ArticleRSC medicinal chemistry2023
Design, synthesis, and biological evaluation of new arjunolic acid derivatives as anticancer agents.
Article in RSC medicinal chemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- A comprehensive review of the medicinal properties ofRSC advances · 2026Review
- Arjunolic Acid From Terminalia ivorensis A. Chev (Combretaceae) Possesses Anti-Breast Cancer Effects In Vitro and In Vivo.Cancer reports (Hoboken, N.J.) · 2025Article
- Selected Pentacyclic Triterpenoids and Their Derivatives as Biologically Active Compounds.Molecules (Basel, Switzerland) · 2025Review
- Amide Derivative of Arjunolic Acid TA-1,4-BiP Enhances ROSmediated Apoptosis in Colorectal Cancer Cells.Current medicinal chemistry · 2025Article
- Anticancer of genusExploration of targeted anti-tumor therapy · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arjunolic acid (AA) is a pentacyclic triterpenoid with promising anticancer properties. A series of novel AA derivatives containing a pentameric A-ring with an enal moiety, combined with additional modifications at C-28, were designed and prepared. The biological activity on the viability of human cancer and non-tumor cell lines was evaluated in order to identify the most promising derivatives. Additionally, a preliminary study of the structure-activity relationship was carried out. The most active derivative, derivative 26, also showed the best selectivity between malignant cells and non-malignant fibroblasts. For compound 26, the anticancer molecular mechanism of action in PANC-1 cells was further studied and the results showed that this derivative induced a cell-cycle arrest at G0/G1 phase and significantly inhibited the wound closure rate of PANC-1 cancer cells in a concentration-dependent manner. Additionally, compound 26 synergistically increased the cytotoxicity of Gemcitabine, especially at a concentration of 0.24 μM. Moreover, a preliminary pharmacological study indicated that at lower doses this compound did not demonstrate toxicity
Identifiers
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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.