High impulsivity would increase the risk of criminal behavior, substance abuse, and suicide. Many experimental drugs have been identified as anti-impulsivity agents, but only a few are clinically available. To further develop anti-impulsivity agents, we have proposed a strategy on the basis of previous findings: we should test clinically available drugs or the metabolites that increase extracellular dopamine levels in the medial prefrontal cortex without increasing them in the ventral striatum. We chose two drugs and examined the effects on impulsive action in rats by using a 3-choice serial reaction time task. We showed that the administration of blonanserin, an atypical antipsychotic, reduced impulsive actions in a U-shaped manner in rats. An active metabolite of buspirone or tandospirone, 1-(2-Pyriidinyl)-piperazine, also slightly reduced impulsive actions, though it impaired motor functions. These results affirm the validity of our strategy for developing anti-impulsivity drugs, though the strategy would need some refinement in the light of these results.