is the major limitation for the broader use of checkpoint inhibitors," said Eric J. Daniels, M.D., Cerenome's Chief Development Officer. “REYOBIQ delivers targeted radiation that injures the tumor, activates further DNA-damage, p53, and apoptosis programs within 24 hours, turning on the innate immune response, while simultaneously lowering IL-10 and macrophage-driven immunosuppression. This sequence may convert cold tumors like ovarian, pancreatic and many CNS cancers, into hot ones. This opens up new combination strategies for these patients. Cerenome, along with its academic collaborators, are now characterizing REYOBIQ's immunomodulatory activity further across a board range of tumors."

More Than a Dose of Radiation

REYOBIQ is designed to deliver a very high dose of beta radiation directly to the tumor or the fluid compartment around it, while minimizing exposure to the rest of the body. Its well-established mechanism of action is radiation-induced DNA damage and tumor cell death. A growing body of translational evidence suggests REYOBIQ may also act substantially on the immune system. In this proposed sequence, local radiation injures tumor cells that then triggers interferon signaling, antigen presentation, cytotoxic T cell and natural killer (NK) cell recruitment to the tumor environment, and dampens immunosuppressive signals.

Ovarian Cancer Models Illustrate the Mechanism

Henriette Balinda, Ph.D., and colleagues in the laboratory of Andrew Brenner, M.D., Ph.D., at The University of Texas Health Science Center at San Antonio (UT Health San Antonio) presented the poster, titled, "186Rhenium-Nanoliposome (186RNL) Remodels the Tumor Microenvironment in Preclinical Ovarian Cancer Models." Epithelial ovarian cancer responds poorly to checkpoint inhibitors given alone, in part because its tumor microenvironment suppresses the immune system. That makes it an attractive model for testing whether local radiation can reverse that suppression. The poster also tracked immune changes in ascites (abdominal fluid).

The poster will be available on the Publications page of Cerenome's website.

Key scientific findings:

• Tumor injury starts the response: Single-cell RNA sequencing showed that DNA-damage, p53 and apoptosis (cell-death) programs switched on within 24 hours of treatment.
  
• The immune system is then activated: By Day 28, interferon signaling, innate immunity, and antigen-presentation programs had increased, and macrophage-associated immunosuppressive programs had decreased.
  
• Lower immunosuppressive signaling: 186RNL substantially lowered IL-10, an immunosuppressive cytokine, compared with untreated controls.
  
• Effector immune cells shift the balance: When 186RNL was combined with anti-PD-1, immune cells (CD45+), T cells (CD3+), CD8+ cytotoxic T cells, CD4+ effector T cells, and NK cells all rose, while monocytes fell. The immune response was dominated by CD8+ T cells. It peaked at 24 hours and lasted through Day 28. CD8+ T-cell activation markers (CD25 and CD69) were higher with the combination than with anti-PD-1 alone.
  
• Dose-dependent antitumor activity: In the ID8agg model, 186RNL improved survival in a dose-dependent manner across doses of 0.075 to 1.257 mCi (p = 0.0003). Bioluminescence imaging showed the deepest and longest-lasting tumor suppression at the highest dose.
  
• Better outcomes with checkpoint blockade: 186RNL plus anti-PD-1 extended median survival to 65 days, longer than control or either agent alone. The combination also reduced tumor burden, and tissue samples showed minimal remaining tumor in the omentum. Weight loss was brief, and the combination showed no evidence of substantial added toxicity.
  
  

"Ovarian cancer has responded poorly to checkpoint inhibitor monotherapy, in part because the tumor environment suppresses the immune system," said Andrew Brenner, M.D., Ph.D., Professor-Research, Kolitz Chair in Neuro-Oncology, UT Health San Antonio. "In these models, REYOBIQ or 186RNL caused early DNA damage in tumor cells, followed by interferon signaling and immune activation. The combination with anti-PD-1 increased CD8+ T cells and NK cells and lowered immunosuppressive signals. Those are the changes you want to see and support an understanding of how REYOBIQ may be used in the future to make checkpoint therapy more effective."

