The first example of rare earth metal-catalyzed [3 + 2] cycloaddition of organic azides with nitroolefins and subsequent elimination reaction is described. In the presence of a catalytic amount of Ce(OTf)3, both benzyl and phenyl azides react with a broad range of aryl nitroolefins containing a range of functionalities selectively producing 1,5-disubstituted 1,2,3-triazoles in good to excellent yields.

No abstract

A highly regioselective synthesis of b-aryl enaminones and 1,4,5-trisubstituted 1,2,3-triazoles from chalcones and benzyl azides based on reaction solvent selection is reported. In the presence of a catalytic amount of CeA C H T U N G T R E N N U N G (OTf) 3 , reactions of chalcones with benzyl azides in DMF at 100 8C afforded densely substituted Z-b-aryl enaminones in good to excellent yields, whereas treatment of chalcones with benzyl azides in toluene at 100 8C selectively produced 1,4,5-trisubstituted 1,2,3-triazoles in excellent yields. COMMUNICATIONSRegioselective Synthesis of b-Aryl Enaminones Scheme 1. A plausible reaction mechanism.

RuCl3·3H2O was found to be an effective catalyst for reactions of indoles, 2-methylthiophene, and 2-methylfuran with aldehydes to afford the corresponding bis(indolyl)methanes, bis(thienyl)methanes, and bis(fur-2-yl)methanes in moderate to excellent yields. Experimental results indicated that mono(indolyl)methanol is not the reaction intermediate under these reaction conditions.

A series of dehydroabietic acid (DHAA) acyl-thiourea derivatives were designed and synthesized as potent antitumor agents. The in vitro pharmacological screening results revealed that the target compounds exhibited potent cytotoxicity against HeLa, SK-OV-3 and MGC-803 tumor cell lines, while they showed lower cytotoxicity against HL-7702 normal human river cells. Compound 9n (IC50 = 6.58 ± 1.11 μM) exhibited the best antitumor activity against the HeLa cell line and even displayed more potent inhibitory activity than commercial antitumor drug 5-FU (IC50 = 36.58 ± 1.55 μM). The mechanism of representative compound 9n was then studied by acridine orange/ethidium bromide staining, Hoechst 33,258 staining, JC-1 mitochondrial membrane potential staining, TUNEL assay and flow cytometry, which illustrated that this compound could induce apoptosis in HeLa cells. Cell cycle analysis indicated that compound 9n mainly arrested HeLa cells in the S phase stage. Further investigation demonstrated that compound 9n induced apoptosis of HeLa cells through a mitochondrial pathway.