203861-62-5Relevant articles and documents
Electrochemical Generation of Hypervalent Bromine(III) Compounds
Francke, Robert,Mohebbati, Nayereh,Sokolovs, Igors,Suna, Edgars
supporting information, p. 15832 - 15837 (2021/06/14)
In sharp contrast to hypervalent iodine(III) compounds, the isoelectronic bromine(III) counterparts have been little studied to date. This knowledge gap is mainly attributed to the difficult-to-control reactivity of λ3-bromanes as well as to their challenging preparation from the highly toxic and corrosive BrF3 precursor. In this context, we present a straightforward and scalable approach to chelation-stabilized λ3-bromanes by anodic oxidation of parent aryl bromides possessing two coordinating hexafluoro-2-hydroxypropanyl substituents. A series of para-substituted λ3-bromanes with remarkably high redox potentials spanning a range from 1.86 V to 2.60 V vs. Ag/AgNO3 was synthesized by the electrochemical method. We demonstrate that the intrinsic reactivity of the bench-stable bromine(III) species can be unlocked by addition of a Lewis or a Br?nsted acid. The synthetic utility of the λ3-bromane activation is exemplified by oxidative C?C, C?N, and C?O bond forming reactions.
Concise Synthesis of Lamellarin Alkaloids by C-H/N-H Activation: Evaluation of Metal Catalysts in Oxidative Alkyne Annulation
Mei, Ruhuai,Zhang, Shou-Kun,Ackermann, Lutz
supporting information, p. 1715 - 1718 (2017/11/27)
The performance of various transition-metal catalysts was explored in the step-economical synthesis of naturally occurring lamellarin alkaloids by C-H/N-H activation. The oxidative alkyne annulation proceeded efficiently by using sustainable ruthenium(II) catalysis, which set the stage for a concise synthesis of lamellarin D, lamellarin H and derivatives thereof.
ISOINDOLINE COMPOSITIONS AND METHODS FOR TREATING NEURODEGENERATIVE DISEASE
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Paragraph 0546; 0550, (2015/09/23)
Isoindoline sigma-2 receptor antagonist compounds, pharmaceutical compositions comprising such compounds, and methods for inhibiting Abeta- associated synapse loss or synaptic dysfunction in neuronal cells, modulating an Abeta-associated membrane trafficking change in neuronal cells, and treating cognitive decline associated with Abeta pathology are provided.
