Objective. This study aims to analyze the results of using bulevirtide, an HBV and HDV entry inhibitor, in real-world practice in patients with chronic hepatitis D in the Moscow region. The analysis focuses on the effectiveness and safety of bulvertide treatment, both as monotherapy and in combination with peginterferon, during the compensated and decompensated stages of liver cirrhosis. Patients and methods. The study evaluated the efficacy and safety of bulevirtide treatment in two patient groups. The first group consisted of 61 patients with compensated disease, including 27 individuals with Child–Pugh class A liver cirrhosis. The second group included 8 patients with Child–Pugh class B cirrhosis. Results. Among patients with compensated disease, a 48-week treatment with bulevirtide resulted in a significant decrease in HDV RNA levels from 6.9 log10 to undetectable (p < 0.001). Furthermore, alanine aminotransferase (ALT) levels decreased from 64.0 to 37.0 U/l (p < 0.001). The median reduction in HDV RNA levels from baseline was -5.1 log10 (monotherapy: -4.2 log10, dual therapy: -5.7 log10). The virological response rate was 94% (monotherapy: 88%, dual therapy: 96%) with «full virological response» (aviremia) observed in 66% of patients and normal ALT levels in 59% of patients (compared to 22% at baseline). Virological efficacy improved over the course of treatment. Similar virological response dynamics were observed in patients with compensated cirrhosis compared to the overall group. In patients with decompensated cirrhosis, a virological response was observed in 6 out of 8 patients during treatment, and a biochemical response (a decrease in ALT levels from 60.0 U/I to 45.0 U/l) in 5 out of 8 patients. After 48 weeks of treatment, all 5 patients who reached this point achieved a virological response (decrease in HDV RNA levels from 5.1 log10 to 3.0 log10, median decrease of -2.5 log10 from baseline). One patient on monotherapy achieved «full virological response» (aviremia). Improvement of liver function was observed, including a reduction in liver damage severity based on Child–Pugh score to the compensated cirrhosis level (6 points), down-staging from Child–Pugh class B to A in 3 patients, and clinical resolution of ascites in 7 out of 8 patients and hepatic encephalopathy in 3 out of 5 patients. Bilirubin, albumin, INR, prothrombin time remained stable. The treatment was well tolerated, no serious adverse events, cases of treatment withdrawal were registered. The reduction in leukocyte and platelet counts, related to interferon, did not necessitate treatment adjustment. Conclusion. The analysis of bulevirtide use in patients with CHD in real-world practice demonstrated high treatment efficacy, safety and good tolerability, even in cases of compensated and decompensated liver cirrhosis. This study also presents the first experience of antiviral therapy for decompensated liver cirrhosis in Russia, supporting the recommendation of bulevirtide for patients with impaired liver function. Furth er development of an optimal treatment algorithm, including for patients with impaired liver function, is needed, as well as clarification of the treatment effect on clinical outcomes and disease prognosis. Key words: bulevirtide, chronic hepatitis D, compensated cirrhosis, decompensated cirrhosis, chronic liver failure