Cancer is a significant health problem responsible for one in four deaths worldwide. Metabolic dysfunction is a hallmark of cancer and contributes to patient morbidity and mortality. As such, small-molecule, allosteric activators that directly bind to and activate 5' adenosine monophosphate-activated protein kinase (AMPK) may have therapeutic merit in cancer. The purpose of this study was to determine the therapeutic efficacy of the pan-AMPK activator, MK8722, in colon cancer. We first examined the in vitro effects of MK8722 on colon-26 (C26) cells. MK8722 (0.1, 1, and 10 µM) increased AMPK activity in C26 cells, which resulted in a dose-dependent reduction in cell proliferation and oxygen consumption rate. We then examined the in vivo effects of MK8722 on cancer survival in a preclinical model of colon cancer. Male BALB/c mice (11-12 weeks of age; n=8 mice/group) were injected with C26 cells (5×10^5 cells/mouse) and treated daily (beginning on day 5) with 0, 1, or 10 mpk MK8722 (i.p.) until humane endpoint criteria, or day 30, was reached. Untreated C26 mice began losing body mass at day 8 which continued throughout the study period. In contrast, treated C26 mice exhibited a dose-dependent preservation of body mass, with improved survival. There were no differences in tumour volume or growth rate with MK8722 treatment. The findings suggest the pan-AMPK activator MK8722 in vivo can extend survival independent to an anti-cancer mechanism. Future studies will determine whether MK8722 alters tumour metabolism and if this impedes cancer progression. Supported by the NHMRC (GNT2013615).