Benitrobenrazide (Hexokinase 2 inhibitor 1) inhibits glycolysis by directly targeting HK2. Benitrobenrazide can induce apoptosis and promote the production of reactive oxygen species to inhibit cancer cell proliferation. Benitrobenrazide can be used in research related to pancreatic cancer and colorectal cancer[1-4].
In vitro, HepG2 and HUH7 human liver cancer cells were treated with Benitrobenrazide (15μM or 57.1μM) for 72 hours. Benitrobenrazide caused DNA damage, increased reactive oxygen species (ROS) production, and disrupted cell cycle progression. Its inhibitory effect may be related to HK2 inhibition and compound aggregation effects[1]. The Hu1545 human hepatocyte cell line was co-treated with Benitrobenrazide (10μM or 30μM) and 400μM palmitate for 8 hours. Benitrobenrazide significantly attenuated palmitate-induced lipid droplet accumulation (steatosis)[2].
In vivo, Benitrobenrazide (200mg/kg) was administered orally once daily for 21 days to BALB/c nude mice bearing MDA-MB-231 tumor xenografts. Benitrobenrazide significantly inhibited tumor growth and did not cause obvious toxic reactions[3].
References:
[1] Juszczak K, Kubicka A, Kitel R, et al. Hexokinase 2 Inhibition and Biological Effects of BNBZ and Its Derivatives: The Influence of the Number and Arrangement of Hydroxyl Groups. Int J Mol Sci. 2022 Feb 27;23(5):2616.
[2] Daniel PV, Puri G, Luo Y, et al. Silencing of S100A11 attenuates murine metabolic dysfunction-associated steatohepatitis. NPJ Gut Liver. 2025;2(1):32.
[3] Zheng M, Wu C, Yang K, et al. Novel selective hexokinase 2 inhibitor Benitrobenrazide blocks cancer cells growth by targeting glycolysis. Pharmacol Res. 2021 Feb;164:105367.
[4] Al-Jabiri MH, Anshasi MA, Ma J, et al. Shapes of Benzyl Benzoate: A Rotational Spectroscopic and Computational Study. J Phys Chem A. 2026 Mar 19;130(11):2443-2450.
Benitrobenrazide (Hexokinase 2 inhibitor 1)通过直接靶向HK2来抑制糖酵解。Benitrobenrazide可诱导细胞凋亡和促进活性氧产生以抑制癌细胞增殖。Benitrobenrazide可用于胰腺癌和结直肠癌的相关研究[1-4]。
在体外，Benitrobenrazide（15μM或57.1μM）处理HepG2和HUH7人肝癌细胞72小时。Benitrobenrazide可导致DNA损伤、增加活性氧（ROS）产生并扰乱细胞周期进程，其抑制作用可能与抑制HK2及化合物聚集效应相关[1]。Benitrobenrazide（10μM或30μM）与400μM棕榈酸共处理Hu1545人肝癌细胞系8小时。Benitrobenrazide可显著减轻棕榈酸诱导的脂质积累（脂肪变性）[2]。
在体内，Benitrobenrazide（200mg/kg）每日一次口服给药于携带MDA-MB-231肿瘤异种移植的BALB/c裸鼠21天。Benitrobenrazide显著抑制了肿瘤生长，且未引起明显的毒性反应[3]。