ArticleFundamental & clinical pharmacology2011
Activity screening and structure-activity relationship of the hit compounds targeting APN/CD13.
Article in Fundamental & clinical pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed, 11 citations in OpenAlex.
- CD13 downregulation mediated by ubenimex inhibits autophagy to overcome 5-FU resistance by disturbing the EMP3/FAK/NF-κB pathway in gastric cancer cells.Translational cancer research · 2022Article
- Ubenimex Reverses MDR in Gastric Cancer Cells by Activating Caspase-3-Mediated Apoptosis and Suppressing the Expression of Membrane Transport Proteins.BioMed research international · 2019Article
- CD13 Inhibition Enhances Cytotoxic Effect of Chemotherapy Agents.Frontiers in pharmacology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aminopeptidase N (APN) plays an important role in tumor progression, which participates in the progress such as proliferation, attachment, angiogenesis, and tumor invasion. All of this makes APN as a good chemical therapeutic anti-tumor target. In this study, a series of chemically synthesized APN inhibitors were tested for the anti-tumor activities, and three most effective compounds were chosen according to the MTT assay. Then, the enzyme inhibitory, anti-tumor, specificity, angiogenesis, and invasion were determined to evaluate the activity of these three compounds. All compounds can markedly inhibit the enzyme activity of APN, angiogenesis of endothelial cells, and the invasion of ES-2 cells. And it had little effect on the viability of K562 which express low level of APN. This data indicated that the tested compounds were APN hit compounds. We also did kinetic assay to determine the inhibition constant and constructed a three-dimensional quantitative structure-activity relationship model to analyze the structure-activity relationship to direct the further design of novel APN inhibitors as anti-tumor agents. These data demonstrate that the tested compounds can be developed as novel candidates of anticancer agent.
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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.