CC260, a selective inhibitor for PI5P4Kα and PI5P4Kβ with Kis of 40 nM and 30 nM respectively, exhibits minimal to no inhibition against other protein kinases like Plk1 and RSK2. It is applicable in the research of cell energy metabolism, diabetes, and cancer[1].

PI5P4Kα:40 nM (Ki), PI5P4Kβ:30 nM (Ki)

In cultured C2C12 myotubes, CC260 (20 μM) enhances insulin-induced phosphorylation of Akt at Thr-308 and Ser-473, inhibits S6K phosphorylation (Thr-389) mediated by mTORC1, and progressively increases acetyl-CoA carboxylase (ACC) phosphorylation in a dose-dependent manner at concentrations from 2.5 μM to 20 μM[1]. CC260 treatment reduces the survival of BT474 cells under serum starvation, which can be reversed by introducing a PI5P4Kβ-resistant mutant, and also leads to increased glycolytic ATP production in BT474 cells[1].