Metformin (1,1-Dimethylbiguanide) is an AMPK activator with blood-brain barrier permeability. Metformin may improve glycemic control by increasing insulin sensitivity and decreasing intestinal glucose uptake, and is commonly used in type 2 diabetes research.

METHODS: Ovarian cancer cells A2780 and SKOV3 were treated with Metformin (0.001-50 mM) for 24-48 h. Cell viability was assayed using the MTS
RESULTS: Micromolar concentrations of Metformin did not statistically reduce the viability of the A2780 or SKOV3 cell lines. At 48 h, millimolar concentrations resulted in cell death. [1]
METHODS: Human colorectal cancer cells HCT29 were treated with Metformin (0.6 mM) for 90 h. Cell motility was detected using the wound healing assay and chamber invasion assay.
RESULTS: Metformin inhibited the migration and invasion of HCT29 cells, and Metformin decreased the motility of tumor cells. [2]

METHODS: To model Metformin-induced diarrhea, Metformin (125-500 mg/kg) was administered orally to healthy and diabetic obese db/db C57BL/6J mice twice daily for thirteen days.
RESULTS: Metformin at 1000 mg/kg/day significantly increased fecal water content. Although no diarrhea symptoms were observed in healthy C57BL/6J mice, the same dose of Metformin induced severe diarrhea in diabetic obese db/db mice. [3]
METHODS: To investigate the protective effect of Metformin in radiation injury, Metformin (200 mg/kg once daily for three days) was administered orally to BALB/c mice, which were then exposed to 6-8 Gy of gamma radiation.
RESULTS: When administered prior to exposure to radiation, Metformin prolonged the survival of mice exposed to 8 Gy-TBI and increased the survival of mice exposed to 6 Gy-TBI. Pretreatment with Metformin attenuated radiation damage. [4]