Comparative Pharmacology
Head-to-head clinical analysis: ATAZANAVIR SULFATE RITONAVIR versus LEXIVA.
Peer-Reviewed Evidence
Head-to-head clinical analysis: ATAZANAVIR SULFATE RITONAVIR versus LEXIVA.
ATAZANAVIR SULFATE; RITONAVIR vs LEXIVA
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Atazanavir is an azapeptide HIV-1 protease inhibitor that inhibits the virus-specific processing of viral Gag and Gag-Pol polyproteins in HIV-1 infected cells, preventing formation of mature virions. Ritonavir is an HIV protease inhibitor that also inhibits CYP3A, boosting atazanavir levels.
Fosamprenavir is a prodrug of amprenavir, a protease inhibitor (PI) that competitively inhibits HIV-1 protease, preventing cleavage of viral Gag-Pol polyprotein, resulting in immature, non-infectious viral particles.
Atazanavir 300 mg with ritonavir 100 mg orally once daily with food.
1400 mg orally twice daily (with ritonavir 100 mg) or 1400 mg orally once daily (with ritonavir 100 mg and cobicistat 150 mg). For treatment-naïve patients, 1400 mg orally once daily with ritonavir 100 mg or cobicistat 150 mg.
None Documented
None Documented
Atazanavir: ~6.5-7 hours (when boosted with ritonavir). Ritonavir: ~3-5 hours. Clinical context: Atazanavir requires ritonavir boosting to achieve therapeutic trough concentrations; once-daily dosing maintains efficacy.
Terminal elimination half-life is 2.8 to 5.7 hours; with ritonavir boosting, half-life increases to 7-10 hours, allowing once-daily dosing.
Biliary/fecal (major route): atazanavir 79% as unchanged drug, 13% as metabolites; ritonavir 86.4% as metabolites, 3.5% unchanged. Renal: atazanavir 7% (20% as unchanged); ritonavir 11.3% (3.5% unchanged).
Renal (approximately 82% in urine, with 14% as parent drug and 68% as metabolites); fecal (approximately 16%, with 7% as parent drug).
Category A/B
Category C
Protease Inhibitor
Protease Inhibitor