Turning tumors into all-in-one immunotherapy bioreactors.
One injection reprograms the tumor to secrete 10+ staged immunotherapy payloads built to address, at once, every mechanism that keeps cold tumors cold.
A comprehensive immunotherapy from a single injection.
Cold tumors combine multiple concurrent mechanisms to evade the immune system — beyond what any single agent or tolerated systemic combination can overcome. Intratumoral multimodal therapy is the answer: it tackles multiple mechanisms locally while avoiding systemic toxicity. First-generation intratumoral approaches, although promising clinically, have their potential limited by several constraints: high procedural and manufacturing burden, insufficient payload secretion, and too few targeted mechanisms.
FIG removes those limits. We've made a discovery that reprograms tumors — historically very poor secretors — into high-output bioreactors capable of secreting, from a single injection, 10+ coordinated payloads in multiple stages, targeting every major immune-evasion mechanism and inducing a robust systemic anti-tumor response in the coldest of tumors — our Symphony™ platform.
Cold tumors are protected by many concurrent mechanisms.
Single-agent cancer immunotherapies have historically failed because tumors do not rely on a single escape route—they suppress immunity on multiple fronts at once. Systemic therapies that try to counter even two of these mechanisms exhibit severe toxicity.
Suppressive immune cells
- M2 macrophages
- MDSCs
- T-regulatory cells
- Cancer-associated fibroblasts
Suppressive signaling & immune masking
- TGF-β, IL-10, VEGF
- Immunosuppressive chemokines
- PD-L1 overexpression
- MHC-I suppression
Structural & metabolic barriers
- Dendritic-cell desert
- Dense extracellular matrix
- Hypoxia
- Acidosis
Intratumoral multimodal immunotherapy — but first-generation approaches hit ceilings.
Only local, multimodal therapy can address every mechanism at once without systemic toxicity. This has led to the rise of intratumoral immunotherapies. However, current approaches have limitations.
Comparison reflects general modality classes; individual programs vary.
Non-replicating viruses should solve this. Tumors don't secrete.
A non-replicating vector could deliver a full multimodal payload without destroying its own producer cell. But tumors are intrinsically poor secretors of therapeutic proteins — the field-wide reason non-replicating intratumoral gene therapy has never lived up to its promise.
We engineered tumors into high-output secretors.
Tumor cells are intrinsically poor secretors of immunotherapeutic payloads — the historical bottleneck limiting intratumoral gene therapy. Holding the promoter constant, we tested a library of rationally designed non-native signal peptides. One resulted in massive secretion — over 700-fold greater than native — an effect observed only in tumor cells.
Our discovery broke the bottleneck and has made intratumoral gene immunotherapy with high-capacity non-replicating viruses feasible for the first time.
From that foundation, we engineered the Symphony™ platform, designed to remove each limitation of first-generation approaches: a single injection that reprograms tumors into bioreactors of 10+ coordinated payloads, targeting every major immune-evasion mechanism and inducing a robust systemic anti-tumor response in the coldest of tumors.
See the Symphony™ platformRepresentative experiment. Holding CMV promoter constant, FIG SP3 drives >700× secretion vs native SP on average across experiments; observed in tumor cells only.
SP = signal peptide
Prostate first — a large, underserved market fit to the platform.
About 25% of prostate cancer patients—~70,000 U.S. cases a year — have high-risk localized disease. More than half of these patients have recurrence despite definitive treatment, driven by micrometastasis. Our therapy recruits the immune system to train itself against the cancer cells, find, and then clear those cells before castration is ever needed.
Our concurrent entry point is mCRPC, where early clinical precedent has shown multimodal intratumoral therapy can drive complete responses. FIG delivers those same mechanisms from one injection.
From there, the same architecture expands to any tumor a needle can reach — other cold, high-recurrence cancers, out-of-options metastatic disease, and unresectable tumors where the therapy acts as an in situ microsurgeon.
See the pipeline