Anisomycin

Peritumoral administration of anisomycin (5 mg/kg) significantly suppresses Ehrlich ascites carcinoma (EAC) growth resulting in the survival of approximately 60% of the mice 90 days after EAC inoculation.[4]

Anisomycin (3 μM) decreases protein synthesis in MDA16 and MDA-MB-468 cells, and reduces colony formation by MDA-MB-468 cells. Anisomycin causes an increase in the number of apoptotic cells in MDA-MB-468 cultures, but not in MDA16 cultures. Anisomycin actives JNK phosphorylation in MDA-MB-468 cells.[2] In U251 and U87 cells, anisomycin?(0.01-8 μM) inhibits the cell growth in time- and concentration-dependent manners with the IC50 (48 h) values of 0.233 and 0.192 μmol/L, respectively. Anisomycin?(4 μM) causes 21.5% and 25.3% of apoptosis proportion in U251 and U87 cells, respectively, and activates p38 MAPK and?JNK, while inactivated ERK1/2. Anisomycin?(4 μM) reduces the level of PP2A/C subunit in a time-dependent manner in U251 and U87 cells.[3] Anisomycin inhibits EAC cell proliferation in concentration-dependent manner.[4]

DMSO:26.5 mg/mL (100 mM),Ethanol:13.3 mg/mL (50 mM)

For the assay, EAC cells are plated in 96-well plates at a density of 10,000 cells/well/200 μL of medium. The cells are treated with the different concentrations of anisomycin for 48 h. Adriamycin (500 ng/mL) is used as a positive control. 0.5 mg/mL of MTT is added to each well. 4 h later, the formazan product of MTT reduction is dissolved in DMSO, and absorbance is measured at 570 nm using a Model 680 microplate reader.(Only for Reference)