GPR120-IN-1 causes a concentration-dependent response to recruiting β-arrestin-2 in both human and mouse Gpr120 expressing cells(EC50s: ~0.35 μM). GPR120-IN-1 produces concentration-dependent increases in IP3 production from both human and mouse Gpr120 expressing cells. GPR120-IN-1 strongly and comparably inhibits LPS-induced phosphorylation of Ikkβ, Tak1, and Jnk and blocked IκB degradation.

GPR120-IN-1 treatment has beneficial effects on hepatic lipid metabolism. It causes decreased liver triglycerides, decreased hepatic steatosis, and DAGs, as well as decreased saturated free fatty acid content. GPR120-IN-1 causes improved insulin sensitivity with increased glucose infusion rates. It also enhanced the insulin stimulated-glucose disposal rate. Only in WT mice, along with a marked increase in the ability of insulin to suppress hepatic glucose production.