Overview

• University of Cambridge researchers reported the strategy in Nature Chemistry (DOI: 10.1038/s41557-025-01930-9).
• The approach combines a caged STING agonist, identified as MSA2, with a second inert component that reacts only within the tumor microenvironment.
• β‑Glucuronidase present in tumors uncages MSA2, enabling the two components to form an active STING agonist locally.
• In engineered zebrafish and mouse studies, activation occurred predominantly in tumors, with minimal activity detected in healthy tissues.
• Vital organs including the liver, kidney, and heart were largely spared, and the team notes the platform could be adapted for other precision medicines.