GPR120 Agonist 3

Research use only, not for human use.

GPR120-IN-1 is a selective agonist of Gpr120 ( logEC50: -7.62).

GPR120-IN-1 is a selective agonist of Gpr120 ( logEC50: -7.62).(In Vitro):GPR120-IN-1 causes a concentration-dependent response to recruit 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 is fully selective for Gpr120 (logEC50=?7.62) with negligible activity towards Gpr40. (In Vivo):GPR120-IN-1 treatment has beneficial effects on hepatic lipid metabolism. Which causing decreased liver triglycerides, decreased hepatic steatosis, and DAGs, as well as decreased saturated free fatty acid conten. GPR120-IN-1 causes improved insulin sensitivity with increased glucose infusion rates. It also enhanced insulin stimulated-glucose disposal rate. Only in WT mice, along with a marked increase in the ability of insulin to suppress hepatic glucose production.

GPR120 Agonist 3 is fully selective for Gpr120 (logEC50=?7.62) with negligible activity towards Gpr40. GPR120 Agonist 3 produces concentration dependent increases in IP3 production from both human and mouse Gpr120 expressing cells. GPR120 Agonist 3 leads to a concentration-dependent response to recruit β-arrestin-2 in both human and mouse Gpr120 expressing cells, with EC50s of ~0.35 μM. GPR120 Agonist 3 strongly and comparably inhibits LPS-induced phosphorylation of Tak1, Ikkβ, and Jnk and blocked IκB degradation .

GPR120 Agonist 3 causes improved insulin sensitivity with increased glucose infusion rates, enhanced insulin stimulated-glucose disposal rate, along with a marked increase in the ability of insulin to suppress hepatic glucose production only in WT mice. GPR120 Agonist 3 treatment has beneficial effects on hepatic lipid metabolism, causing decreased hepatic steatosis, decreased liver triglycerides, and DAGs, along with reduced saturated free fatty acid conten.

——

Cell Cycle/DNA Damage

GPR

——

——

——

1599477-75-4

405.84

C19H23ClF3NO3

>98% (HPLC)

In Vitro:?DMSO : ≥ 50 mg/mL (123.20 mM)

OC(=O)CC1CCC2(CC1)CCN(CC2)c1cc(OC(F)(F)F)ccc1Cl

——

(-20℃)

With Ice Pack

≥ 2 years