On October 21, 2026 Cerenome, Inc. (Nasdaq: CNSY) ("Cerenome" or the "Company") reported that new preclinical data presented at the 16th 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.

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"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.

(Press release, Cerenome, OCT 21, 2026, View Source [SID1234673643])