Mifepristone　(RU486)　is　marketed　and　used　widely　by　women　as　an　abortifacient,　and　experimentally　for　psychotic　depression　and　anticancer　treatments.　After　administration,　metapristone　is　found　to　be　the　most　predominant　metabolite　of　mifepristone.　We　hypothesized　that　adhesion　of　circulating　tumor　cells　(CTCs)　to　vascular　endothelial　bed　is　a　crucial　starting　point　in　metastatic　cascade,　and　that　metapristone　can　serve　as　a　cancer　metastatic　chemopreventive　agent　that　can　interrupt　adhesion　and　invasion　of　CTCs　to　the　intima　of　microvasculature.　In　the　present　study,　we　modified　the　synthesis　procedure　to　produce　grams　of　metapristone,　fully　characterized　its　spectral　properties　and　in　vitro　cellular　activities,　including　its　cytostatic　effects,　cell　cycle　arrest,　mitochondrial　membrane　potential,　and　apoptosis　on　human　colorectal　cancer　HT-29　cells.　Metapristone　concentration　dependently　interrupted　adhesion　of　HT-29　cells　to　endothelial　cells.　Metapristone　may　potentially　be　a　useful　agent　to　interrupt　metastatic　initiation.