ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Truncated pardaxin derivative D18.13 induces selective breast cancer apoptosis via predicted targeting of MAPK8.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. 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.
- m6A modification and its clinical applications in gynaecological cancer.Apoptosis : an international journal on programmed cell death · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cancer remains a global health issue, whereby the adverse effects of conventional drugs urge the discovery of modalities for replacement, such as anticancer peptides with higher selectivity against cancer cells. Bioactive peptide pardaxin has anticancer effects, but its concurrent haemolytic effects possess limitations. This study aimed to discover shortened pardaxin derivatives using in silico analyses, followed by the study of their cytotoxic effects on breast cancer and normal cells. Pardaxin was truncated to 27 or 18 residues, and then single residue replacement was induced using AntiCP 2.0. The generated sequences were further predicted to identify potential derivatives with anticancer, non-toxic, low haemolysis, conserved alpha-helices structure, and stronger docking affinity towards FAS death receptor. Synthesised potential derivatives were validated using MTT assay on breast cancer and normal cells, haemolytic assay, FITC-Annexin V binding, and lactate dehydrogenase (LDH) assay for apoptosis and necrosis investigation. Potential targets in the MAPK/JNK pathway to induce apoptosis were determined using HDOCK docking screening and validated via molecular dynamics (MD) simulation and MM/GBSA calculation. Among the synthesised peptides, D18.13 demonstrated the highest potential due to its breast cancer-killing ability, lowest toxicity on normal cells, and with alleviated haemolytic effects. The D18.13-treated breast cancer cells showed remarkable apoptotic effects. The D18.13 potentially targets MAPK8 to induce MAPK/JNK-mediated apoptosis, with MM/GBSA revealing a free binding energy (-67.40 kcal/mol) similar to that of parental pardaxin (-68.88 kcal/mol). The in silico method enhanced anticancer peptide discovery such as D18.13, which has the potential to treat breast cancer with minimal side effects.
Indexed as
Identifiers
41065835What 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.