Following 14 days of hypoxia, a 7-day treatment with Triciribine reverses vascular thickening, as evidenced by immunohistochemistry and Western analyses, indicating its potential in treating hypoxia-induced conditions. Unlike Triciribine, Rapamycin fails to prevent hypoxia-induced pulmonary alveolar hemorrhage and congestion. Triciribine also shows the ability to moderately halt the progressive pruning of the vasculature^[4].

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].

While Triciribine does not efficiently inhibit the U87MG human cell line, it shows selective inhibition against other astrocytoma cell lines based on their grade. The WHO II K1861-10 line shows a partial response (69% maximum inhibition) with a GI50 of 1.7 μM. Optimal growth suppression by Triciribine occurs between 1-10 μM, reducing Akt phosphorylation and the activity of downstream p70S6K to baseline levels at 100 μM (IC50=130 nM) in KR158 cells^[2].

Triciribine, a novel tricyclic compound with antitumor properties, demonstrates effectiveness against HIV-1 in a syncytial plaque assay at concentrations of 0.01-0.02 μM. Additionally, it is active against various strains of HIV-1 and HIV-2, with IC50 values ranging from 0.02 to 0.46 μM in a microtiter XTT assay^[3].