The cGAS–STING pathway is a central regulator of innate immune activation and type I interferon signaling. In diseases marked by chronic pathway activation, STING signaling can contribute to sustained neuroinflammation and tissue injury.
Zermatt is developing CNS-penetrant small-molecule STING inhibitors designed to reduce pathological inflammatory signaling in rare interferonopathies and broader CNS disease settings.
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, IFIH1Additional preclinical data are available upon request for qualified partners.
"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
Zermatt is advancing a CNS-focused STING inhibitor pipeline beginning with rare interferon-driven neuroinflammatory diseases and expanding toward broader CNS indications with shared innate immune biology.
Additional preclinical data are available upon request for qualified partners.