Design and synthesis of 1,2,4-oxadiazole-functionalized funtumine derivatives as potent anticancer agents
A series of innovative 1,2,4-oxadiazole-functionalized funtumine derivatives were designed, synthesized, and assessed for their antiproliferative effects on HCT116, HeLa, and HepG2 human cancer cell lines to discover new natural product-derived anticancer agents. The majority of these compounds demonstrated favorable anticancer efficacy, with compound 4m exhibiting better activity against HepG2 cells (IC 50 = 3.15 μ M) while maintaining low cytotoxicity towards normal human cells. Mechanistic investigations indicated that 4m triggered apoptosis in a dose-dependent manner and modified the transcriptomic profile of HepG2 cells, affecting crucial pathways such as chemical carcinogenesis-DNA adducts, steroid hormone biosynthesis, and cytochrome P450-mediated xenobiotic metabolism. Protein-protein interaction network analysis identified cytochrome P450 1A2 (CYP1A2) and UDP glucuronosyltransferase family 2 member B11 (UGT2B11) as potential targets, which were corroborated by molecular docking studies revealing strong binding interactions with 4 m. Density functional theory calculations revealed the electronic properties and reactivity of 4m, highlighting its potential for targeted engagement. These results highlight 4m as a promising, low-toxicity anticancer candidate worthy of further development.
Authors
- Long Zhang (ORCID: https://orcid.org/0000-0002-0483-952X)
- Juan Zou (ORCID: https://orcid.org/0000-0001-7524-4489)
- Yafang Chen (ORCID: https://orcid.org/0000-0003-3432-4508)
- Xiang Yu (ORCID: https://orcid.org/0000-0003-0685-0420)
- Kang He
- Mingjiang Lu (ORCID: https://orcid.org/0009-0005-2845-6573)
- Wenyu Li
Institutions
- Guiyang College of Traditional Chinese Medicine (CN)
- Guizhou University (CN)
Publication Details
- Journal
- Arabian Journal of Chemistry
- Published
- 2026-08-24
- DOI
- https://doi.org/10.25259/ajc_1399_2025
- Primary Topic
- Cancer therapeutics and mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00