Epirubicin is an orally active, specific inhibitor of DNA topoisomerase II with an IC50 of 12μM[1]. Epirubicin forms a complex with DNA, blocks the re-ligation of DNA double strands, causes DNA damage, and interferes with DNA, RNA, and protein synthesis, thereby exerting broad-spectrum antitumor activity[2]. Epirubicin is commonly used in research on solid tumors such as breast, liver, and gastric cancers, as well as malignant lymphomas[3].
In vitro, Epirubicin (0.5-100μM; 48h) dose-dependently suppressed U-87 glioma cell proliferation, reduced MMP-9 secretion, lowered VEGF release, and inhibited cell migration[4]. Treatment of HCT116 and SW620 colorectal cancer cells with Epirubicin (125nM; 48h) significantly upregulated TRAIL and enhanced TRAIL-induced apoptosis[5].
In vivo, Epirubicin (2.5mg/kg; every other day for 16 days; i.v.) reduced tumor volume and increased tumor cell apoptosis in 4T1 breast cancer-bearing BALB/c mice[6]. Epirubicin (7mg/kg; every 4 days ×3; i.v.) reduced tumor massin R-27 human breast carcinoma-bearing nude mice without increasing toxic death[7].
References:
[1] Cersosimo RJ, Hong WK. Epirubicin: a review of the pharmacology, clinical activity, and adverse effects of an adriamycin analogue. J Clin Oncol. 1986;4(3):425-439.
[2] Luiz MT, Dutra JAP, Di Filippo LD, et al. Epirubicin: Biological Properties, Analytical Methods, and Drug Delivery Nanosystems. Crit Rev Anal Chem. 2023;53(5):1080-1093.
[3] Robert J. Clinical pharmacokinetics of epirubicin. Clin Pharmacokinet. 1994;26(6):428-438.
[4] Wang XF, Zhao ZF, Chen MH, Yuan QH, Li YL, Jiang CL. Epirubicin inhibits growth and alters the malignant phenotype of the U87 glioma cell line. Mol Med Rep. 2015;12(4):5917-5923.
[5] Caldiran F, Berkel C, Yilmaz E, et al. Combination treatment of bortezomib and epirubicin increases the expression of TNFRSF10 A/B, and induces TRAIL-mediated cell death in colorectal cancer cells. Biochem Biophys Res Commun. 2023;675:33-40.
[6] Wu J, Xue X, Zhang B, et al. Enhanced antitumor activity and attenuated cardiotoxicity of Epirubicin combined with Paeonol against breast cancer. Tumour Biol. 2016;37(9):12301-12313.
[7] Asanuma F, Yamada Y, Kawamura E, et al. Antitumor activity of paclitaxel and epirubicin in human breast carcinoma, R-27. Folia Microbiol (Praha). 1998;43(5):473-474.
Epirubicin是一种具有口服活性的DNA topoisomerase II特异性抑制剂,IC50为12μM[1]。Epirubicin与DNA形成复合物,阻断DNA双链的重新连接,导致DNA损伤,并干扰DNA、RNA及蛋白质合成,从而发挥广谱抗肿瘤活性[2]。Epirubicin常用于乳腺癌、肝癌、胃癌等实体瘤及恶性淋巴瘤的研究[3]。
在体外,Epirubicin(0.5-100μM;48小时)可浓度依赖性地抑制U-87胶质瘤细胞增殖,减少MMP-9分泌,降低VEGF释放,并抑制细胞迁移[4]。Epirubicin(125nM;48小时)处理HCT116和SW620结直肠癌细胞后,显著上调TRAIL并增强TRAIL诱导的细胞凋亡[5]。
在体内,Epirubicin(2.5mg/kg;隔日一次,持续16天;静脉注射)可减少4T1乳腺癌荷瘤BALB/c小鼠的肿瘤体积并增加肿瘤细胞凋亡[6]。Epirubicin(7mg/kg;每4天一次,共3次;静脉注射)在R-27人乳腺癌荷瘤裸鼠中降低肿瘤质量,且未增加毒性死亡[7]。
















