Figure 6.

Overview of working model for STINGPOX’s therapeutic effects. In healthy cells, STING signaling is active, and STINGPOX replication would be significantly hindered due to increased activation of IFN signaling. In several cancer types, immune signaling, and more specifically, STING signaling is deficient; therefore STINGPOX-induced cyclic di-AMP production does not enhance IFN signaling/production in infected cells enabling viral replication and expression of disA. disA catalyzes synthesis of c-di-AMP. Through lysis or secretion, c-di-AMP is transferred to extrinsic phagocytic cells, including dendritic cells, which help promote an anti-tumor response.