ArticleThe Journal of antibiotics2026
Repurposing Tirazone as an effective quorum-sensing inhibitor against Pseudomonas aeruginosa virulence and biofilm formation.
Article in The Journal of antibiotics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibiotic resistance has emerged as a critical global public health challenge. Quorum sensing (QS), a density-dependent regulatory mechanism, plays a pivotal role in bacterial pathogenesis by coordinating virulence factor expression, making it a critical target for antivirulence therapy. Leveraging a drug repositioning strategy, this study investigated the antivirulence potential of drugs in the database of DrugBank on the common opportunistic pathogen Pseudomonas aeruginosa by virtual screening. Molecular docking analysis predicted that the antitumor drug, Tirazone, could bind to the core QS regulatory proteins, LasR, RhlR, and PqsR of P. aeruginosa with abundant active sites, whereas the binding free energies were higher than those of the native QS signals. In vitro experiments demonstrated that Tirazone significantly suppressed virulence factor secretion, cell motilities, and biofilm formation in the model P. aeruginosa strain PAO1, and downregulated the expression of a series of QS-related genes with low effective concentration (≤ 8 μM). A competitive binding model of QS signal molecules further elucidated that Tirazone interfered with QS signaling by competitively inhibiting the function of LasR, RhlR, and PqsR. Additionally, Tirazone treatment significantly protected Caenorhabditis elegans and mouse models from P. aeruginosa infection, and reduced the bacterial loads and pathological lesions in mouse lungs. Moreover, Tirazone demonstrated synergistic effects with polymyxin B, levofloxacin, and amikacin, significantly enhancing their bactericidal efficacy in treating P. aeruginosa. This study reveals the molecular mechanism underlying Tirazone's multi-target intervention in the QS system, and provides an experimental foundation for developing combination therapies based on antivirulence strategies.
Indexed as
Identifiers
41708876What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.