Evidence map›Paper›PMID 38939155›Full record

ArticleChemical science2024

Development of an inhibitor of the mutagenic SOS response that suppresses the evolution of quinolone antibiotic resistance.

Jacob D Bradbury, Thomas Hodgkinson, Adam M Thomas, Omprakash Tanwar, Gabriele La Monica, Vanessa V Rogga, Luke J Mackay, Emilia K Taylor, Kiera Gilbert, Yihua Zhu and 7 more

Abstract read
In one paragraph

Article in Chemical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Base excision repair inFrontiers in microbiology · 2026
    Review
  7. Review
  8. Article
  9. Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Jacob D BradburyDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.ORCID https://orcid.org/0000-0003-2016-833X
Thomas HodgkinsonDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.
Adam M ThomasDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.ORCID https://orcid.org/0000-0002-8780-8795
Omprakash TanwarDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.
Gabriele La MonicaDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.ORCID https://orcid.org/0000-0001-6510-1943
Vanessa V RoggaDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.
Luke J MackayDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.
Emilia K TaylorDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.
Kiera GilbertDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.
Yihua ZhuFred Hutchinson Cancer Center Seattle WA 98109-1024 USA.ORCID https://orcid.org/0000-0002-6112-4272
Amber Y SeftonDepartment of Infectious Disease, Faculty of Medicine, Imperial College London W2 1NY UK.
Andrew M EdwardsDepartment of Infectious Disease, Faculty of Medicine, Imperial College London W2 1NY UK.ORCID https://orcid.org/0000-0002-7173-7355
Charlotte J Gray-HammertonIneos Oxford Institute for Antimicrobial Research, Sir William Dunn School of Pathology, University of Oxford OX1 3RE UK.ORCID https://orcid.org/0009-0006-2183-6116
Gerald R SmithFred Hutchinson Cancer Center Seattle WA 98109-1024 USA.
Paul M RobertsChemistry Research Laboratory, Department of Chemistry, University of Oxford OX1 3TA UK.
Timothy R WalshIneos Oxford Institute for Antimicrobial Research, Sir William Dunn School of Pathology, University of Oxford OX1 3RE UK.
Thomas Lanyon-HoggDepartment of Pharmacology, University of Oxford OX1 3QT UK thomas.lanyon-hogg@pharm.ox.ac.uk.ORCID https://orcid.org/0000-0002-7092-8096

Funding

Molecular analysis of genetic recombination and DNA break repairR35GM118120 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI SMITH, GERALD R · 2016 to 2025
$9.3M
NIGMS NIH HHS R35 GM118120
6 · The paper itself

Abstract

Antimicrobial resistance (AMR) is a growing threat to health globally, with the potential to render numerous medical procedures so dangerous as to be impractical. There is therefore an urgent need for new molecules that function through novel mechanisms of action to combat AMR. The bacterial DNA-repair and SOS-response pathways promote survival of pathogens in infection settings and also activate hypermutation and resistance mechanisms, making these pathways attractive targets for new therapeutics. Small molecules, such as IMP-1700, potentiate DNA damage and inhibit the SOS response in methicillin-resistant

Identifiers

PMID38939155
PMCPMC11206376

What OpenQuestion holds

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Registered trials

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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.