20691-71-8Relevant articles and documents
Synthesis and characterization of 8-aminoquinolines, substituted by electron donating groups, as high-affinity copper chelators for the treatment of Alzheimer's disease
Huang, Ju,Nguyen, Michel,Liu, Yan,Robert, Anne,Meunier, Bernard
, p. 419 - 427 (2019)
The deregulation of copper homeostasis generates copper–amyloid aggregation and strongly participates in neuron damage in the brains of patients with Alzheimer's disease. Therefore, copper chelators able to regulate copper homeostasis should be considered
2 -aryl quinoxaline compound with affinity with Tau protein as well as preparation method and application thereof (by machine translation)
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Paragraph 0034; 0083; 0084, (2020/12/30)
The invention provides 2 -arylquinoxaline compounds with affinity with Tau protein, and the structure is as shown in a formula (I). The invention further provides a preparation method of the compound of the formula (I). The compound can be directly used a
Potent, Selective, and Cell Active Protein Arginine Methyltransferase 5 (PRMT5) Inhibitor Developed by Structure-Based Virtual Screening and Hit Optimization
Mao, Ruifeng,Shao, Jingwei,Zhu, Kongkai,Zhang, Yuanyuan,Ding, Hong,Zhang, Chenhua,Shi, Zhe,Jiang, Hualiang,Sun, Dequn,Duan, Wenhu,Luo, Cheng
, p. 6289 - 6304 (2017/08/02)
PRMT5 plays important roles in diverse cellular processes and is upregulated in several human malignancies. Besides, PRMT5 has been validated as an anticancer target in mantle cell lymphoma. In this study, we found a potent and selective PRMT5 inhibitor by performing structure-based virtual screening and hit optimization. The identified compound 17 (IC50 = 0.33 μM) exhibited a broad selectivity against a panel of other methyltransferases. The direct binding of 17 to PRMT5 was validated by surface plasmon resonance experiments, with a Kd of 0.987 μM. Kinetic experiments indicated that 17 was a SAM competitive inhibitor other than the substrate. In addition, 17 showed selective antiproliferative effects against MV4-11 cells, and further studies indicated that the mechanism of cellular antitumor activity was due to the inhibition of PRMT5 mediated SmD3 methylation. 17 may represent a promising lead compound to understand more about PRMT5 and potentially assist the development of treatments for leukemia indications.