Originally reported as an inhibitor of Protein Kinase C isoforms with selectivity for PKCδ. However, more recent studies have shown Rottlerin did not block PKCδ activity but did block other kinase and non-kinase proteins in vitro and activated multiple Ca²⁺-sensitive K⁺ channels with high potency. It uncouples mitochondria and affects mitochondrial production of reactive oxygen species (ROS). Also induces autophagy through inhibition of mTORC1.