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Introduction. Thyronamines belong to agonists of TAAR1 - trace amine receptors in the brain. The mechanism of activation of the processes of autophagy and neuroplasticity under the action of a synthetic analogue of thyronamines – 4-(4-(2-aminoethoxy)benzyl)aniline is described. Since cerebrovascular disorders remain the most common among neurological diseases, the development and implementation of drugs with neuroprotective properties is considered a promising strategy for the treatment and rehabilitation of patients with ischemic stroke. The aim of the study was to elucidate the effect of 4-(4-(2-aminoethoxy)benzyl)aniline on the activity of GPO, SOD and the dynamics of changes in the level of TBARS in the brain of rats after modeling focal ischemia by transient occlusion of the left middle cerebral artery. Materials and methods. The 4-(4-(2-aminoethoxy)benzyl)aniline was synthesized. Changes in the activity of antioxidant enzymes and the accumulation of secondary LPO products that react with thiobarbituric acid (TBARS) in rat brain homogenates were observed after injection of the studied compound in different dosages, as well as 24 hours after modeling focal ischemia. A neurological deficit in experimental rats was detected by the Garcia scale and the vibrissae-evoked forelimb placing test. Results. Compilation of data made it possible to find a strong relationship between the amount of the injected analogue and the growth of GPO activity in the neurons of healthy animals. In 80% of rats, occlusion of the middle cerebral artery induced evident sensorimotor disorders. 24 hours after the administration of a synthetic analogue of thyronamine in the homogenates of the affected left hemisphere, the activity of glutathione peroxidase significantly increased, and the content of TBARS decreased, and a tendency to activation of SOD was also observed. Conclusions. The obtained data indicate a positive effect of 4-(4-(2-aminoethoxy) benzyl) aniline on antioxidant enzymes in the intact rat brain and after modeling of focal ischemia, which is the basis to continue research for the purpose of finding long-term neuroprotective effects.