ArticleChemical biology & drug design2018
Analogue synthesis reveals decoupling of antibiofilm and β-lactam potentiation activities of a lead 2-aminoimidazole adjuvant against Mycobacterium smegmatis.
Article in Chemical biology & drug design, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Biofilm Formation in Mycobacterial Genus; Mechanism of Biofilm Formation and Anti-mycobacterial Biofilm Agents.Current pharmaceutical biotechnology · 2025Review
- Synergistic antibacterial effects of ultrasound combined nanoparticles encapsulated with cellulase and levofloxacin onFrontiers in microbiology · 2023Article
- 2-Aminoimidazoles InhibitInternational journal of molecular sciences · 2022Article
- Design, Synthesis, and Biological Evaluation of HDAC Degraders with CRBN E3 Ligase Ligands.Molecules (Basel, Switzerland) · 2021Article
- Small Molecule Potentiation of Gram-Positive Selective Antibiotics againstACS infectious diseases · 2019Article
- Identification of Anti-Mycobacterial Biofilm Agents Based on the 2-Aminoimidazole Scaffold.ChemMedChem · 2019Article
- Using 2-aminobenzimidazole derivatives to inhibitMedChemComm · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Biofilm formation is one of the many mechanisms bacteria utilize to survive antibiotic treatment. It has been demonstrated that when Mycobacterium tuberculosis exists in a biofilm in vitro, it expresses phenotypic resistance to antimicrobial drugs. As the in vivo survival of M. tuberculosis following drug treatment is potentially linked to a biofilm-like expression of drug tolerance, it is hypothesized that biofilm dispersion should increase antibiotic susceptibility and reduce the duration of the current antibiotic treatment regimen. Previously, we have identified a 2-aminoimidazole (2-AI) compound capable of dispersing and inhibiting M. tuberculosis and M. smegmatis biofilms in vitro. Additionally, this compound potentiated the activity of carbenicillin against M. tuberculosis and, to a lesser degree, M. smegmatis. Here, we describe a SAR study on this compound evaluating each derivative for biofilm dispersion and β-lactam potentiation capabilities against M. smegmatis. This study identified a compound that improved upon the biofilm dispersion capabilities of the lead compound. Interestingly, a different compound was identified with an increased ability to potentiate a subset of β-lactam antibiotics. These compounds indicate that biofilm dispersion and potentiation capabilities may not be associated.
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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 OpenQuestion graph.