STING-IN-16 is an inhibitor of STING, with an IC50 value of 44 nM in humans and 32 nM in mice. This compound effectively suppresses the activation of the STING pathway in both human and mouse cells. STING-IN-16 aids in restoring kidney mitochondrial function, inhibits the production of reactive oxygen species (ROS), and reduces apoptosis. It exhibits significant anti-inflammatory effects in vivo and is a valuable tool for researching autoimmune and autoinflammatory diseases.

STING-IN-16 (Compound 5c) at a concentration of 1 μM for 24 hours inhibits the activation of STING, with an IC50 of 44 nM in THP1-Blue-ISG cells and 32 nM in RAW-Lucia-ISG cells. At concentrations ranging from 0.3 to 3 μM over 3 to 6 hours, it suppresses STING agonist-induced signaling activation in THP1 cells, bone marrow-derived macrophages (BMDM), mouse embryonic fibroblasts (MEF), and mouse macrophages (RAW264.7), while also significantly enhancing the thermal stability of STING. Additionally, at 1 μM for 6 hours, STING-IN-16 inhibits the activation of the cGAS-STING pathway triggered by cisplatin-induced DNA damage in HK2 cells, thereby reducing ROS accumulation and apoptosis.

STING-IN-16 (Compound 5c) administered intraperitoneally at 10 mg/kg once daily for three days alleviates cisplatin-induced inflammation in mice. Additionally, a single intraperitoneal dose of STING-IN-16 (10 mg/kg) demonstrates anti-inflammatory properties in a mouse model induced by MSA-2.