Novel Anticancer Drug Development and Toxicity Reduction Strategies

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: 25 October 2025 | Viewed by 138

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Guest Editor
Department of Cytobiology, Pharmaceutical Faculty, Jagiellonian University Medical College, Medyczna 9, 30-688 Krakow, Poland
Interests: anticancer activity; plant phenolics; leukemia; apoptosis; cell cycle; DNA repair; flow cytometry
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Special Issue Information

Dear Colleagues,

Oncologists have emphasized that the possibilities of conventional cancer therapy in using cytotoxic drugs are reaching the limits of effectiveness. Therefore, intensive research is underway on new therapeutic strategies that can increase the effectiveness of treatment and at the same time reduce side effects. One means of achieving this is to use innovative synthetic methodologies that allow for the modification of bioactive molecules and the creation of new compounds with strong anticancer activity. Molecular docking is also used to find the best orientation of the ligand in the binding site of the molecule and form a stable complex, which allows the acceleration of the identification of molecules with increased specificity towards molecular targets in anticancer therapy. A combination treatment strategy is also being developed, using drugs already in use and natural bioactive compounds to achieve synergy of action in cancer cells. Furthermore, attempts are being made to use methods that allow the drug to reach the target more precisely. An example of this is the use of tumour-targeted nanocarriers, which enable increased intracellular drug uptake and accumulation in the tumour. Another interesting application is the use of hydrogels sensitive to specific properties of the microenvironment that promote tumour growth, which can be used to increase the effectiveness of anticancer therapy. With this, the aim of this Special Issue is to publish original or review articles on the latest strategies used to improve the selective action of drugs on cancer cells while limiting their toxicity to healthy tissues.

Dr. Monika Papież
Guest Editor

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Keywords

  • cancer
  • targeted therapy
  • anticancer drug
  • structure-based computational technique
  • combination therapy
  • nanocarriers
  • hydrogels

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Published Papers (1 paper)

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Research

29 pages, 9652 KiB  
Article
Curcumin Derivative CU4c Exhibits HDAC-Inhibitory and Anticancer Activities Against Human Lung Cancer Cells In Vitro and in Mouse Xenograft Models
by Narissara Namwan, Gulsiri Senawong, Chanokbhorn Phaosiri, Pakit Kumboonma, La-or Somsakeesit, Pitchakorn Sangchang and Thanaset Senawong
Pharmaceuticals 2025, 18(7), 960; https://doi.org/10.3390/ph18070960 (registering DOI) - 26 Jun 2025
Abstract
Background/Objectives: Drug resistance and severe side effects caused by gemcitabine (Gem) and cisplatin (CDDP) are common. This study aimed to investigate the combined effects of CU4c and Gem or CDDP on lung cancer cells in vitro and in nude mouse xenograft models. [...] Read more.
Background/Objectives: Drug resistance and severe side effects caused by gemcitabine (Gem) and cisplatin (CDDP) are common. This study aimed to investigate the combined effects of CU4c and Gem or CDDP on lung cancer cells in vitro and in nude mouse xenograft models. Methods: Antiproliferative activity and drug interaction were evaluated using MTT and Chou–Talalay methods, respectively. Apoptosis induction and cell cycle arrest were analyzed by flow cytometry. The expression levels of proteins were evaluated by Western blot analysis. The HDAC-inhibitory activity of CU4c was confirmed in vitro, in silico, and in A549 cells. Results: CU4c inhibited the proliferation of A549 cells in a dose- and time-dependent manner but had little effect on the growth of noncancerous Vero cells. CU4c synergistically enhanced the antiproliferative activities of CDDP (at 24 h) and Gem (at 48 and 72 h) against A549 cells. Combined CU4c and CDDP notably inhibited A549 proliferation by triggering cell cycle arrest at S and G2/M phases at 24 h with elevated levels of p21 and p53 proteins. Combined CU4c and Gem induced cell cycle arrest at both the S and G2/M phases at 48 h via upregulating the expression of the p21 protein. CU4c enhanced the apoptotic effects of CDDP and Gem by increasing the Bax/Bcl-2 ratio, pERK1/2, and Ac-H3 levels. Combined CU4c and Gem significantly reduced tumor growth while minimizing visceral organ damage in animal study. Conclusions: These results suggest that CU4c enhances the anticancer activity of CDDP and Gem and reduces the toxicity of Gem in animal studies. Full article
(This article belongs to the Special Issue Novel Anticancer Drug Development and Toxicity Reduction Strategies)
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