PRIMA-1 is converted to compounds that form adducts with thiols in mutant p53. Modification of thiol groups in mutant p53 by PRIMA-1 conversion products is sufficient to restore its tumor suppressor activity.[2]. PRIMA-1 inhibits the growth of pancreatic cancer cell lines and induces cell cycle arrest and decreases DNA synthesis. It selectively induces apoptosis and cell death in mutant p53-expressing pancreatic cancer cells and also leads to activation of p53-dependent apoptotic pathways. PRIMA-1 enhances the cytotoxicity of chemotherapeutic agents active against mutant p53 pancreatic cancer cells[1]. PRIMA-1 has antileukemic properties in acute promyelocytic leukemia-derived NB4 cells. PRIMA-1-triggered apoptosis is in a dose-dependent and time-dependent manner as indicated by the MTT assay and annexin-V staining. Apoptosis induction by PRIMA-1 is associated with caspase-9, caspase-7 activation and PARP cleavage. PRIMA-1 does not show any significant apoptotic effect in normal human peripheral blood mononuclear cells[4].

Intravenous (i.v.) injections of PRIMA-1 in mice does not cause any obvious changes in weight or behavior compared with untreated animals. PRIMA-1 has in vivo antitumor activity in this animal tumor model. It suppresses in vivo tumor growth in a mutant p53-dependent manner[3].