JoEllyn M McMillan, Denise A Cobb, Zhiyi Lin, Mary G Banoub, Raghubendra S Dagur, Amanda A Branch Woods, Weimin Wang, Edward Makarov, Ted Kocher, Poonam S Joshi, Rolen M Quadros, Donald W Harms, Samuel M Cohen, Howard E Gendelman, Channabasavaiah B Gurumurthy, Santhi Gorantla, Larisa Y Poluektova
Antiretroviral drug (ARV) metabolism is linked largely to hepatic cytochrome P450 activity. One ARV drug class known to be metabolized by intestinal and hepatic CYP3A are the protease inhibitors (PIs). Plasma drug concentrations are boosted by CYP3A inhibitors such as cobisistat and ritonavir (RTV). Studies of such drug-drug interactions are limited since the enzyme pathways are human specific. While immune-deficient mice reconstituted with human cells are an excellent model to study ARVs during human immunodeficiency virus type 1 (HIV-1) infection, they cannot reflect human drug metabolism...
May 2018: Journal of Pharmacology and Experimental Therapeutics