ArticleClinical and translational science2025
Characterization of Drug-Drug Interactions for Remdesivir, an Intravenous Antiviral for SARS-CoV-2, in Healthy Participants.
Article in Clinical and translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Thorough QT/QTc Clinical Study to Evaluate the Effect of Remdesivir on Cardiac Repolarization in Healthy Participants.Clinical and translational science · 2026Trial
- Pharmacokinetic Drug Interaction Studies of Limnetrelvir with Midazolam and Itraconazole in Healthy Participants.Clinical drug investigation · 2026Article
- Characterization of Drug-Drug Interactions for Remdesivir, an Intravenous Antiviral for SARS-CoV-2, in Healthy Participants.Clinical and translational science · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Remdesivir is an intravenous antiviral approved worldwide for the treatment of COVID-19 in adults and children. Remdesivir, as a prodrug inhibitor of RNA polymerase, undergoes intracellular activation to form the active metabolite along with 2 inactive circulating metabolites, GS-704277 and GS-441524. Based on drug-drug interaction (DDI) risks identified in vitro, three Phase 1 crossover DDI studies were conducted to evaluate remdesivir as a potential (i) object, (ii) inhibitor, or (iii) inducer of enzymes and transporters. As an object of organic anion transporting polypeptide (OATP) 1B1/1B3 and P-glycoprotein inhibition (cyclosporine A), remdesivir and GS-704277 exposures increased 2-fold and 3-fold, respectively, while GS-441524 was unchanged. Increased exposures were not clinically relevant as remdesivir and GS-704277 exposures remained transient (approximately 1-h half-life) and were unlikely to affect the formation of the active metabolite. As an object of strong cytochrome P450 (CYP) 3A induction (carbamazepine), exposure changes of remdesivir and its metabolites were not clinically significant. As an inhibitor, single-dose remdesivir did not impact pitavastatin (OATP1B1/1B3 substrate) exposures but increased midazolam (CYP3A substrate) C
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