4420-46-6Relevant articles and documents
Cyclometalated cinchophen ligands on iridium(iii): Towards water-soluble complexes with visible luminescence
Smith, Rebecca A.,Stokes, Emily C.,Langdon-Jones, Emily E.,Platts, James A.,Kariuki, Benson M.,Hallett, Andrew J.,Pope, Simon J. A.
, p. 10347 - 10357 (2013)
Eight cationic heteroleptic iridium(iii) complexes, [Ir(epqc) 2(N^N)]+, were prepared in high yield from a cyclometalated iridium bridged-chloride dimer bearing two ethyl-2- phenylquinoline-4-carboxylate (epqc) ligands. Two X-ray cry
Palladium-Catalyzed Three-Component Cascade Reaction of Nitriles: Synthesis of 2-Arylquinoline-4-carboxylates
Zhao, Zhiwei,Zeng, Ge,Chen, Yinan,Zheng, Jinming,Chen, Zhongyan,Shao, Yinlin,Zhang, Fangjun,Chen, Jiuxi,Li, Renhao
, p. 7955 - 7960 (2021/10/20)
A new method for converting easy availability starting materials 2-(2-oxoindolin-3-yl)acetonitrile, arylboronic acids, and alcohols into 2-arylquinoline-4-carboxylates is reported. The procedure involves a three-component addition/ring expansion/esterification reaction in the presence of Pd(II) catalyst with high functional group tolerance under mild conditions. In addition, the photophysical properties of the resulting product were investigated and exhibited excellent polarity-sensitive fluorescence properties and AIE property.
New quinoline/1,2,4-triazole hybrids as dual inhibitors of COX-2/5-LOX and inflammatory cytokines: Design, synthesis, and docking study
Abdel-Aziz, Mohamed,Abdelhamid, Dalia,Fujita, Mikako,Gomaa, Hesham A. M.,Gouda, Ahmed M.,Hassan, Heba A.,Mohassab, Aliaa M.,Otsuka, Masami,Radwan, Mohamed O.,Youssif, Bahaa G. M.
, (2021/07/06)
A novel series of 19 quinoline/1,2,4-triazole hybrid 6a-i and 7a-j was synthesized and evaluated in vitro as dual COX-2/5-LOX inhibitors. Compounds 6e, 6i, and 7e displayed the highest potency and selectivity for inhibiting COX-2 activity (IC50 = 7.25, 8.13, and 8.48 nM, respectively; selectivity index (COX-1/COX-2) = 44.89, 30.30, and 33.47, respectively) in comparison to celecoxib (COX-2 IC50 = 42.60 nM; selectivity index (SI) = 8.05). The anti-inflammatory activity of the newly synthesized compounds was further examined in vivo using a carrageenan induced paw edema assay. Interestingly, the in vitro findings of the COX inhibitory assay were consistent with the in vivo assay. Moreover, 6e, 6i, and 7e showed a substantial reduction in serum concentrations of PGE2, TNF-α, IL-6. Molecular docking analysis of compounds 6e, 6f, 6i, 7e, and 7f revealed high binding affinities toward COX-2 compared to COX-1, which was matched with the experimental results. In addition, these compounds exhibited different binding orientations into the active site of COX-2, which were dependent on the type of substitutions on N4 of the triazole ring. Among the tested derivatives, compounds 6e, 6i and 7e which showed high selectivity to COX-2, exhibited hydrogen bonding interactions with key amino acids in COX-2 such as Arg120, Arg513, and/or Glu524. In addition, the tested compounds also showed multiple hydrogen bonds with the Arg101, Val110, Arg138 or His130 in 5-LOX. These findings show, taken together, that those derivatives are good leads to potential anti-inflammatory agents with lowest gastric damage.
NO-releasing STAT3 inhibitors suppress BRAF-mutant melanoma growth
Kaoud, Tamer S.,Mohassab, Aliaa M.,Hassan, Heba A.,Yan, Chunli,Van Ravenstein, Sabrina X.,Abdelhamid, Dalia,Dalby, Kevin N.,Abdel-Aziz, Mohamed
, (2019/12/09)
Constitutive activation of STAT3 can play a vital role in the development of melanoma. STAT3-targeted therapeutics are reported to show efficacy in melanomas harboring the BRAFV600E mutant and also in vemurafenib-resistant melanomas. We designed and synthesized a series of substituted nitric oxide (NO)-releasing quinolone-1,2,4-triazole/oxime hybrids, hypothesizing that the introduction of a STAT3 binding scaffold would augment their cytotoxicity. All the hybrids tested showed a comparable level of in vitro NO production. 7b and 7c exhibited direct binding to the STAT3-SH domain with IC50 of ～ 0.5 μM. Also, they abrogated STAT3 tyrosine phosphorylation in several cancer cell lines, including the A375 melanoma cell line that carries the BRAFV600E mutation. At the same time, they did not affect the phosphorylation of upstream kinases or other STAT isoforms. 7c inhibited STAT3 nuclear translocation in mouse embryonic fibroblast while 7b and 7c inhibited STAT3 DNA-binding activity in the A375 cell line. Their anti-proliferating activity is attributed to their ability to trigger the production of reactive oxygen species and induce G1 cell cycle arrest in the A375 cell line. Interestingly, 7b and 7c showed robust cell growth suppression and apoptosis induction in two pairs of BRAF inhibitor-na?ve (-S) and resistant (-R) melanoma cell lines containing a BRAF V600E mutation. Surprisingly, MEL1617-R cells that are known to be more resistance to MEK inhibition by GSK1120212 than MEL1617-S cells exhibit a similar response to 7b and 7c.
