Fibroblast activation protein-alpha (FAP alpha) is highly expressed in tumor-associated cells and has become one of the most attractive targeting sites in cancer diagnosis and therapy. To ameliorate the rapid metabolism of FAP alpha inhibitor (FAPI), here, a multifunctional binding agent was introduced to simultaneously achieve At-211 radiolabeling and tumor retention prolongation of corresponding radiolabeled drug. At-211-APBA-FAPI was successfully synthesized by conjugating At-211 with the designed FAPI carrier in satisfactory radiochemical yield (>60 %). At-211-APBA-FAPI exhibited excellent in vitro stability, significant tumor affinity and specific killing effect on FAP alpha-positive U87MG cells. Molecular docking reveals that FAPI decorated with albumin binder can bind with FAP alpha protein via multiple intermolecular interactions with a considerable binding energy of -9.66 kcal/mol At-211-APBA-FAPI exhibits good targeting in murine xenograft models, showing obviously longer tumor retention than previously-reported radioastatinated compound. As a result, At-211-APBA-FAPI presents pronounced therapeutic effect with ignorable normal organs/tissues biotoxicity. All these indicate that introducing a multifunctional binding agent can effectively enhance the availability of FAPI for At-211 conjugation and tumoricidal effect, providing vital hints for the translation of targeted-alpha therapy based on radiolabeled FAPI derivatives.