Patients with HER2-positive and triple negative breast cancer (TNBC) are associated with increased risk to develop metastatic disease including reoccurring disease that is resistant to standard and targeted therapies. The α V β 3 has been implicated in BC including metastatic disease. The aims of this study were to investigate the potential of α V β 3 -targeted peptides to deliver radioactive payloads to BC tumors expressing α V β 3 on the tumor cells or limited to the tumors' neovascular. Additionally, we aimed to assess the pharmacokinetic profile of the targeted α-particle therapy (TAT) agent [ 225 Ac]Ac-DOTA-cRGDfK dimer peptide and the in vivo generated decay daughters. The expression of α V β 3 in a HER2-positive and a TNBC cell line were evaluated using western blot analysis. The pharmacokinetics of [ 111 In]In-DOTA-cRGDfK dimer, a surrogate for the TAT-agent, was evaluated in subcutaneous mouse tumor models. The pharmacokinetic of the TAT-agent [ 225 Ac]Ac-DOTA-cRGDfK dimer and its decay daughters were evaluated in healthy mice. Selective uptake of [ 111 In]In-DOTA-cRGDfK dimer was shown in subcutaneous tumor models using α V β 3 -positive tumor cells as well as α V β 3 -negative tumor cells where the expression is limited to the neovasculature. Pharmacokinetic studies demonstrated rapid accumulation in the tumors with clearance from non-target organs. Dosimetric analysis of [ 225 Ac]Ac-DOTA-cRGDfK dimer showed the highest radiation absorbed dose to the kidneys, which included the contributions from the free in vivo generated decay daughters. This study shows the potential of delivering radioactive payloads to BC tumors that have α V β 3 expression on the tumor cells as well as limited expression to the neovascular of the tumor. Furthermore, this work determines the radiation absorbed doses to normal organs/tissues and identified key organs that act as suppliers and receivers of the actinium-225 free in vivo generated α-particle-emitting decay daughters.