ArticleBMC microbiology2026
Mechanistic insights into phthalylsulfacetamide-induced restoration of meropenem bactericidal activity in NDM-1-positive Escherichia coli.
Article in BMC 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
7 authors.
Funding
Abstract
The emergence and global spread of New Delhi metallo-β-lactamase-1 (NDM-1) pose a severe threat to the efficacy of carbapenems, which are considered the last line of defense against infections caused by multidrug-resistant gram-negative bacteria. In this study, through virtual screening and enzyme activity inhibition assays, phthalylsulfacetamide (PSA) was identified as a compound exhibiting inhibitory activity against NDM-1. PSA dose-dependently inhibited NDM-1, with a 50% inhibitory concentration (IC50) of 15.4 ± 0.3 µM and an inhibition rate (IR%) of 89.2%. In vitro antibacterial activity assays, confirmed that PSA effectively restored the antibacterial activity of meropenem (MEM) against NDM-1-positive Escherichia. coli (E. coli), reducing the minimum inhibitory concentration (MIC) of MEM by 32-fold and demonstrating rapid bactericidal effects within 3 h. The combination of PSA and MEM had a significant synergistic effect with a fractional inhibitory concentration index (FICI) of 0.156. In vivo, the combination therapy significantly reduced the bacterial load, decreased inflammatory cytokine levels, alleviated histopathological damage and increased survival rates in a murine systemic infection model. Molecular dynamics simulation and site-directed mutagenesis revealed that PSA stably binds to the active hydrolysis center of NDM-1, interacts with Zn2+, and strongly interacts with the key amino acid residues Val73 and His122. Furthermore, the observed rapid bactericidal activity suggests that PSA’s mechanism of action may extend beyond NDM-1 inhibition. Molecular docking analysis indicates that PSA may potentially interact with LpxC, a key enzyme involved in lipopolysaccharide synthesis; however, this observation remains preliminary and requires further experimental validation. These results highlight PSA as a promising therapeutic agent against NDM-1-mediated carbapenem resistance.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.