Literature DB >> 33693561

Randomized Trial of Ruxolitinib in Antiretroviral-Treated Adults With Human Immunodeficiency Virus.

Vincent C Marconi1,2,3,4, Carlee Moser5, Christina Gavegnano1, Steven G Deeks6, Michael M Lederman7, Edgar T Overton8, Athe Tsibris9, Peter W Hunt6, Amy Kantor5, Rafick-Pierre Sekaly7, Randall Tressler10, Charles Flexner11, Selwyn J Hurwitz1, Daniela Moisi7, Brian Clagett7, William R Hardin12, Carlos Del Rio1,2, Raymond F Schinazi1, Jeffrey J Lennox1.   

Abstract

BACKGROUND: Inflammation is associated with end-organ disease and mortality for people with human immunodeficiency virus (PWH). Ruxolitinib, a Jak 1/2 inhibitor, reduces systemic inflammation for individuals without human immunodeficiency virus (HIV) and HIV reservoir markers ex vivo. The goal of this trial was to determine safety and efficacy of ruxolitinib for PWH on antiretroviral therapy (ART).
METHODS: AIDS Clinical Trials Group (ACTG) A5336 was an open-label, multisite, randomized controlled trial (RCT). Participants were randomly assigned (2:1) using centralized software to ruxolitinib (10 mg twice daily) plus stable ART for 5 weeks vs ART alone, stratified by efavirenz use. Eligible participants were suppressed on ART for ≥2 years, without comorbidities, and had >350 CD4+ T cells/µL. Primary endpoints were premature discontinuation, safety events, and change in plasma interleukin 6 (IL-6). Secondary endpoints included other measures of inflammation/immune activation and HIV reservoir.
RESULTS: Sixty participants were enrolled from 16 May 2016 to 10 January 2018. Primary safety events occurred in 2.5% (1 participant) for ruxolitinib and 0% for controls (P = .67). Three participants (7.5%) prematurely discontinued ruxolitinib. By week 5, differences in IL-6 (mean fold change [FC], 0.93 vs 1.10; P = .18) and soluble CD14 (mean FC, 0.96 vs 1.08; relative FC, 0.96 [90% confidence interval {CI}, .90-1.02]) levels for ruxolitinib vs controls was observed. Ruxolitinib reduced CD4+ T cells expressing HLA-DR/CD38 (mean difference, -0.34% [90% CI, -.66% to -.12%]) and Bcl-2 (mean difference, -3.30% [90% CI, -4.72% to -1.87%]).
CONCLUSIONS: In this RCT of healthy, virologically suppressed PWH on ART, ruxolitinib was well-tolerated. Baseline IL-6 levels were normal and showed no significant reduction. Ruxolitinib significantly decreased markers of immune activation and cell survival. Future studies of Jak inhibitors should target PWH with residual inflammation despite suppressive ART. CLINICAL TRIALS REGISTRATION: NCT02475655. Published by Oxford University Press for the Infectious Diseases Society of America 2021.

Entities:  

Keywords:  HIV; Jak inhibitors; immune activation; inflammation; reservoir

Mesh:

Substances:

Year:  2022        PMID: 33693561      PMCID: PMC8752257          DOI: 10.1093/cid/ciab212

Source DB:  PubMed          Journal:  Clin Infect Dis        ISSN: 1058-4838            Impact factor:   20.999


  31 in total

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Journal:  PLoS One       Date:  2014-10-23       Impact factor: 3.240

9.  Long-term treatment with ruxolitinib for patients with myelofibrosis: 5-year update from the randomized, double-blind, placebo-controlled, phase 3 COMFORT-I trial.

Authors:  Srdan Verstovsek; Ruben A Mesa; Jason Gotlib; Vikas Gupta; John F DiPersio; John V Catalano; Michael W N Deininger; Carole B Miller; Richard T Silver; Moshe Talpaz; Elliott F Winton; Jimmie H Harvey; Murat O Arcasoy; Elizabeth O Hexner; Roger M Lyons; Ronald Paquette; Azra Raza; Mark Jones; Deanna Kornacki; Kang Sun; Hagop Kantarjian
Journal:  J Hematol Oncol       Date:  2017-02-22       Impact factor: 17.388

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8.  Pharmacokinetics of Ruxolitinib in HIV Suppressed Individuals on Antiretroviral Agent Therapy from the ACTG A5336 Study.

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