ArticleInternational journal of molecular sciences2024
Probenecid Inhibits Extracellular Signal-Regulated Kinase and c-Jun N-Terminal Kinase Mitogen-Activated Protein Kinase Pathways in Regulating Respiratory Syncytial Virus Response.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Review
- Probenecid is a dual-acting antiviral/anti-inflammatory therapy for diverse respiratory viruses.Frontiers in pharmacology · 2026Article
- Article
- Probenecid Treatment Inhibits Replication of the Edmonston Measles Virus Strain in Vero Cells.Viruses · 2025Article
- The MAPK Response to Virus Infection Is Modified by Probenecid.Current issues in molecular biology · 2025Review
- Probenecid Inhibits NLRP3 Inflammasome Activity and Mitogen-Activated Protein Kinases (MAPKs).Biomolecules · 2025Article
- Pharmacological mechanisms of probenecid for SARS-CoV-2 and RSV co-infection: findings of system pharmacology, molecular docking, molecular dynamics simulation, and structure-activity relationship.Frontiers in microbiology · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
We examined the effect of probenecid in regulating the ERK and JNK downstream MAPK pathways affecting respiratory syncytial virus replication.
backgroundWe have previously shown that probenecid inhibits RSV, influenza virus, and SARS-CoV-2 replication in vitro in preclinical animal models and in humans. In a Phase two randomized, placebo-controlled, single-blind, dose range-finding study using probenecid to treat non-hospitalized patients with symptomatic, mild-to-moderate COVID-19, we previously showed that a 1000 mg twice daily treatment for 5 days reduced the median time to viral clearance from 11 to 7 days, and a 500 mg twice daily treatment for 5 days reduced the time to viral clearance from 11 to 9 days more than the placebo.
methodsIn this study, we sought to determine the mechanism of action of the probenecid inhibition of RSV replication in human respiratory epithelial (A549) cells.
resultsWe show that probenecid inhibits the RSV-induced phosphorylation of JNKs and ERKs and the downstream phosphorylation of c-jun, a component of the AP-1 transcription complex needed for virus replication. The inhibition of JNKs by probenecid reversed the repression of transcription factor HNF-4.
conclusionThe probenecid inhibition of JNK and ERK phosphorylation involves the MAPK pathway that precludes virus replication.
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