15644-90-3Relevant articles and documents
Synthesis and antibacterial activities of some quinoline substituted quinoxaline derivatives
Anukumari,Anand Rao,Dubey
, p. 3129 - 3130 (2015)
p-Anisidine (1) on treatment with ethyl acetoacetate gave 1-(ethyl-3-[(4-methoxyphenyl)imino]butanoate) (2), which on cyclization in hot Dowtherm oil gave 4-hydroxy-6-methoxy-2-methylquinoline (3). The latter, on chlorination with SO2Cl2/
Design, synthesis, and biological evaluation of new quinoline-based heterocyclic derivatives as novel antibacterial agents
Mahal, Ahmed,Salman, Ghazwan Ali,Zinad, Dhafer S.
, p. 1621 - 1628 (2020)
A novel series of quinolone-based heterocyclic derivatives including thiadiazine, thiadiazoles, and triazole were synthesized and their in vitro antibacterial activity against Gram-positive and Gram-negative bacteria were evaluated. Newly synthesized deri
Design, synthesis, and evaluation of new 2-(quinoline-4-yloxy)acetamide-based antituberculosis agents
Abbadi, Bruno Lopes,Basso, Luiz Augusto,Bizarro, Cristiano Valim,Borsoi, Ana Flávia,Macchi, Fernanda Souza,Machado, Diana,Machado, Pablo,Paz, Josiane Delgado,Pissinate, Kenia,Rambo, Raoní S.,Ramos, Alessandro Silva,Sperotto, Nathalia,Viveiros, Miguel
, (2020/02/29)
Using a classical molecular simplification approach, a series of 36 quinolines were synthesized and evaluated as in vitro inhibitors of Mycobacterium tuberculosis (M. tuberculosis) growth. Structure–activity relationship (SAR) studies leaded to potent antitubercular agents, with minimum inhibitory concentration (MIC) values as low as 0.3 μM against M. tuberculosis H37Rv reference strain. Furthermore, the lead compounds were active against multidrug-resistant strains, without cross-resistance with some first- and second-line drugs. Testing the molecules against a spontaneous mutant strain containing a single mutation in the qcrB gene (T313A) indicated that the synthesized quinolines targeted the cytochrome bc1 complex. In addition, leading compounds were devoid of apparent toxicity to HepG2 and Vero cells and showed moderate elimination rates in human liver S9 fractions. Finally, the selected structures inhibited M. tuberculosis growth in a macrophage model of tuberculosis infection. Taken together, these data indicate that this class of compounds may furnish candidates for the future development of antituberculosis drugs.
Syntheses and evaluation of new Quinoline derivatives for inhibition of hnRNP K in regulating oncogene c-myc transcription
Shu, Bing,Zeng, Ping,Kang, Shuangshuang,Li, Peng-Hui,Hu, Dexuan,Kuang, Guotao,Cao, Jiaojiao,Li, Xiaoya,Zhang, Meiling,An, Lin-Kun,Huang, Zhi-Shu,Li, Ding
, p. 1 - 17 (2019/01/04)
Aberrant overexpression of heterogeneous nuclear ribonucleoprotein K (hnRNP K) is a key feature in oncogenesis and progression of many human cancers. hnRNP K has been found to be a transcriptional activator to up-regulate c-myc gene transcription, a critical proto-oncogene for regulation of cell growth and differentiation. Therefore, down-regulation of c-myc transcription by inhibiting hnRNP K through disrupting its binding to c-myc gene promoter is a potential approach for cancer therapy. In the present study, we synthesized and screened a series of Quinoline derivatives and evaluated their binding affinity for hnRNP K. Among these derivatives, (E)-1-(4-methoxyphenyl)-3-(4-morpholino-6-nitroquinolin-2-yl)prop-2-en-1-one (compound 25) was determined to be the first-reported hnRNP K binding ligand with its KD values of 4.6 and 2.6 μM measured with SPR and MST, respectively. Subsequent evaluation showed that the binding of compound 25 to hnRNP K could disrupt its unfolding of c-myc promoter i-motif, resulting in down-regulation of c-myc transcription. Compound 25 showed a selective anti-proliferative effect on human cancer cell lines with IC50 values ranged from 1.36 to 3.59 μM. Compound 25 exhibited good tumor growth inhibition in a Hela xenograft tumor model, which might be related to its binding with hnRNP K. These findings illustrated that inhibition of DNA-binding protein hnRNP K by compound 25 could be a new and selective strategy of regulating oncogene transcription instead of targeting promoter DNA secondary structures such as G-quadruplexes or i-motifs.