Cerenome Announces New Dual Mechanism of Action Featuring Lethal DNA Damage and Beneficial Immunomodulation Supporting Lead Investigational Drug REYOBIQ™
Key Highlights
- ➤REYOBIQ plus anti-PD-1 extended median survival to 65 days in ovarian cancer models
- ➤186RNL improved survival dose-dependently across 0.075 to 1.257 mCi doses
- ➤Combination treatment increased CD8+ T cells and NK cells while reducing immunosuppressive signals
- ➤Cerenome is evaluating REYOBIQ in three clinical trials for CNS cancers
Expert Statements
Eric J. Daniels, Chief Development Officer of Cerenome
“Turning ‘cold’ or immunologically resistant tumors into ‘hot’ or immunologically responsive tumors is the major limitation for the broader use of checkpoint inhibitors”
Eric J. Daniels, Chief Development Officer of Cerenome
“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.”
Eric J. Daniels, Chief Development Officer of Cerenome
“This sequence may convert cold tumors like ovarian, pancreatic and many CNS cancers, into hot ones.”
Eric J. Daniels, Chief Development Officer of Cerenome
“This opens up new combination strategies for these patients.”
Eric J. Daniels, Chief Development Officer of Cerenome
“Cerenome, along with its academic collaborators, are now characterizing REYOBIQ's immunomodulatory activity further across a board range of tumors.”
Andrew Brenner, Professor-Research and Kolitz Chair in Neuro-Oncology at UT Health San Antonio
“Ovarian cancer has responded poorly to checkpoint inhibitor monotherapy, in part because the tumor environment suppresses the immune system,”
Andrew Brenner, Professor-Research and Kolitz Chair in Neuro-Oncology at UT Health San Antonio
“In these models, REYOBIQ or 186RNL caused early DNA damage in tumor cells, followed by interferon signaling and immune activation.”
Andrew Brenner, Professor-Research and Kolitz Chair in Neuro-Oncology at UT Health San Antonio
“The combination with anti-PD-1 increased CD8+ T cells and NK cells and lowered immunosuppressive signals.”
Andrew Brenner, Professor-Research and Kolitz Chair in Neuro-Oncology at UT Health San Antonio
“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.”
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
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