ArticleArchives of microbiology2026
Evaluation of the antimicrobial and NorA and MepA efflux pump inhibitory activity of a hydrazone derivative of hydralazine against Staphylococcus aureus.
Article in Archives of microbiology, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial resistance represents one of the major challenges in contemporary public health, compromising the effectiveness of conventional antibiotics. In this context, research focused on the discovery of new compounds and resistance modulators has gained increasing attention. The present study aimed to evaluate the antimicrobial activity and the antibiotic-modulating potential of a hydrazone derivative of hydralazine against Staphylococcus aureus strains harboring efflux pumps. The compound (E)-2-((2-(phthalazin-1-yl)hydrazineylidene)methyl)phenol (HDZH2OH) was synthesized from hydralazine and isoniazid and evaluated using the Minimum Inhibitory Concentration (MIC) assay by the broth microdilution method, as well as resistance modulation assays in association with specific antibiotics and ethidium bromide. The cell viability assay showed that HDZH2OH reduced macrophage viability in a concentration-dependent manner, with viability decreasing from 74.8 ± 3.0% at 3.25 µM to 27.25 ± 1.25% at 25 µM. MIC values ≥ 1024 µg/mL (3.88 mM) against both tested strains, indicating the absence of intrinsic antibacterial activity. However, in the S. aureus 1199B strain, a reduction in the MIC of norfloxacin from 256 µg/mL to 101.59 µg/mL (0.802 mM to 0.334 mM) was observed, suggesting a partial potentiating effect. In the K2068 strain, no potentiation of ciprofloxacin was observed; however, a significant reduction in the MIC of ethidium bromide from 8 µg/mL to 2 µg/mL (0.020 mM to 0.005 mM) was detected (p < 0.001). Molecular docking indicated that HDZH2OH strongly interacts with S. aureus efflux pumps, showing high affinity and selective binding. It overlaps with substrate sites in MepA and NorA, suggesting competitive inhibition. Its interactions, including hydrogen bonds, enhance stability, highlighting its potential to inhibit efflux activity and restore antimicrobial effectiveness. HDZH2OH shows favorable drug likeness consistent with Lipinski and Veber rules. It is mostly neutral at physiological pH (pKa 4.05), supporting good permeability and oral absorption. CNS MPO score (4.47) suggests potential CNS activity and BBB penetration. It has high plasma protein binding and moderate toxicity risk, with possible CYP inhibition and hepatotoxicity concerns. These findings indicate that the compound acts as a selective efflux pump modulator, with greater affinity for the MepA system, highlighting its potential as a therapeutic adjuvant in combating bacterial resistance.
Indexed as
Identifiers
What 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.