ArticleFrontiers in pharmacology2026
Antihistamine drug terfenadine suppressed the cycle progression of gastric cancer cells by targeting PI3K/AKT/mTOR signaling.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, highlighting the urgent need for effective and accessible therapies. Drug repurposing offers a cost-effective strategy to identify novel candidates from approved drugs. Terfenadine, a classical antihistamine with an established safety profile, has demonstrated antitumor activity in various malignancies; however, its efficacy and mechanism in GC have not been systematically explored. This study investigates the therapeutic potential of terfenadine in GC and elucidates its underlying molecular mechanisms. Methods: Cytotoxicity was assessed in AGS, HGC27, and MKN45 GC cell lines. Effects on proliferation, colony formation, migration, apoptosis, cell cycle distribution, and mitochondrial membrane potential were examined. Mechanisms were explored through bioinformatics analysis, molecular docking, and Western blotting. Synergy with 5-fluorouracil (5-Fu) was evaluated using checkerboard assays and analyzed by SynergyFinder. Results: Terfenadine exhibited potent cytotoxicity against GC cells, with IC Conclusion: This study demonstrates that terfenadine exerts multifaceted antitumor effects in GC through modulation of the PI3K/AKT/mTOR pathway, exhibits synergistic activity with 5-Fu, and shows
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