AMP-activated protein kinase (AMPK) regulates cellular energy consumption during metabolic stress by activating catabolic processes and inhibiting anabolic processes. Current first-line therapeutics for diabetes indirectly activate AMPK, which in turn lowers plasma glucose and inhibits lipid synthesis1 . Dephosphorylation of the activation loop of AMPK has been identified as a main mechanism of AMPK inhibition2 , and phosphatase inhibition reverses the diabetic phenotype in some cells3 . Novel compounds have been characterised here by their ability to induce resistance to dephosphorylation by the phosphatase PPM1A at the activation loop.