BMS-470539 dihydrochloride is a selective and highly potent melanocortin 1 receptor (MC-1 R) agonist with anti-inflammatory activity. BMS-470539 attenuates oxidative stress and neuronal apoptosis via the MC1R/cAMP/PKA/Nurr1 signaling pathway in a neonatal hypoxia-ischemia rat model.

MC1R:28 nM (EC50), MC1R:120 nM

METHODS: BMS-470539 dihydrochloride (0-1μM, 15 minutes) was used to treat HBL cells stably transfected with NF-B luciferase reporter gene, and then treated with 0.5 ng/mL TNF-α for 4 hours to study its effect on stable transfection. Effects of NF-B luciferase reporter gene on TNF-α-stimulated luciferase activation in HBL cells.
RESULTS:BMS-470539 dihydrochloride treatment of HBL cells with NF-B luciferase reporter gene caused a dose-dependent significant reduction in TNF-α-stimulated NF-B luciferase activity. [2]

METHODS: BMS-470539 dihydrochloride (2.05-18.47 mg/kg, intravenous injection, 125 minutes) was used to treat WT and MC1 receptor-negative e/e mice to study its effects on mesenteric microcirculation.
RESULTS:BMS-470539 dihydrochloride treatment of mice inhibited cell adhesion and migration, had no effect on cell rolling, and also inhibited the tissue expression of two chemokines, CXCL1 and CCL2. [3]