Triciribine is a DNA synthesis inhibitor, also inhibits Akt and HIV-1/2 with IC₅₀ of 130 nM, and 0.02-0.46 μM, respectively. IC50 & Target: DNA synthesis^[1]
IC50: 130 nM (Akt)^[2]
IC50: 0.02-0.46 μM (HIV-1/2)^[3] In Vitro: The nucleoside analog Triciribine (TCN) is a purine analog which is initially shown to inhibit DNA synthesis. Triciribine selectively inhibits the phosphorylation and activation of all three Akt isoforms. At a concentration of 10 μM Triciribine Akt phosphorylation is inhibited at both Thr308 and Ser473. Triciribine effectively inhibits the phosphorylation and consequently the catalytic activity of Akt in PC-3 cells^[1]. The Akt inhibitor Triciribine (TCN) does not effectively inhibit the human cell line U87MG but inhibits other astrocytoma cell lines in a grade-dependent manner. The WHO II K1861-10 line is incompletely inhibited (69% maximum inhibition) with a GI₅₀ value of 1.7 µM for Triciribine. Triciribine exhibits maximum growth inhibition around 1-10 µM and inhibits phosphorylation of Akt, as well as downstream p70S6K, to basal levels at 100 µM (IC₅₀=130 nM) in KR158 cells^[2]. Triciribine (TCN) is a novel tricyclic compound with known antitumor activity. Using a syncytial plaque assay, Triciribine is active against HIV-1 at 0.01-0.02 μM. Using a microtiter XTT assay, Triciribine is active against a panel of HIV-1 and HIV-2 strains at IC₅₀ values ranging from 0.02 to 0.46 μM^[3]. In Vivo: Triciribine (TCBN) treatment, administered for 7 days after 14 days of hypoxia until 21 days of hypoxia is reached, reversed the vascular thickening as shown by immunohistochemistry and Western analyses. On the other hand, Rapamycin treatment did not prevent hypoxia-induced pulmonary alveolar haemorrhage and congestion. Triciribine partially inhibits progressive pruning of the vasculature^[4].