β-羰基化合物的抗癌机制

IF 3.2 4区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Chemical Biology & Drug Design Pub Date : 2024-04-23 DOI:10.1111/cbdd.14521
Shivam Mishra, Aditi Gupta, Shweta Jain, Ankur Vaidya
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引用次数: 0

摘要

在药物化学中,β-咔啉核对治疗多种疾病,尤其是癌症具有重要的治疗价值。β-咔啉具有强效和广泛的活性,因此成为治疗癌症的重要药理支架。据报道,许多衍生物,如四氢 β-咔啉、金属络合 β-咔啉、单、双和三取代 β-咔啉都具有动态抗癌活性。这些不同取代的 β-咔啉衍生物显示出不同的作用机制,在抗癌药物的发现和开发中发挥着重要作用。这篇综述介绍了 β-咔啉的最新化学成分,包括通过不同靶点作用于癌细胞的合成物和天然物。此外,还总结了通过将 β-羰基化合物与其他机制相结合而设计的多靶点分子治疗肿瘤的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Anticancer mechanisms of β-carbolines

β-Carboline nucleus is therapeutically valuable in medicinal chemistry for the treatment of varied number of diseases, most importantly cancer. The potent and wide-ranging activity of β-carboline has established them as imperative pharmacological scaffolds especially in the cancer treatment. Numerous derivatives such as Tetrahydro β-carbolines, metal complexed β-carbolines, mono, di and tri substituted β-carbolines have been reported to possess dynamic anticancer activity. These different substituted β-carboline derivatives had shown different mechanism of action and plays important role in anticancer drug discovery and development. The review is an update of the chemistry of β-carbolines, both synthetic and natural origin acting through various targets against cancerous cells. In addition to this, studies of multitarget molecules designed by coupling β-carbolines along with other mechanisms for treatment of neoplasm are also summarized.

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来源期刊
Chemical Biology & Drug Design
Chemical Biology & Drug Design 医学-生化与分子生物学
CiteScore
5.10
自引率
3.30%
发文量
164
审稿时长
4.4 months
期刊介绍: Chemical Biology & Drug Design is a peer-reviewed scientific journal that is dedicated to the advancement of innovative science, technology and medicine with a focus on the multidisciplinary fields of chemical biology and drug design. It is the aim of Chemical Biology & Drug Design to capture significant research and drug discovery that highlights new concepts, insight and new findings within the scope of chemical biology and drug design.
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