Severe neurological symptoms emerging in infancy or early childhood.
Loss-of-function mutations in nucleic-acid-handling enzymes trigger chronic type-I IFN signaling.
Current standard of care is supportive only.
TREX1, RNASEH2A/B/C, SAMHD1, ADAR1, IFIH1Stats pending final scientific review. Contact our team for updated references.
"Dysregulated innate immune signaling drives chronic neuroinflammation in AGS."
A three-step mechanism-first approach — from upstream drivers to therapeutic candidates.
Identify upstream pathway drivers using mechanistic AI on patient multi-omics data.
Validate mechanistic targets in disease-relevant biology — patient-derived cells and models.
Develop therapeutic candidates against validated targets — small molecule, biologic, or modality-agnostic.
Our mechanistic platform is designed to generalize across innate-immunity-driven disease.
Shared interferon signaling pathways
Type-I IFN-driven pathology
Monogenic immune dysregulation
Current programs across discovery and preclinical stages.
| Program | Indication | Discovery | Preclinical | IND-Enabling | Phase 1 |
|---|---|---|---|---|---|
| ZMT-001 | Aicardi–Goutières Syndrome | ||||
| ZMT-102 | Neuroinflammation (TBD) | ||||
| ZMT-205 | Autoimmune (TBD) |
Filled squares represent current progress within stage. Hover rows for context. Contact us for pipeline detail.