ArticleActa pharmaceutica Sinica. B2024
Carrimycin inhibits coronavirus replication by decreasing the efficiency of programmed -1 ribosomal frameshifting through directly binding to the RNA pseudoknot of viral frameshift-stimulatory element.
Article in Acta pharmaceutica Sinica. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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
11 citing papers in PubMed.
- hnRNPC facilitates coronavirus replication by directly binding the frameshift-stimulatory element of viral genomic RNA.PLoS pathogens · 2026Article
- Open questions on viral frameshifting: Exploiting the structural plasticity of the frameshifting element for therapeutic intervention.Biophysical journal · 2026Review
- SARS-CoV-2 Antivirals Identified from Small Molecule Modulators of Programmed -1 Ribosomal Frameshifting.ACS infectious diseases · 2026Article
- Drugs against broad-spectrum of coronaviruses.Frontiers in immunology · 2026Review
- Uncovering Anticancer Mechanisms of Spiramycin Derivatives Using Transcriptomic and Metabolomic Analyses.Metabolites · 2025Article
- Efficacy of carrimycin againstMicrobiology spectrum · 2025Article
- Carrimycin exhibited broad spectrum inhibitory activities against coronaviruses replication through down-regulating host factor TMEM41B.Acta pharmacologica Sinica · 2025Article
- Stem loop binding protein promotes SARS-CoV-2 replication via -1 programmed ribosomal frameshifting.Signal transduction and targeted therapy · 2025Article
- The synergistic antitumour effect of Carrimycin combined with 5-fluorouracil on colorectal cancer.Scientific reports · 2025Article
- Mycophenolate mofetil exerts broad-spectrum antiviral activity against coronaviruses including SARS-CoV-2.Virology journal · 2025Article
- Review
Corrections and comments
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pandemic of SARS-CoV-2 worldwide with successive emerging variants urgently calls for small-molecule oral drugs with broad-spectrum antiviral activity. Here, we show that carrimycin, a new macrolide antibiotic in the clinic and an antiviral candidate for SARS-CoV-2 in phase III trials, decreases the efficiency of programmed -1 ribosomal frameshifting of coronaviruses and thus impedes viral replication in a broad-spectrum fashion. Carrimycin binds directly to the coronaviral frameshift-stimulatory element (FSE) RNA pseudoknot, interrupting the viral protein translation switch from ORF1a to ORF1b and thereby reducing the level of the core components of the viral replication and transcription complexes. Combined carrimycin with known viral replicase inhibitors yielded a synergistic inhibitory effect on coronaviruses. Because the FSE mechanism is essential in all coronaviruses, carrimycin could be a new broad-spectrum antiviral drug for human coronaviruses by directly targeting the conserved coronaviral FSE RNA. This finding may open a new direction in antiviral drug discovery for coronavirus variants.
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Registered trials
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