Coordinating the four signals of anti-tumor immunity from a single injection.
A multimodal, non-oncolytic gene therapy — 1 drug substance, 1 drug product, 1 injection — that turns the tumor itself into a lasting source of many coordinated immune signals. Long sought but never achievable, because tumors are poor secretors. FIG changed that.
What makes it feasible for the first time.
Two years of research. A multi-layer, wholly owned IP moat. Every historical limitation of non-replicating viral immunotherapy — resolved.
Engineered non-native signal peptide
>700-fold tumor secretion. The foundational discovery that lets a non-replicating virus turn a tumor into a bioreactor.
Immune-sensing delayed promoter
Initial + delayed promoter systems separating early recruitment and priming from later lysis, checkpoint blockade, and DC licensing.
Gene-encoded secretable lysis
Tumor lysis delivered from within the tumor as a staged payload. No prodrug, no device, no repeat dosing.
Superpotent constructs
Tumor-anchoring IL-12, CD40 agonist, CTLA-4 antagonist, and PD-L1 antagonist — a complete suite of superpotent, retention-tuned payloads engineered for staged release. Zero licensing overhead.
Secrete therapy first. Lyse last. Preserve the bioreactor.
Non-replicating HD-Ad delivery avoids reliance on viral-replication-mediated lysis entirely. Initial + delayed promoter systems separate early recruitment and priming from later lysis, checkpoint blockade, and DC licensing — preserving the bioreactor while staging immunity.
- Dendritic-cell recruitment & expansion
- T-cell and NK recruitment & activation
- Treg depletion and CTLA-4 antagonism
- TME remodeling — stroma, hypoxia, TGF-β
- PD-L1 checkpoint blockade
- CD40 superagonism for durable priming
- T-cell memory, survival & expansion signals
- Secreted tumor-lysis module
- Indication-specific payload swaps
- Further-delayed extension layer
- Tunable lysis kinetics
- Same architecture, re-pointed
10+ payloads. Six functional classes. Secreted in multiple stages.
Secretion of 10+ payloads validated at clinically meaningful levels in tumor-cell models.
The tumor is programmed to robustly secrete a broad portfolio of immune-modulating proteins. Each class is timed to its optimal point in the immune cascade.
Recruit dendritic cells, T cells, and NK cells into the tumor microenvironment (TME).
Activate and expand T/NK and dendritic cells. Reverse immunosuppression in TME. Delayed cytokines promote survival and immune memory.
Drive dendritic-cell licensing and durable T-cell priming. Enhance T cell survival. Reverse hypoxia and induce Tertiary Lymphoid Structures.
Relieve PD-L1 and CTLA-4 suppression locally, without systemic exposure.
Neutralize stromal and regulatory immunosuppression in the tumor bed.
Delayed, secreted tumor-cell killing — no prodrug, no device, no repeat dosing.
Superpotent proteins, purpose-built.
We engineer improved variants of existing molecules to establish wholly owned IP, and build novel proteins from the ground up where needed. Everything is tuned for potency and staged release; TME retention is engineered specifically for systemically toxic payloads such as IL-12 — with no licensing overhead and no inherited ceiling.
Single-chain IL-12
Engineered single-chain IL-12 with a collagen-binding tail — retained in the tumor microenvironment rather than leaking systemically. Substantially more potent than wild-type IL-12.
CD40 superagonist
Proprietary superagonist CD40 module — drives dendritic-cell licensing and long-lived T-cell priming at potencies beyond the intratumoral CD40L therapies in the clinic today.
CTLA-4 antagonist
Superpotent anti-CTLA-4 fragment delivered locally — Treg depletion and checkpoint relief inside the tumor, without the systemic toxicity ceiling of IV anti-CTLA-4.
PD-L1 blockade
Secreted PD-L1 blocker released during Stage 2, timed to arrive after immune priming — sustaining T-cell function exactly when the tumor tries to shut it down.
One dose. Strong primary and distant abscopal control.
Validated in one of the hardest models a tumor can face: aggressive, enzalutamide-resistant mCRPC xenograft, HLA-matched CD34+ humanized SGM3-IL15 mice. An HD-Ad "stuffer" control isolates the effect of the secreted payloads themselves.
Primary Tumor
Abscopal Tumor
Six independent pillars.
100% owned. Multiple independent platform and composition-of-matter claim families.