ArticleFrontiers in pharmacology2025
SB218078 inhibits angiogenesis and epithelial-mesenchymal transition in breast cancer.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Beyond conventional therapies: the evolution of targeted agents and immunotherapies in triple-negative breast cancer.Acta pharmacologica Sinica · 2026Review
- Sphingomonas paucimobilis-Driven Epithelial-Endothelial Transition in Adenomyosis Pathogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
7 authors.
Funding
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Abstract
Purpose: Small-molecule inhibitors of vascular endothelial growth factor receptor 2 (VEGFR2) face clinical limitations due to adverse effects. This study aimed to evaluate the novel compound SB218078 as a dual-targeting agent against both tumor angiogenesis and epithelial-mesenchymal transition (EMT) in breast cancer, while exploring its mechanisms of action. Methods: The anti-angiogenic effects of SB218078 were investigated using Results: SB218078 effectively suppressed angiogenesis by inhibiting endothelial cell functions and disrupting developmental vascular networks in zebrafish. It also impeded breast cancer cell aggressiveness and tumor growth Conclusion: SB218078 emerges as a promising dual-action therapeutic candidate for breast cancer, simultaneously blocking angiogenesis and EMT through the Chk1-ZEB1 axis. Its specificity for ZEB1, distinct from other EMT regulators, offers a novel strategy to overcome the limitations of traditional VEGFR2 inhibitors, warranting further preclinical development.
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