FIG Therapeutics

Turning tumors into all-in-one immunotherapy bioreactors.

Our Symphony™ platform turns tumors into all-in-one immunotherapy bioreactors. One injection. Ten-plus staged, secreted payloads. A non-replicating gene therapy engineered to solve — at once — every mechanism that keeps cold tumors cold.

>700×
Increase in tumor secretion from our engineered signal peptide
10+
Staged, secreted payloads from a single intratumoral injection
$100B+
Solid-tumor immuno-oncology TAM; mCRPC $21B → $92B by 2034
1
Drug substance, 1 drug product, 1 injection
Executive Summary

Turning tumors into all-in-one immunotherapy bioreactors.

Cold tumors combine immunosuppressive cells, antigen suppression, checkpoint overexpression, T-cell neutralization and immune-cell exclusion behind dense stromal barriers — beyond what any single agent or tolerated systemic combination can overcome.

Intratumoral multimodal therapy is the answer, yet first-generation modalities encounter distinct biological and operational barriers. Intratumoral cryolysis-based multi-payload therapy has effectively been validated as an approach, but its clinical implementation involves higher procedural and manufacturing complexity, including device-based delivery and multi-agent regimens. Conversely, armed oncolytic viruses consolidate multi-pathway delivery into a single therapeutic agent; however, premature viral-mediated oncolysis can inherently restrict the window for sustained, robust payload expression.

Over two years we made the discoveries that resolve every one of these limitations — engineered secretion, staged logic-gated promoters, secretable lysis modules, and superpotent proteins — packaged into a single non-replicating HD-Ad vector. Wholly owned.

The Problem

Cold tumors are protected by many concurrent mechanisms.

Systemic multi-agent immunotherapy cannot safely cover this network. FIG delivers a once-injected gene therapy designed to address all of these mechanisms at once — locally, from inside the tumor.

Suppressive

Suppressive immune cells

  • M2 macrophages
  • MDSCs
  • T-regulatory cells
  • Cancer-associated fibroblasts
Suppressive

Suppressive signaling & immune masking

  • TGF-β, IL-10, VEGF
  • Immunosuppressive chemokines
  • PD-L1 overexpression
  • MHC-I suppression
Physical

Physical & metabolic barriers

  • Dendritic-cell desert
  • Dense extracellular matrix
  • Hypoxia
  • Acidosis
The Answer

Intratumoral multimodal immunotherapy — but first-generation approaches hit ceilings.

Only local, multimodal therapy can address every mechanism at once without systemic toxicity. The rise of intratumoral immunotherapy — armed oncolytic viruses, multi-agent device-delivered regimens, intratumoral mRNA, prodrug adenovirus — validates the thesis. Each also reveals where its format falls short.

Approach
What it validates
Where it falls short
Armed oncolytic viruses
Local immune activation works, including activity after anti-PD-1 failure.
Coupling payload expression to viral replication and lysis can limit the sustained payload-expression window before the producer cell is cleared.
Cryolysis + multi-agent intratumoral regimens
Multimodal local therapy in mCRPC has produced notable complete responses in heavily pretreated patients.
High procedural and manufacturing complexity — device-dependent delivery alongside multiple separate agents, each with its own stability and handling requirements.
Intratumoral mRNA
Local multimodal expression from mRNA (e.g., OX40L, IL-23, IL-36γ).
Transient expression kinetics characteristic of non-replicating mRNA may necessitate frequent redosing.
Prodrug-activated adenoviral gene therapy
Intratumoral adenoviral gene delivery + prodrug; survival signals.
Mechanism is primarily localized cytotoxicity, with limited immune-cell recruitment, checkpoint relief, or microenvironment remodeling.
Local single-cytokine strategies
Local single-cytokine strategies (tumor-retained IL-12, interferons).
A single cytokine generally cannot orchestrate the full coordinated sequence of recruitment, priming, checkpoint relief, remodeling, and antigen release.

Comparison reflects general modality classes; individual programs vary.

The Bottleneck

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 spent two years obsessing over each of these barriers — engineered secretion, staged logic-gated promoters, secretable lysis modules, and superpotent proteins — and built the Symphony™ platform on multiple independent layers of wholly owned IP.

The Discovery

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.

This foundational unlock makes multimodal intratumoral gene immunotherapy feasible for the first time.

See the Symphony™ platform
IFN-γ secretion · 22Rv1 tumor cells
pg / mL
Native SP
41.2
IGK SP
95.4
FIG SP2
75.3
FIG SP3
26,034

Holding CMV promoter constant. FIG signal peptide 3 unlocked >700× secretion vs native, in tumor cells only.

SP = signal peptide

Lead Indication

Prostate first — a large, underserved market fit to the platform.

A $100B+ solid-tumor immuno-oncology TAM, with mCRPC alone projected to grow from $21B to $92B by 2034. ~70,000 U.S. high-risk localized cases per year, more than half recurring despite surgery or radiation — and a needle-accessible tumor architected around exactly the immune barriers Symphony™ is built to solve.

See the pipeline
$100B+
Solid-tumor IO TAM
$21B → $92B
mCRPC market, 2025–2034
~70,000 / yr
U.S. high-risk localized cases
>50%
Recurrence despite surgery or radiation