ABSTRACT
An operationally simple method for the synthesis of bridged dibenzo[b,f][1,5]diazocines and bridged spiromethanodibenzo[b,e]azepines exhibiting bridged eight-membered and seven-membered molecular architecture is reported. This unique approach is based on substrate selective mechanistic pathway, including an unprecendented aerial oxidation-driven mechanism for the synthesis of bridged spiromethanodibenzo[b,e]azepines. The reaction is highly atom economic, and in addition, it allows the construction of two rings and four bonds in a single operation under metal-free condition. The easy availability of ß enaminone and ortho phathalaldehyde as starting materials and the simple operation make this approach suitable for the preparation of important dibenzo[b,f][1,5]diazocine and spiromethanodibenzo[b,e]azepine cores.
ABSTRACT
Metal-free radical nitration of the ß C-H bond of 3-alkylidene-2-oxindoles with tert-butyl nitrite (TBN) has been explored. Interestingly, (E)-3-(2-(aryl)-2-oxoethylidene)oxindole and (E)-3-ylidene oxindole give different diastereomers on nitration. The mechanistic investigation revealed that the diastereoselectivity was controlled by the size of the functional group. Another transformation of 3-(nitroalkylidene) oxindole into 3-(tosylalkylidene) oxindole was performed through metal and oxidant-free tosylhydrazine-mediated sulfonation. Both methods have the advantages of readily available starting materials and operational simplicity.
ABSTRACT
An efficient tosylhydrazine-mediated conjugate reduction of 3-phenacylideneoxindole and sequential Michael/intramolecular aldol reaction is reported under base-catalyzed conditions towards the formation of densely substituted dispirocyclopentanebisoxindole derivatives. The reaction proceeded in a diastereoselective manner to afford four chiral stereocenters. The method also has advantages of wide substrate scope, readily available starting materials and operational simplicity through one pot reaction.
ABSTRACT
The human mitochondrion is a unique semi-autonomous organelle with a genome of its own and also requires nuclear encoded components to carry out its functions. In addition to being the powerhouse of the cell, mitochondria plays a central role in several metabolic pathways. It is therefore challenging to delineate the cause-effect relationship in context of mitochondrial dysfunction. Several studies implicate mutations in mitochondrial DNA (mtDNA) in various complex diseases. The human mitochondrial DNA (mtDNA) encodes a set of 37 genes, 13 protein coding, 22 tRNAs and two ribosomal RNAs, which are essential structural and functional components of the electron transport chain. As mentioned above, variations in these genes have been implicated in a broad spectrum of diseases and are extensively reported in literature and various databases. A large number of databases and prediction methods have been published to elucidate the role of human mitochondrial DNA in various disease phenotypes. However, there is no centralized resource to visualize this genotype-phenotype data. Towards this, we have developed MtBrowse: an integrative genomics browser for human mtDNA. As of now, MtBrowse has four categories - Gene, Disease, Reported variation and Variation prediction. These categories have 105 tracks and house data on mitochondrial reference genes, around 600 variants reported in literature with respect to various disease phenotypes and predictions for potential pathogenic variations in protein-coding genes. MtBrowse also hosts genomic variation data from over 5000 individuals on 22 disease phenotypes. MtBrowse may be accessed at http://ab-openlab.csir.res.in/cgi-bin/gb2/gbrowse.
