Cheonggukjang is a soybean paste made by fermenting whole cooked soybeans with Bacillus subtilis. Cheonggukjang contains a fibrinolytic enzyme that could provide clinical applications for removing blood clots. In the present study,the term “cheonggukjang kinase”(CGK) was used to refer to this fibrinolytic enzyme. The thrombolytic effects of CGK were analyzed in a rat model of cerebral embolic stroke produced by middle cerebral artery occlusion(MCAO) . Results from fibrin and platelet-rich clot lysis assays demonstrated that thrombolytic activity was greatest in CGKs,which were cultured for 40 hours. In addition,T50,the time needed to decompose 50% of the clot,did not change with plasminogen treatment,indicating that CGK was not a plasminogen activator,but was rather presumed to act as a plasmin-like protein. An intravenous infusion of CGK(1 U plasmin-like activity/100 μg CGK/kg) at 1 hour after MCAO resulted in removal of clots in a rat model of cerebral embolic stroke. CGK-treated groups exhibited a significant dose-dependent reduction in infarct volume. CGK treatment also improved functional recovery,as assessed by neurological deficit scores. Decreased infarct volume and improved functional recovery following CGK treatment was greater compared with recombinant tissue plasminogen activator(10 mg/kg) . These results suggested that CGK effectively reduced infarct volume and improved functional recovery following ischemic brain injury. CGK exhibits a number of potential clinical applications in the treatment of cerebral embolic stroke. Cheonggukjang is a soybean paste made by fermenting whole cooked soybeans with Bacillus subtilis. Cheonggukjang contains a fibrinolytic enzyme that may provide clinical applications for removing blood clots. In the present study, the term “cheonggukjang kinase ” (CGK) was used to refer to this fibrinolytic enzyme. The thrombolytic effects of CGK were analyzed in a rat model of cerebral embolic stroke produced by middle cerebral artery occlusion (MCAO). Results from fibrin and platelet-rich clot analysis assay for that thrombolytic activity was greatest in CGKs, which were added for 40 hours. In addition, T50, the time needed to decompose 50% of the clot, did not change with plasminogen treatment, indicating that CGK was not a plasminogen activator, but was rather presumed to act as a plasmin-like protein . An intravenous infusion of CGK (1 U plasmin-like activity / 100 μg CGK / kg) at 1 hour after MCAO resulted in removal of clots in a rat model of cerebral embolic stroke. CGK-treated groups showed a significant dose-dependent reduction in infarct volume. CGK treatment also improved functional recovery, as assessed by neurological deficit scores. Decreased infarct volume and improved functional recovery following CGK treatment was greater than with recombinant tissue plasminogen activator (10 mg / kg) . These results suggested that CGK effectively reduced infarct volume and improved functional recovery following ischemic brain injury. CGK exhibits a number of potential clinical applications in the treatment of cerebral embolic stroke.