API-1

API-1 is a potent selective Akt/PKB inhibitor that reduces the level of phosphorylated Akt (IC₅₀ = 0.8 μM). API-1 binds to the PH domain and inhibits Akt membrane translocation. API-1 induces c-FLIP degradation. API-1 reduces cell proliferation and induces apoptosis. API-1 decreases tumor growth in mouse xenograft model^[1][2][3]. In Vitro:API-1 (0.625-10 μM, 3 d) effectively inhibits the growth of non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC) cell lines^[1].
API-1 (5-10 μM, 24 h) effectively induces apoptosis in API-1-sensitive NSCLC and HNSCC cell lines^[1].
API-1 (1.25-5 μM, 24 h) synergizes with factor-related apoptosis-inducing ligand (TRAIL) to induce apoptosis in H1229 and 22A^[1].
API-1 (0.625-10 μM, 2-24 h) reduces the levels of c-FLIP (through facilitating ubiquitin/proteasome-mediated degradation) without increasing the expression of DR4 or DR5 in NSCLC and HNSCC cells^[1].
API-1 (0.625-10 μM, 2-24 h) inhibits the phosphorylation of Akt in NSCLC and HNSCC cells^[1].
API-1 (0.5-20 μM, 12-72 h) induces GSK3-dependent, β-TrCP- and FBXW7-mediated Mcl-1 degradation, resulting in induction of apoptosis in NSCLC cell lines^[2].
In Vivo:API-1 (10 mg/kg; i.p.; daily for 6-8 weeks) selectively inhibits the growth of tumors with hyperactivated Akt in OVCAR3 and PANC-1 xenograft mice model^[3].