Overview
- The system pairs a β‑glucuronidase‑uncaged version of the STING agonist MSA2 with a second inert component that combine only in the tumor microenvironment.
- In zebrafish and mouse studies engineered to produce β‑glucuronidase, the active compound formed almost exclusively in tumors and spared liver, kidney, and heart.
- The components were largely inactive on their own yet triggered the pathway at very low concentrations when assembled under tumor conditions.
- Researchers designed the chemistry to favor rapid, selective coupling at disease sites to address the systemic inflammation that has limited STING agonists.
- The approach remains preclinical, with the team proposing broader safety studies and potential application of the two-component concept to other potent therapies.