Tenovin-1 (92 mg/kg, i.p.) suppresses tumor growth in SCID mice originating from BL2 cells or ARN8 cells^[5].

Tenovin-1 shields p53 from degradation mediated by MDM2, while minimally affecting p53 synthesis. It targets factor(s) upstream of p53, influencing not only p53 function but also other cellular pathways. At a concentration of 10 μM, Tenovin-1 inhibits the deacetylase activity of SirT2^[1].

Tenovin-1 (1-10 μM) elicits a concentration-dependent, bell-shaped cell death response in SK-N-MC cells. It modulates the gene and protein expression of Bcl-2 family members, exhibiting a more pronounced effect on mRNA and protein expression at lower concentrations compared to higher ones. Additionally, Tenovin-1-induced cytotoxicity in p53 wild-type WE-68 cells relies on caspases, whereas it is independent of caspases in p53 null SK-N-MC cells. AIF predominantly contributes to Tenovin-1-induced cell death in p53 null SK-N-MC cells, whereas in p53 wild-type WE-68 cells, its role is less significant. Furthermore, reactive oxygen species participate in Tenovin-1-mediated cell death in SK-N-MC cells. Moreover, Tenovin-1 induces DNA damage in SK-N-MC cells^[3].

Tenovin-1 (5 μM) enlarges the nuclear size in both glioblastoma cells and rat primary astrocytes. Furthermore, Tenovin-1 induces cellular senescence, a process seemingly independent of cell death^[4].

Tenovin-1 (10 μM) diminishes the proliferation and anchorage-independent growth of NSCLC cells. Moreover, it impedes the growth of H358 lung cancer cells^[5].