STING-IN-5, a potent inhibitor of the Stimulator of Interferon Genes (STING) pathway, significantly suppresses lipopolysaccharide (LPS)-induced nitric oxide (NO) synthesis in macrophages, exhibiting an IC50 of 1.15 μM. This compound dampens the inflammatory response and offers potential for research into anti-inflammatory diseases and sepsis [1].

STING-IN-5 (compound 30) (40 μM; 24 h) exerts minimal impact on the viability of RAW264.7 cells [1]. At concentrations of 2.5 and 5 μM for 2 hours, STING-IN-5 inhibits nitric oxide (NO) production in LPS-stimulated RAW264.7 cells, with inhibition rates of 69.28 ± 2.36% and 78.66 ± 2.73% respectively, and an IC 50 of 1.15 ± 0.15 μM [1]. Furthermore, STING-IN-5 (0.5-2 μM; 2 h) suppresses STING activation and subsequent TBK1/IRF3/NF-κB signaling [1].

STING-IN-5, administered orally at doses ranging from 1.25 to 5 mg/kg once daily for three consecutive days, showed significant protective effects against acute hepatic injury in mice with sepsis [1]. The pharmacokinetic parameters of STING-IN-5 in male Sprague-Dawley rats include a peak concentration time (Tmax) of 1 hour, a maximum concentration (Cmax) of 66.52 ng/mL, an area under the curve from time zero to the last quantifiable concentration (AUC0-t) of 81.08 ng/mL·h, an area under the curve from time zero to infinity (AUC0-∞) of 135.7 ng/mL·h, a half-life (T1/2) of 1.11 hours, a mean residence time from time zero to the last quantifiable concentration (MRT0-t) of 0.99 hours, and a mean residence time from time zero to infinity (MRT0-∞) of 2.02 hours [1].