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Abstract: Two novel blue light-emitting materials based on bis(tert-butyl)anthracenyl-imidazophenanthrolines (BAIPs) have been synthesized and extensively characterized. Both materials exhibited a non-aggregate feature with high fluorescent quantum efficiency and excellent thermal stability. They can serve both as emissive and electron-transporting materials used in electroluminescence (EL) device for blue emission with high luminescence and external quantum efficiency. This study demonstrates that they are potentially useful for a wide range of applications in EL technology. [Copyright &y& Elsevier]

A series of thiochromeno[2,3- c ]quinolin-12-one derivatives with various substitutions were synthesized and evaluated as topoisomerase (Topo) inhibitors. Six (8 , 10 , 12 , 14 , 19 , and 26) of 23 compounds showed strong inhibitory activities against Topo-mediated DNA relaxation and proliferation of five human cell lines including breast (MDA-MB-231, MDA-MB-468 and MCF7), colorectal (HCT116) and non-small cell lung (H1299) cancers. Among these, compounds 14 and 26 exhibited full inhibitory activities against Topo I at 3 μM and Topo IIα at 1 μM. Cancer cells treated with 26 accumulated DNA damage and were arrested at the G 2 /M phase. With time, cells proceeded to apoptosis, as revealed by increased amounts of cells with fragmented DNA and cleavage of caspase-8 and -9. In contrast, normal breast epithelial cells showed low sensitivity to 26. Taken together, our study identifies 26 as a potent Topo dual-inhibitor with low toxicity to normal cells, and elucidates that the terminal amino group of N -2-aminoethylamino or N -3-aminopropylamino at the 6th position and 8,10-di-halogen substituents on thiochromeno[2,3- c ]quinolin-12-one are critical for the Topo-inhibiting and cancer-killing activities. Image 1 • Six compounds identified as dual Topo inhibitors. • 26 exhibits the highest toxicity in five cancer cell lines but is less toxic in normal breast epithelial cells. • 26 traps Topo I and IIα on chromatin and suppresses their activities. • 26 triggers DNA damage, cell-cycle arrest at the G 2 /M phase, followed by apoptosis. [ABSTRACT FROM AUTHOR]

The small-molecule naphtha [2,3-f]quinoxaline-7,12-dione (NSC745887) can effectively inhibit the proliferation of various cancers by trapping DNA-topoisomerase cleavage. The aim of this study was to elucidate cellular responses of NSC745887 in human glioblastoma multiforme (GBM, U118MG and U87MG cells) and investigate the underlying molecular mechanisms. NSC745887 reduced the cell survival rate and increased the sub-G 1 population in dose- and time-dependent manners in GBM cells. Moreover, NSC745887 increased expression of γH2AX and caused DNA fragmentation leading to DNA damage. Furthermore, Annexin V/propidium iodide and Br-dTP staining showed the apoptotic effect of NSC745887 in GBM cells. DNA repair proteins of ataxia-telangiectasia mutated (ATM), ATM and Rad3-related, and decoy receptor 3 also decreased with NSC745887 treatment. In addition, NSC745887 caused apoptosis by the caspase-8/9-caspase-3-poly(ADP-ribose) polymerase cascade. An in vivo study indicated that NSC745887 suppressed the [ 18 F]-FDG-specific uptake value in brain tumors. Histological staining also indicated a decrease in Ki-67 and increases in γH2AX and cleaved caspase-3 in the brain tumor area. These data provide preclinical evidence for NSC745887 as a potential new small molecule drug for managing glioblastomas., Competing Interests: CONFLICTS OF INTEREST The authors disclose no potential conflicts of interest.

This study synthesized a europium (Eu(3+)) complex Eu(DBM)(3)Cl-MIP (DBM = dibenzoyl methane; Cl-MIP = 2-(2-chlorophenyl)-1-methyl-1H-imidazo[4,5-f][1,10]phenanthroline) dispersed in a benzyl methacrylate (BMA) monomer and treated with ultraviolet (UV) light for polymerization. Spectral results showed that the europium complex containing an antenna, Cl-MIP, which had higher triplet energy into the Eu(3+) energy level, was an energetically enhanced europium emission. Typical stacking behaviors of π-π interactions between the ligands and the Eu(3+)-ion were analyzed using single crystal X-ray diffraction. Regarding the luminescence performance of this europium composite, the ligand/defect emission was suppressed by dispersion in a poly-BMA (PBMA) matrix. The underlying mechanism of the effective enhancement of the pure Eu(3+) emission was attributed to the combined effects of structural modifications, defect emissions, and carrier charge transfer. Fluorescence spectra were compared to the composite of optimized Eu3+ emission where they were subsequently chelated to four metal ions via carboxylate groups on the BMA unit. The optical enhanced europium composite clearly demonstrated highly efficient optical responses and is, therefore a promising application as an optical detection material.