No abstract

ZuschriftenAnders als bei der asymmetrischen Hydrierung von a-Dehydroaminosäure-Derivaten unterscheiden sich die abgebildeten diastereomeren Komplexe mit b-Acylaminoacrylaten nicht gravierend in ihrer Reaktivität, sodass -abweichend vom klassischen Major-Minor-Konzept -das Hauptintermediat im Sinne des Schlüssel-Schloss-Konzepts die Selektivität bestimmt. Mehr dazu erfahren Sie in der Zuschrift von D. Heller et al. auf den folgenden Seiten.

The diastereomeric complexes of b-acylaminoacrylates shown do not differ much in reactivity, in contrast to intermediates in the asymmetric hydrogenation of a-dehydroamino acids. As a result, the major intermediate determines the selectivity of the reaction in terms of the lock-and-key principle rather than the major-minor concept. D. Heller et al. describe the reaction mechanism in more detail on the following pages.

The crystal structure of the title compound, C15H18N2O·H2O, exhibits four independent hydrogen bonds, of types N—H⋯O and O—H⋯O. The water mol­ecules participate in extensive hydrogen bonding and link mol­ecules into a two‐dimensional network.

Chemotherapeutic agents, which contain the Michael acceptor, are potent anticancer molecules by promoting intracellular reactive oxygen species (ROS) generation. In this study, we synthesized a panel of PL (piperlongumine) analogs with chlorine attaching at C2 and an electron-withdrawing/electron-donating group attaching to the aromatic ring. The results displayed that the strong electrophilicity group at the C2–C3 double bond of PL analogs plays an important role in the cytotoxicity whereas the electric effect of substituents, which attached to the aromatic ring, partly contributed to the anticancer activity. Moreover, the protein containing sulfydryl or seleno, such as TrxR, could be irreversibly inhibited by the C2–C3 double bond of PL analogs, and boost intracellular ROS generation. Then, the ROS accumulation could disrupt the redox balance, induce lipid peroxidation, lead to the loss of MMP (Mitochondrial Membrane Potential), and ultimately result in cell cycle arrest and A549 cell line death. In conclusion, PL analogs could induce in vitro cancer apoptosis through the inhibition of TrxR and ROS accumulation.