Viridion Therapeutics
Preventing Cancer Recurrence
Through Immune Reprogramming.
3
Therapeutic molecules / construct
60–80%
Recurrence within 3–5 years
3
Independent mechanisms
0
Approved combined therapies
Yale-origin science · CARG-2020 exclusively licensed from CaroGen Corporation (Yale spin-off) · AVIDIO™ VLV platform.
The Problem
Why Cancer Comes Back.
Immune Exhaustion
Tumors upregulate PD-L1, switching off T-cells that would otherwise attack residual
disease.
Tumor-Promoting Inflammation
The IL-17 pathway creates a chronic inflammatory shield that protects surviving cancer cells from immune attack.
Immune Exclusion
Suppressive signaling physically prevents T-cells from entering the tumor microenvironment — rendering even activated immune cells ineffective.
No Existing Solution
Current immunotherapies target a single immune axis. Durable control requires addressing all three mechanisms simultaneously.
Our Approach
Multifunctional Immune Reprogramming.
IL-12
Activates Immunity
Converts suppressed immunity to an active anti-tumor T-cell response
IL-17
Blocks Inflammation
Removes the inflammatory shield protecting residual tumors
PD-L1
Silences Checkpoints
Prevents tumors from hiding via checkpoint escape
The result is a converted tumor microenvironment — one that supports durable, systemic immune memory rather than enabling recurrence.
Scientific Foundation
Yale-Origin Science. Peer-Reviewed Validation.
- Yale School of Medicine Origin
Multifunctional immunotherapy approach originated in Yale’s ovarian cancer and reproductive immunology research programs under the leadership of Drs. Gil Mor and Thomas Rutherford.
- Peer-Reviewed Publications
Published in Cancer Immunology Research (2023), Acta Pharmaceutica Sinica B (2024), and Scientific Reports (2025).
- AVIDIO™ Delivery Platform
The proprietary virus-like vesicle platform enables co-expression of multiple therapeutic payloads from a single construct.
- Multi-Indication Validation
Therapeutic activity demonstrated across ovarian, melanoma, and triple-negative breast cancer models without construct modification.
Explore the Lead Program.
Or review the preclinical validation data