Gabriel Birkus

TL;DR: Treatment of various human cell types with tenofovir at concentrations that greatly exceed those required for it both to have in vitro anti-HIV type 1 activity in peripheral blood mononuclear cells and to achieve therapeutically relevant levels in plasma is not associated with mitochondrial toxicity.

TL;DR: The clinical observation of elevated serum creatinine in patients taking cobicistat is likely a result of OCT2 transport, facilitating intracellular accumulation, and MATE1 inhibition, establishing OAT2 as a likely relevantCreatinine transporter and further challenging the traditional view that Creatinine is solely transported by a cationic pathway.

TL;DR: Crystal structures were determined with wild-type and K103N HIV-1 reverse transcriptase with etravirine and rilpivirine, revealing a similar binding mode for TMC125 and TMC278, whether bound to wild- type or K103n RT.

TL;DR: The main enzymatic activity responsible for the initial step in the intracellular activation of GS-7340 and GS-9131 was isolated from human peripheral blood mononuclear cells and identified as lysosomal carboxypeptidase A (CatA; EC 3.4.5).

TL;DR: In conclusion, tenofovir exhibited weak cytotoxic effects in all cell types tested with less in vitro cytotoxicity than the majority of NRTIs currently used for the treatment of HIV disease.