Ritonavir is an inhibitor of aspartyl proteases of  for oral administration, the active peptide mimetic. Inhibition of HIV protease prevents rupture of gag-pol polyprotein connection that leads to the formation of immature and unable to virus infection.Ritonavir has selective affinity for the winstrol protease and exhibits little activity against human aspartyl proteases.

Antiviral Activity in vitro data in vitro suggest that ritonavir is active against all types of HIV tested on various human transformed and primary cell lines. The concentration of drug that inhibited 50% and 90% of viral replication in vitro is suitably about 0.02 uM and 0.11 uM. Similar activity has been demonstrated using a sensitive azidothymidine (AZT-sensitive) and AZT-resistant HIV strains. In studies conducted in which the definition of direct cell toxicity of ritonavir on several cell lines showed no direct toxicity when using the drug in concentrations up to 35 uM; wherein the therapeutic index in vitro was at least 1000.

Resistance HIV-1 isolates resistant to ritonavir were isolated in vitro .Genotypic analysis of isolates showed the presence of mutations in HIV protease gene, which led to the specific amino acid substitutions at codons 84 (Isoleucine to Valine), 82 (phenylalanine to valine), 71 (alanine to valine) and 46 (isoleucine for methionine). Genotypic and phenotypic analysis of isolates obtained in clinical trials (I / II phase) showed that mutations in the HIV protease gene and appeared gradually in order. Baseline mutation occurred at positions 82 (alanine to valine / phenylalanine), 54 (valine to isoleucine), 71 (alanine to valine / Threonine) and 36 (isoleucine to leucine) followed by subsequent additional combinations of mutations in five amino acid positions. It has been found that the presence of 82 mutations necessary but not sufficient for the formation of phenotypic resistance. Phenotypic resistance was defined as a decrease in the sensitivity of the virus in 5 times or more compared to baseline in vitro. The clinical relevance of phenotypic and genotypic changes associated with treatment with ritonavir, is not currently installed.

Renal clearance is less than 0.1 L / h and relatively constant when using different dosages. The absolute bioavailability of ritonavir has not been established because there is no dosage form for parenteral administration. Plasma concentrations of ritonavir after administration of a single dose of 100 mg tablets is approximately: 121,7 ± 53,8 ug h / mL. In the appointment of the drug during the meal there is a slight decrease in the bioavailability of ritonavir tablets. When winstrol assigning a single dose tablets ritonavir 100 mg simultaneously with the reception of a moderately fatty meal. It was found that the residual concentration of ritonavir decreased slightly over time, perhaps due to the induction of enzymes, however, it had stabilized by the end of two weeks. The equilibrium concentration in the blood plasma while taking the drug at a dose of 600 mg 2 times a day, it is achieved by the end of two weeks, with a maximum concentration (C max ) and a residual plasma concentration (C trough ) are respectively 11.2 g / ml and 3, 7 mg / ml. In equilibrium apparent clearance in patients treated with 600 mg twice daily, an average of 8,8 ± 3,2 l / h. The half-life of 3-5 hours of ritonavir. Clinically significant difference AUC and C max in men and women has not been observed. No statistically significant relationship between the parameters of the pharmacokinetics of ritonavir and body weight were found.

The patients older age pharmacokinetics of ritonavir patients 50-70 years when used in a dose of 100 mg in combination with lopinavir or at higher doses, but no HIV protease inhibitors did not differ from that in younger patients. patients with impaired renal function currently specific data relative to this no group of patients. However, because ritonavir is actively binds to a protein, it is unlikely that it will be largely displayed by hemodialysis or peritoneal dialysis. Patients with impaired liver function in patients with mild hepatic insufficiency effect of ritonavir 400 mg when taking 2 times a day corresponded to that effect in the control group at a dose of 500 mg 2 times a day. Thus, patients with mild hepatic impairment correction dose is not winstrol required. Sufficient data on the use of ritonavir in patients with moderate hepatic insufficiency is not. Liver failure mild or moderate no effect on the binding of ritonavir plasma proteins.



  • established hypersensitivity to ritonavir or one of the formulation components;
  • severe hepatic impairment;
  • Children under 3 years of age;

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