The kinase Akt (also known as protein kinase B or PKB) modulates cell proliferation, metabolism, and survival, as well as angiogenesis.[1],[2] Akt inhibitor XI is a cell-permeable, copper-containing 3-formylchromone derivative that inhibits Akt in an array of cancer cells (IC50s = 10-34 μM).[3] It also causes NF-κB inactivation in an orthotopic pancreatic tumor model using COLO 357 cells.3 Molecular modeling indicates that this inhibitor interacts with the pleckstrin homology and kinase domains of Akt. Akt inhibitor XI is commonly used in the range of 1-20 μM to assess the role of Akt in cellular responses.[4],[5],[6]

Reference:
[1]. Manning, B.D., and Cantley, L.C. AKT/PKB signaling: Navigating downstream. Cell 129(7), 1261-1274 (2007).
[2]. Yuan, T.L., and Cantley, L.C. PI3K pathway alterations in cancer: Variations on a theme. Oncogene 27(41), 5497-5510 (2008).
[3]. Barve, V., Ahmed, F., Adsule, S., et al. Synthesis, molecular characterization, and biological activity of novel synthetic derivatives of chromen-4-one in human cancer cells. Journal of Medicinal Chemistry 49(13), 3800-3808 (2006).
[4]. Frampton, G., Invernizzi, P., Bernuzzi, F., et al. Interleukin-6-driven progranulin expression increases cholangiocarcinoma growth by an Akt-dependent mechanism. Gut 61(2), 268-277 (2012).
[5]. Rybchyn, M.S., Slater, M., Conlgrave, A.D., et al. An Akt-dependent increase in canonical Wnt signaling and a decrease in sclerostin protein levels are involved in strontium ranelate-induced osteogenic effects in human osteoblasts. The Journal of Biological Chemisty 286(27), 23771-23779 (2011).
[6]. Zareen, N., Biswas, S.C., and Greene, L.A. A feed-forward loop involving Trib3, Akt and FoxO mediates death of NGF-deprived neurons. Cell Death and Differentiation 20(12), 1719-1730 (2013).