Evidence map›Paper›PMID 40172295›Full record

ArticleBiomolecules & biomedicine2025

Unveiling the synergistic power of 3-hydrazinoquinoxaline-2-thiol and vancomycin against MRSA: An

Ohood S Alharbi, Mohanned Talal Alharbi, Mazen A Ismail, Ahmad M Sait, Mohammed Mufrrih, Wafaa Alhazmi, Bandar Hasan Saleh, Manal A Zubair, Noha A Juma, Noof R Helmi and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules & biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

18 authors.

Ohood S AlharbiDepartment of Microbiology and Parasitology, Faculty of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia.
Mohanned Talal AlharbiDepartment of Basic Medical Sciences, College of Medicine, University of Jeddah, Jeddah, Saudi Arabia.
Mazen A IsmailDepartment of Medical Education, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Ahmad M SaitDepartment of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia; Regenerative Medicine Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Mohammed MufrrihDepartment of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia; Special Infectious Agents Unit BSL-3, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Wafaa AlhazmiDepartment of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.
Bandar Hasan SalehDepartment of Clinical Microbiology and Immunology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Clinical Microbiology Laboratory, King Abdulaziz University Hospital, Jeddah, Saudi Arabia.
Manal A ZubairDepartment of Clinical Microbiology and Immunology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Noha A JumaDepartment of Clinical Microbiology and Immunology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Noof R HelmiDepartment of Clinical Microbiology and Immunology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Hatoon A NiyaziDepartment of Clinical Microbiology and Immunology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Hanouf A NiyaziDepartment of Clinical Microbiology and Immunology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Hussam DaghistaniRegenerative Medicine Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University Jeddah, Saudi Arabia.
Taghreed ShamraniDepartment of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University Jeddah, Saudi Arabia; Food, Nutrition and Lifestyle Unit, King Fahd Medical Research Centre, King Abdulaziz University, Jeddah, Saudi Arabia.
Waiel S HalabiDepartment of Optometry, Faculty of Applied Medical Sciences, University of Jeddah, Saudi Arabia.
Abdalbagi AlfadilDepartment of Clinical Microbiology and Immunology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; Centre of Research Excellence for Drug Research and Pharmaceutical Industries, King Abdulaziz University, Jeddah, Saudi Arabia.
Hisham N AltaybDepartment of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia.
Karem IbrahemDepartment of Clinical Microbiology and Immunology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Clinical Microbiology Laboratory, King Abdulaziz University Hospital, Jeddah, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methicillin-resistant Staphylococcus aureus (MRSA) is a major pathogen causing infections ranging from skin disorders to severe conditions like infective endocarditis. Its evolving resistance, including resistance to β-lactams and last-resort antibiotics, such as vancomycin, daptomycin, and linezolid, necessitates alternative therapies. This study investigates the synergistic efficacy of vancomycin and 3-hydrazinoquinoxaline-2-thiol (3HL) against 23 clinical MRSA isolates. Susceptibility testing was performed using broth microdilution and checkerboard assays, while in silico analyses assessed interactions between vancomycin and 3HL. Vancomycin exhibited minimum inhibitory concentrations (MICs) ranging from 0.25 to 1 µg/mL, whereas 3HL showed higher MICs of 16-32 µg/mL. Synergistic interactions were confirmed via checkerboard assays, with fractional inhibitory concentration index (FICI) values between 0.236 and 0.5, indicating enhanced vancomycin efficacy. Notably, vancomycin MICs decreased significantly when combined with 3HL. In silico docking revealed interactions with penicillin-binding protein 2a (PBP2a), suggesting promising therapeutic potential. Vancomycin exhibited superior docking scores (-8.9 kcal/mol) and stabilizing hydrogen bonds, effectively targeting key protein grooves. Both compounds demonstrated potential for overcoming PBP2a's structural occlusions, suggesting their role in combating β-lactam-resistant strains through targeted protein inhibition and structural stabilization.

Indexed as

Anti-Bacterial AgentsMethicillin-Resistant Staphylococcus aureusQuinoxalinesVancomycinComputer SimulationDrug SynergismHumansMicrobial Sensitivity TestsMolecular Docking SimulationPenicillin-Binding ProteinsAnti-Bacterial AgentsPenicillin-Binding ProteinsQuinoxalinesVancomycin

Identifiers

PMID40172295
PMCPMC12451975

What OpenQuestion holds

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LicenceCC BY
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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.