Cancer Program
TP-317: Enabling Checkpoint Inhibitor Response in Cold Tumors
The Checkpoint Inhibitor Ceiling
Immune checkpoint inhibitors (ICI) release the brakes on the body’s natural ability to kill tumor cells. However, ICI only work when cytotoxic T cells are primed with tumor antigens to find and kill tumors.
The micro-environment of “cold" tumors frequently lacks primed T cells to respond to checkpoint blockade.
Cancer cells evade immune surveillance by downregulating antigen presentation or secreting immunosuppressive signals that suppress cytotoxic T cells.
TP-317: Priming Cold Tumors for Checkpoint Inhibitor Response
Activating the immune system upstream of checkpoint blockade
TP-317 promotes immunogenic phagocytosis of tumor debris — activating the antigen presentation machinery that checkpoint inhibitors require but cannot provide, while reducing tumorigenic inflammation.
TP-317 converts cold tumors to hot by priming T-cells and reprogramming tumor cells to present tumor antigens — an effect confirmed by single-cell RNA analysis.
Preclinical Validation
Dual SOC = [anti-PD-1 + chemo] or [anti-PD-1 + anti-CTLA-4]
Huang S, et al. Resolvin E1 sensitizes tumors to immune checkpoint inhibition by stimulating tumor antigen presentation. Cancer Res (2025) 85 (8_Supplement_1): 6912. https://doi.org/10.1158/1538-7445.AM2025-6912