About REYOBIQ™ (rhenium Re186 obisbemeda)

REYOBIQ is an investigational injectable radiotherapeutic in which the radioisotope rhenium-186 is chelated and trapped inside a nanoliposome. It is designed to deliver targeted, high-dose beta radiation directly to tumors through local delivery, such as convection-enhanced delivery or an intraventricular (Ommaya) catheter, while keeping exposure to the rest of the body low. REYOBIQ is being evaluated for the treatment of leptomeningeal metastases, recurrent glioblastoma and pediatric brain cancers in the ReSPECT-LM, ReSPECT-GBM and ReSPECT-PBC clinical trials. Results from the multicenter Phase 1 ReSPECT-GBM trial were published in Nature Communications in 2025 (Brenner AJ, et al. Nat Commun. 2025;16:2079). REYOBIQ is investigational and has not been approved by the U.S. Food and Drug Administration or any other regulatory authority for any use.

About Cerenome

Cerenome (Nasdaq: CNSY) is a CNS oncology company advancing an integrated platform that combines precision diagnostics, targeted therapeutics, and artificial intelligence to improve outcomes for patients with central nervous system cancers. The Company's CNSide® Diagnostics platform supports the detection, molecular characterization, and longitudinal monitoring of CNS cancers through cerebrospinal fluid-based testing. Its lead therapeutic platform, REYOBIQ™ (rhenium Re186 obisbemeda), is being evaluated in clinical trials for leptomeningeal metastases, recurrent glioblastoma, and pediatric brain cancers. The data & artificial intelligence platform is designed to integrate diagnostic, molecular, imaging, and clinical data into actionable insights that support precision oncology and therapeutic innovation. By integrating commercial diagnostics, targeted therapeutics, proprietary longitudinal data, and artificial intelligence within a single organization, Cerenome is building a differentiated CNS oncology platform designed to improve patient care while creating long-term shareholder value. For more information, visit https://www.cerenome.com.

Forward-Looking Statements

This press release contains statements that may be deemed "forward-looking statements" within the meaning of U.S. securities laws. All statements in this press release other than statements of historical fact are forward-looking statements. These forward-looking statements may be identified by future verbs, as well as terms such as "expect," "potential," "may," "could," "suggest," "support," "plan" and similar expressions or the negatives thereof. These statements include, without limitation, statements about the potential immunomodulatory properties of REYOBIQ and rhenium (186Re) obisbemeda; the potential of REYOBIQ to change the tumor immune microenvironment or improve response to immune checkpoint inhibitors; the potential of REYOBIQ in combination with immunotherapy in CNS cancers or other indications; whether preclinical results will be reproduced in further preclinical studies or in human clinical trials; and the Company's research and clinical development plans for REYOBIQ. These statements are based on assumptions and assessments made by management in light of their experience, their view of historical trends, current conditions, expected future developments and other factors they believe are appropriate. Preclinical results may not predict clinical outcomes. Actual results could differ materially because of risks and uncertainties, including those described under "Risk Factors" in the Company's filings with the U.S. Securities and Exchange Commission. The Company undertakes no obligation to update any forward-looking statement, except as required by law.

Investor Contact
CORE IR
IR@cerenome.com

A PDF accompanying this announcement is available at http://ml.globenewswire.com/Resource/Download/b41783e3-1ede-4509-a02d-c887a38bcfd6

FAQ

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What did Cerenome's REYOBIQ ovarian cancer combination study show?

In mouse models, REYOBIQ's active agent combined with anti-PD-1 extended median survival to 65 days, longer than control or either agent alone. The combination also reduced tumor burden and showed no evidence of substantial added toxicity, although weight loss occurred briefly.

What dual mechanism do Cerenome's REYOBIQ findings suggest?

The preclinical findings suggest REYOBIQ may combine radiation-induced tumor DNA damage with immune-system activation. Mouse-model analyses showed early DNA-damage and cell-death activity, followed by increased immune-response programs and reduced immune-suppressing signals.

Which REYOBIQ doses improved survival in Cerenome's ovarian cancer mouse study?

In the ID8agg mouse model, 186RNL improved survival in a dose-dependent manner across 0.075 to 1.257 mCi doses (p = 0.0003). Imaging showed the deepest and longest-lasting tumor suppression at the highest dose.