15450-72-3Relevant articles and documents
Yamamoto et al.
, p. 3489,3493 (1978)
Selenophenol quinoline derivative as well as preparation method and application thereof
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Paragraph 0095; 0098-0101, (2020/12/30)
The invention discloses a selenophenol quinoline derivative as well as a preparation method and application thereof. The structure of the selenophenol quinoline derivative is shown as a formula I, a formula II or a formula III, wherein R1 is hydrogen, a C1-6 alkyl group, a C1-6 alkoxy group, a substituted ketone group, a phenyl group, a benzyl group, a substituted phenyl group or a substituted benzyl group; R1 is a monovalent metal cation; R2 is one or more of hydrogen, halogen, a C1-4 alkyl group, a C1-4 alkoxy group or a C1-4 haloalkyl group; R3 is a substituted five-membered heterocyclicring or a substituted six-membered heterocyclic ring; and a heteroatom is one or more of N, O, S or Se. The compound disclosed by the invention is novel in structure, simple in preparation process and relatively good in inhibition effect on various cancer cells, particularly the compounds 34, 44, 45, 98, 104, 115 and 116 have excellent inhibition effects on various cancer cells, the effects of the compounds are equivalent to those of a positive control DDP, and the compounds can be used to prepare anti-cancer drugs to be applied under 5 [mu]M or below, so that the prospect is wide.
Discovery of β-arrestin-biased β2-adrenoceptor agonists from 2-amino-2-phenylethanol derivatives
Woo, Anthony Yiu-Ho,Ge, Xin-yue,Pan, Li,Xing, Gang,Mo, Yong-mei,Xing, Rui-juan,Li, Xiao-ran,Zhang, Yu-yang,Wainer, Irving W.,Cheng, Mao-sheng,Xiao, Rui-ping
, p. 1095 - 1105 (2019/01/19)
β-Arrestins are a small family of proteins important for signal transduction at G protein-coupled receptors (GPCRs). β-Arrestins are involved in the desensitization of GPCRs. Recently, biased ligands possessing different efficacies in activating the G protein- versus the β-arrestin-dependent signals downstream of a single GPCR have emerged, which can be used to selectively modulate GPCR signal transduction in such a way that desirable signals are enhanced to produce therapeutic effects while undesirable signals of the same GPCR are suppressed to avoid side effects. In the present study, we evaluated agonist bias for compounds developed along a drug discovery project of β2-adrenoceptor agonists. About 150 compounds, including derivatives of fenoterol, 2-amino-1-phenylethanol and 2-amino-2-phenylethanol, were obtained or synthesized, and initially screened for their β-adrenoceptor-mediated activities in the guinea pig tracheal smooth muscle relaxation assay or the cardiomyocyte contractility assay. Nineteen bioactive compounds were further assessed using both the HTRF cAMP assay and the PathHunter β-arrestin assay. Their concentration-response data in stimulating cAMP synthesis and β-arrestin recruitment were applied to the Black–Leff operational model for ligand bias quantitation. As a result, three compounds (L-2, L-4, and L-12) with the core structure of 5-(1-amino-2-hydroxyethyl)-8-hydroxyquinolin-2(1H)-one were identified as a new series of β-arrestin-biased β2-adrenoceptor agonists, whereas salmeterol was found to be Gs-biased. These findings would facilitate the development of novel drugs for the treatment of both heart failure and asthma.
