A Minimal Causal Model of Crohn's Disease
Defines the five-node causal circuit (NOD2, ATG16L1/IRGM, XBP1, IL23R, MUC2) and the rationale for repairing upstream nodes to enable durable remission.
Read on Zenodo (10.5281/zenodo.17989512)Crohn's disease circuit repair
ViroDyn is building a gene-editing program to repair the core causal circuit that drives ileal Crohn's disease. Our model prioritizes upstream restoration of the damaged network to move beyond chronic suppression and toward durable remission.
We are prioritizing restoration of NOD2-mediated microbial sensing as the entry point to repairing the full Crohn's circuit. By correcting this upstream node, we aim to normalize downstream autophagy, epithelial stress responses, IL-23/Th17 amplification, and mucus-barrier integrity.
ViroDyn is a research company focused on curing Crohn's disease through gene editing. We translate a minimal causal model of Crohn's into a practical repair strategy for the upstream circuit that drives disease initiation and persistence.
A circuit-repair platform that pairs causal biology with precise gene-editing design, focusing first on NOD2 restoration and then expanding across the full five-node module.
We start with a falsifiable causal model, define measurable rescue endpoints, and partner with translational teams to validate edits that restore function upstream of inflammation.
Repairing the minimal causal circuit of Crohn's disease with gene editing, beginning with the NOD2 node and expanding through the full pathway.
This five-node circuit captures the upstream drivers most consistently linked to ileal Crohn's: microbial sensing (NOD2), autophagy and Paneth cell function (ATG16L1/IRGM), epithelial stress response (XBP1), IL-23/Th17 amplification (IL23R), and mucus-barrier integrity (MUC2). We start with NOD2 because it is a high-impact entry point and provides clear functional readouts for downstream recovery across the pathway.
Our pipeline is structured around circuit repair, with a first-in-class NOD2 program and a staged expansion across the remaining core nodes.
Gene-editing strategies to recover microbial sensing and upstream control of the inflammatory cascade.
After NOD2, our next program targets ATG16L1 to complete the core repair. Other nodes are typically non-mutant or become clinically relevant only when upstream dysfunction (NOD2 or ATG16L1) is present.
Partnerships for vector design, in-vitro and in-vivo validation, and translational readiness.
Defines the five-node causal circuit (NOD2, ATG16L1/IRGM, XBP1, IL23R, MUC2) and the rationale for repairing upstream nodes to enable durable remission.
Read on Zenodo (10.5281/zenodo.17989512)Interested in investing, partnering on delivery, or following our program milestones? Share a note and we will respond.
For investment, strategic partnerships, or validation inquiries, please contact Alex.