To investigate the impact of infusion therapy with Remaxol® on liver function in patients with intrahepatic cholestasis in chronic liver diseases (metabolic, drug, alcoholic hepatitis, chronic hepatitis B, C, autoimmune hepatitis, primary biliary cirrhosis, cross autoimmune syndrome). Subjects and methods. 102 patients aged 25 to 80 years, with intrahepatic cholestasis syndrome with chronic liver diseases different etiology were examined. Patients of the main group (n = 68) in the complex therapy received an infusion hepatoprotector Remaxol® daily intravenously drip 400.0 ml once a day for 11 days. Patients of the comparison group (n = 34) in the complex therapy received lyophilizate to prepare a solution for intravenous and intramuscular administration of ademetionine 400 mg diluted in the original solvent. Results. Infusion therapy with Remaxol® for chronic liver diseases of various etiologies (viral, metabolic, toxic, autoimmune), with intrahepatic cholestasis promotes: regression of the main clinical syndromes (pain abdominal from 68% to 25%, dyspeptic, 80% to 26% asthenic from 92% to 52% (p <0.05), cholestatic from 100% to 24% (p <0.05). A statistically significant difference in the dynamics of cholestasis was demonstrated by the change in the GGT value between the groups studied: the relative values of reduction in GGT levels in the patients of the main group were 38% compared to 19% in the comparison group patients (p <0.05). In the patients of the main group, the level of total cholesterol was reduced in dynamics from 10,10 ± 1,20 to 6,23 ± 0,31 mmol/l (p <0,001); improvement of protein-synthetic liver function; an increase in the absolute number of lymphocytes from 1.05 ± 0.08 x 109/l to 1.53 ± 0.06 x 109/l, (p <0.05). Conclusion. The effectiveness of Remaxol® in patients with intrahepatic cholestasis indicates the role of hepatoprotective, anticholestatic, cytoprotective effect of antioxidant therapy in restoring the functional status of the liver, immunoreactivity cells, as well as the presence of a lipid-regulating effect of the drug.