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 multiple coordinated immune signals. Long sought but never achievable, because tumors are poor secretors. FIG changed that.
Antigen recognition
Tumor lysis, antigen release, dendritic-cell recruitment & antigen presentation
Co-stimulation
Dendritic-cell licensing & co-stimulatory receptor agonism
Cytokine support
T-cell / NK-cell activation, survival, polarization & memory support
TME access & metabolism
Hypoxia modulation, vascular/TME remodeling & reversal of suppressive stromal barriers
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, CD8 T, and NK cells into the TME. Our DPP4-resistant variants are designed to resist degradation by these enzymes overexpressed by tumors.
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.