Triciribine is a cell-permeable unnatural nucleoside that inhibits the phosphorylation and signalling of all three family members of Akt - Akt-1, Akt-2 and Akt-3.

These are serine/threonine protein kinases in the phosphoinositide 3-kinase (PI3K) signalling pathway that play a critical role in the regulation of cell proliferation and survival.

Following recruitment of Akt to the plasma membrane, phosphorylation at threonine 308 and serine 473 (Akt-1 numbering) by PDK-1 or PDK-2 results in full activation of the enzyme.

[1] Triciribine, first synthesized in 1971,[2] was found to have definite anti-cancer properties[3] and a phosphate ester of the drug went into clinical trials in the 1980s because it had improved solubility.

[citation needed] In the early 2000s Said Sebti at the H. Lee Moffitt Cancer Center & Research Institute in Tampa, Fl and Jin Cheng at the University of South Florida established that Triciribine would be effective against tumours with hyperactivated AKT.