Our study was based on the hypothesis that a non competitive antagonist of NMDA receptors can improve clinical effects of antipsychotic therapy in a subgroup of patients with schizophrenia with clinical signs of glutamatergic hyperfunction such as catatonic symptoms and disorganization. The study design was open and non-comparative. The duration of the study for each patient was 6 months, the target dosage of acatinol was 20 mg. Forty stable patients with schizophrenia with predominance of signs of disorganization and subcatatonic symptoms were included. The following instruments were used: PANSS, NSA, CGI, BACS, UKU. Adding of acatinol to the antipsychotic treatment improved clinical symptoms, cognitive functioning and social functioning and decreased the number of side effects. The drug was well-tolerated.