Atazanavir (sulfate)

Atazanavir (BMS-232632) sulfate is a highly selective and orally active HIV-1 protease inhibitor with blood-brain barrier permeability. Atazanavir sulfate is a substrate and inhibitor of CYP3A4, and an inhibitor of P-glycoprotein (P-gp). Atazanavir sulfate is also a SARS-CoV 3CL^pro inhibitor with an IC₅₀ of 3.49 μM. Atazanavir sulfate inhibits cardiac fibrosis, hyperlipidemia and induces malignant glioma death^{[1][2][3][4][5][6][7][8][9]}. IC50 & Target:HIV-1 protease^[1]
CYP3A4, P-gp^[2] In Vitro: Atazanavir (1-10 μM, 72 h) attenuates hypoxia induced rat cardiac fibroblasts (rCFs) s proliferation by modulating the HMGB1/TLR 9 pathway^[4].
Atazanavir (1-10 μM, 72 h) inhibits collagen I, collagen III, HMGB1, p-IκBα and p-NF-κB expression levels in rat cardiac fibroblasts^[4].
Atazanavir (1-10 μM, 48 h) inhibits the growth of A, U251, T98G, LN229 cells and induces ESR (endoplasmic reticulum stress response) in U251, T98G, and LN229 cells^[6].
Atazanavir (6.0 μM) elicites Ca2+ transients and blebbing of the plasma membranes of C2C12 skeletal muscle myotubes^[7].
In Vivo: Atazanavir (30 mg/kg, i.g., daily, 4 weeks) reduces collagen deposition and inhibits cardiac remodeling in myocardial infarction (MI) model rats^[4].
Atazanavir sulfate has poor blood-brain barrier (BBB) ??permeability, but it can be verified in vitro using human BBB models^[8][9].