Coptisine is an efficient uncompetitive IDO inhibitor with a K _i value of 5.8 μM and an IC ₅₀ value of 6.3 μM. Coptisine (0.1-100 μM) inhibits the proliferation of A549, H460, H2170, MDA-MB-231 and HT-29 cells, with IC ₅₀ s of 18.09, 29.50, 21.60, 20.15 and 26.60?μM, respectively. Coptisine (12.5, 25, 50 μM) upregulates the expression of pH2AX and p21, reduces expression of cyclin B1, cdc2, and cdc25C, and induces G2/M arrest and apoptosis of A549 cells in a concentration-dependent manner. Coptisine (12.5, 25, 50 μM) also induces mitochondrial dysfunction and activates caspases activities in A549 cells. Furthermore, Coptisine (50 μM) increases ROS levels in a time-dependent manner (0.5, 1, 2, 4, 12, and 24?h).

Coptisine shows increased toxicity in mice in a concentration dependent manner, with LD ₅₀ value of 880.18 mg/kg. Coptisine (154 mg/kg/day, 90 days) shows no toxicity on SD rats. Coptisine (23.35, 46.7, 70.05 mg/kg, p.o.) dose-dependently decreases the levels of TC, TG, and LDL-c and increases HDL-c content in serum of hamsters to different degree, slows down weight gain induced by the HFHC diet, and raises the level of cholesterol and TBA in feces dose-dependently in hamsters. Coptisine (70.05 mg/kg, p.o.) suppresses HMGCR protein expression level and induces the protein expression of SREBP-2, LDLR, and CYP7A1 involved in cholesterol metabolism.