Palmitoleic acid is a constituent of the triglycerides of human adipose tissue. Palmitoleic acid-based diets raise low-density lipoprotein cholesterol and diminish high-density lipoprotein cholesterol.

O-304 is a first-in-class, orally available pan-AMPK activator, which increases AMPK activity by suppressing the dephosphorylation of pAMPK. O-304 exhibits a great potential as a drug to treat type 2 diabetes (T2D) and associated cardiovascular complications [1][2].

HTH-01-015 is a selective NUAK1 inhibitor, but not NUAK2, with IC50 of 100 nM, suppressing NUAK1-mediated MYPT1 phosphorylation.

Gomisin J is a natural product isolated and purified from the fruits of Schizandra chinensis with vasodilatory activity that mediates mainly by calcium-dependent activation of eNOS with subsequent production of endothelial NO, and inhibits LPO in rat liver mitochondria and protects cultured myocardial cells from being injured by calcium paradox.

COH-SR4 is an AMPK activator with anticancer properties. It significantly inhibited adipocyte differentiation in a dose-dependent manner in 3T3-L1 cells. It significantly reduced intracellular lipid accumulation and downregulated the expression of key adipogenesis-related transcription factors and lipogenic proteins in differentiating adipocytes.

ASP4132 is a new type of AMPK activator with EC50 value of 18nM. It showed attractive selective growth inhibition against human cancer cells.

PF-06409577 is a potent and selective allosteric activator of AMPK with EC50 value of 7 nM for AMPKα1β1γ1, but >40000 nM for AMPKα1β2γ1.

IM156 is a metformin derivative which has been reported to ameliorate various types of fibrosis and inhibit in vitro and in vivo tumors by inducing AMPK activation more potently than metformin. IM156 treatment impaired the function of virus-specific memory CD8+ T cells, indicating that excessive AMPK activation weakens memory T cell differentiation, thereby suppressing recall immune responses. IM156 activated AMPK in a dose-dependent manner, and produced shortening of the circadian period and enhanced degradation of the clock genes PER2 and CRY1.