Using　copper-ionophores　to　translocate　extracellular　copper　into　mitochondria　is　a　clinically　validated　anticancer　strategy　that　has　been　identified　as　a　new　type　of　regulated　cell　death　termed　＂cuproptosis.＂　This　study　reports　a　mitochondria-targeting　Cu(I)　complex,　Cu(I)Br(PPh3)(3)　(CBP),　consisting　of　a　cuprous　ion　coordinated　by　three　triphenylphosphine　moieties　and　a　Br　atom.　CBP　exhibited　antitumor　and　antimetastatic　efficacy　in　vitro　and　in　vivo　by　specifically　targeting　mitochondria　instigating　mitochondrial　dysfunction.　The　cytotoxicity　of　CBP　could　only　be　reversed　by　a　copper　chelator　rather　than　inhibitors　of　the　known　cell　death,　indicating　copper-dependent　cytotoxicity.　Furthermore,　CBP　induced　the　oligomerization　of　lipoylated　proteins　and　the　loss　of　Fe-S　cluster　proteins,　consistent　with　characteristic　features　of　cuproptosis.　Additionally,　CBP　induced　remarkable　intracellular　generation　of　reactive　oxygen　species　(ROS)　through　a　Fenton-like　reaction,　indicating　a　complex　antitumor　mechanism.　This　is　a　proof-of-concept　study　exploiting　the　antitumor　activity　and　mechanism　of　the　Cu(I)-based　mitochondria-targeting　therapy.