ArticleArchiv der Pharmazie2025
Evernic Acid: A Low-Toxic and Selective Alternative to Chemotherapeutic Agents in the Treatment of Ovarian Cancer.
Article in Archiv der Pharmazie, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Inhibition of thioredoxin reductase 1 by evernic and vulpinic acids: a promising anticancer strategy on A549 cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
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
Evernic acid (EA) has emerged as a potential therapeutic agent with its low toxicity and anticancer properties. In this study, the anticancer effect of EA on ovarian cancer cell lines and normal ovarian surface epithelial cells (OSE) was evaluated. The antiproliferative effect of EA was evaluated by xCELLigence Real-Time Cell analysis, colony formation assay, and acridine orange and DAPI staining methods. Genotoxicity analysis was performed by comet assay. The effect of EA on cell migration was analyzed by wound healing assay. The potential of EA to induce apoptosis was also determined by evaluating the changes in gene and protein expression levels by qRT-PCR and Western blot analysis, respectively. EA was found to be a promising potential therapeutic agent for ovarian cancer without showing significant cytotoxic effect on normal cells. Furthermore, EA decreased the ability of ovarian cancer cells for migration, increased the rate of apoptosis by inhibiting BIRC5 and activating CASP3, triggered cell cycle arrest in the G2/M phase, and caused a decrease in mitochondrial membrane potential and genotoxic effects. The results have shown that EA could be an effective candidate molecule for ovarian cancer treatment.
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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.