Cobicistat: Review of a Pharmacokinetic Enhancer for HIV Infection

Clin Ther. 2015 Sep 1;37(9):1876-93. doi: 10.1016/j.clinthera.2015.07.022. Epub 2015 Aug 25.

Abstract

Purpose: This article reviews the clinical pharmacology, pharmacodynamic and pharmacokinetic (PK) properties, clinical efficacy and tolerability, drug interactions, and dosing and administration of cobicistat.

Methods: Searches of MEDLINE and International Pharmaceutical Abstracts from 1964 to February 2015 were conducted using the search terms cobicistat and GS-9350. Relevant information was extracted from the identified clinical trials and review articles. Abstracts from the Conference on Retroviruses and Opportunistic Infections (2014-2015) and the Interscience Conference on Antimicrobial Agents and Chemotherapy (2013-2014) were also searched.

Findings: Cobicistat is a PK enhancer lacking antiviral activity that, via selective cytochrome P-450 (CYP) 3A inhibition, inhibits the metabolism of certain antiretroviral medications and is used for prolonging their effect. Cobicistat has been studied as a booster of elvitegravir, a second-generation integrase inhibitor, and of the protease inhibitors atazanavir and darunavir. Data on its clinical efficacy and tolerability have been presented in 2 Phase II trials and in 9 Phase III trials, which reported durable efficacy in terms of achievement of sustained suppression of HIV-1 RNA levels to <50 copies/mL for at least 48 weeks. Cobicistat was generally well-tolerated in these studies. Cobicistat may increase serum creatinine levels via the inhibition of proximal renal tubular cell transporters and thus reduce estimated glomerular filtration rate, although it does not appear to affect actual glomerular filtration rate. Given the potent CYP3A inhibition by cobicistat, its coadministration with drugs metabolized by CYP3A may result in increased plasma concentrations of such agents. Moreover, as cobicistat is metabolized predominantly by CYP3A, plasma concentrations may increase or decrease on coadministration with CYP3A inhibitors or inducers, respectively.

Implications: With potent durability through 48 weeks, a tolerability profile comparable to other first- and second-line antiretroviral therapies, and a convenient dosing schedule with low daily pill burden in fixed-dose combination tablets, cobicistat is a potential addition to the management of HIV infection as a PK enhancer. However, the effects of cobicistat on serum creatinine and its considerable drug-interaction potential may warrant additional monitoring.

Keywords: GS-9350; HIV; booster; cobicistat; pharmacokinetic enhancer.

Publication types

  • Review

MeSH terms

  • Anti-HIV Agents / pharmacokinetics
  • Anti-HIV Agents / pharmacology*
  • Anti-HIV Agents / therapeutic use
  • Cobicistat / pharmacokinetics
  • Cobicistat / pharmacology*
  • Cobicistat / therapeutic use
  • Cytochrome P-450 CYP3A Inhibitors / pharmacokinetics
  • Cytochrome P-450 CYP3A Inhibitors / pharmacology
  • Cytochrome P-450 CYP3A Inhibitors / therapeutic use
  • Darunavir / pharmacokinetics
  • Darunavir / therapeutic use
  • Drug Interactions
  • Drug Therapy, Combination
  • HIV Infections / drug therapy*
  • HIV Infections / metabolism
  • HIV-1 / drug effects
  • Humans
  • Quinolones / pharmacokinetics
  • Quinolones / therapeutic use

Substances

  • Anti-HIV Agents
  • Cytochrome P-450 CYP3A Inhibitors
  • Quinolones
  • elvitegravir
  • Cobicistat
  • Darunavir