Soliman Sara M, Abdel-Rahman Adel A-H, Nossier Eman S, Hussein Modather F, Sabry Amr, El-Hema Hagar S
Chemistry Department, Faculty of Science, Menoufia University, Shebin El-Kom, 32511, Egypt.
Department of Pharmaceutical Medicinal Chemistry and Drug Design, Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, 11754, Egypt.
Sci Rep. 2025 Jul 31;15(1):27992. doi: 10.1038/s41598-025-12140-1.
Quinazolinone derivatives have been broadly studied as anti-cancer drug candidates due to their potential to inhibit key signaling pathways involved in tumor progression. In the current study, new 2-[(4-substituted-5-methylfuran-3-yl)thio]-3-phenylquinazolin-4(3H)-one derivatives (2-10) were designed and assessed for anti-cancer activity. Cytotoxicity of the compounds was tested against normal WI-38 cells and cancer cell lines HepG-2 (liver), MCF-7 (breast), and HCT-116 (colorectal). In addition, their inhibitory effects on EGFR and VEGFR-2, key targets for tumor growth and angiogenesis, were assessed. Compounds 6b and 10 showed significant cytotoxic activity, with 6b (IC₅₀ = 0.19 ± 0.03 μM) being the most effective EGFR inhibitor, over 10 (IC₅₀ = 0.51 ± 0.04 μM) and as potent as erlotinib (IC₅₀ = 0.23 ± 0.02 μM). Flow cytometry revealed that 6b induced apoptosis in 35.29% of MCF-7 cells and G₂/M phase cell cycle arrest, much better than that of untreated cells (6.81%). In silico ADMET prediction and molecular docking confirmed high EGFR binding affinity and favorable pharmacokinetic properties. Overall, compound 6b showed promising anti-cancer activity via EGFR inhibition, apoptosis, and cell cycle arrest and is a good lead for further development as an EGFR-targeted agent.
喹唑啉酮衍生物因其具有抑制肿瘤进展中关键信号通路的潜力,已被广泛研究作为抗癌药物候选物。在本研究中,设计并评估了新型2-[(4-取代-5-甲基呋喃-3-基)硫代]-3-苯基喹唑啉-4(3H)-酮衍生物(2-10)的抗癌活性。测试了这些化合物对正常WI-38细胞以及癌细胞系HepG-2(肝癌)、MCF-7(乳腺癌)和HCT-116(结直肠癌)的细胞毒性。此外,还评估了它们对肿瘤生长和血管生成的关键靶点EGFR和VEGFR-2的抑制作用。化合物6b和10表现出显著的细胞毒性活性,其中6b(IC₅₀ = 0.19 ± 0.03 μM)是最有效的EGFR抑制剂,优于10(IC₅₀ = 0.51 ± 0.04 μM),且与厄洛替尼(IC₅₀ = 0.23 ± 0.02 μM)效力相当。流式细胞术显示,6b诱导35.29%的MCF-7细胞凋亡并导致G₂/M期细胞周期阻滞,远优于未处理细胞(6.81%)。计算机辅助ADMET预测和分子对接证实了其对EGFR的高结合亲和力和良好的药代动力学性质。总体而言,化合物6b通过抑制EGFR、诱导凋亡和细胞周期阻滞显示出有前景的抗癌活性,是作为EGFR靶向药物进一步开发的良好先导化合物。