Licochalcone A

UGT1A1:0.97 μM

In mice infected with L. major, licochalcone A (5 mg/kg, i.p.) completely prevents lesion development. In mice infected with L. donovani, licochalcone A (150 mg/kg, p.o.) results in > 65 and 85% reductions of parasite loads in the liver and the spleen, respectively. [2] In CT-26 cell-inoculated Balb/c mice, licochalcone A (1 mg/kg, p.o.) inhibits the tumor growth, and alleviates cisplatin-induced nephrotoxicity and hepatotoxicity. [4]

Licochalcone A markedly inhibits the in vitro growth of L. major amastigotes in human MDMs and U937 cells. [1] Licochalcone A shows antibacterial effects against all gram-positive bacteria tested and especially against all Bacillus spp. Tested with MICs of 2 to 3 micrograms/mL. [3] In CT-26 colon cancer cells, Licochalcone A reduces the cell viability and DNA synthesis. [4] Licochalcone A also interferes with MAPK signaling cascades, initiates ROS generation, induces oxidative stress and consequently causes BGC cell apoptosis. [5]

DMSO:67 mg/mL (197.99 mM),Ethanol:67 mg/mL (197.99 mM),H2O:<1 mg/mL,Chloroform:Soluble

The viability of CT-26 mouse colon cancer cells is determined via a MTT assay. In brief, colon cancer cells are seeded onto each well of a 96-well plate with DMEM containing 10% FBS and cultured to adhere overnight. The cells are then treated with various concentrations of LCA in serum-free medium for 24 and 72 hr, respectively. Twenty microlitres of a MTT solution (5 mg/ml) is added to each well, and the cells are incubated for 4 hr at 37°. The medium is then removed, and 200 μL of dimethyl sulfoxide is added to each well. The absorbance is determined at 570 nm using a microplate reader.(Only for Reference)