121788-87-2Relevant articles and documents
Tetrahydrosalen Uranyl(VI) Complexes: Crystal Structures and Solution Binding Study
Zhao, Xiao,Zhang, Di,Yu, Ren,Chen, Shusen,Zhao, Dahui
, p. 1185 - 1191 (2018)
A pair of uranyl complexes incorporating tetrahydrosalen and N,N-dimethyltetrahydrosalen ligands are synthesized and studied. These new ligands, with saturated secondary and tertiary amines, exhibit higher chemostability than the prototype Schiff base (sa
Glycosylated tetrahydrosalens as multifunctional molecules for Alzheimer's therapy
Storr, Tim,Scott, Lauren E.,Bowen, Meryn L.,Green, David E.,Thompson, Katherine H.,Schugar, Harvey J.,Orvig, Chris
supporting information; experimental part, p. 3034 - 3043 (2009/08/08)
The tetrahydrosalens N,N′-bis(2-hydroxybenzyl)-ethane-1,2-diamine (H2L1), N,N′-bis(2-hydroxybenzyl)-(-)-1,2- cyclohexane-(1R,2R)-diamine (H2L2), N,N′-bis(2- hydroxybenzyl)-N,N′-dimethyl-ethane-1,2-diamine (H2L 3), N,N′-bis(2-hydroxybenzyl)-N,N′-dibenzyl-ethane-1,2- diamine (H2L4), and N,N′-bis(2-(4-tert-butyl) hydroxybenzyl)-ethane-1,2-diamine (H2L5), as well as their prodrug glycosylated forms, GL1-5, have been prepared and evaluated in vitro for their potential use as Alzheimer's disease (AD) therapeutics. Dysfunctional interactions of metal ions, especially those of Cu, Zn, and Fe, with the amyloid-β (Aβ) peptide are hypothesised to play an important role in the aetiology of AD, and disruption of these aberrant metal-peptide interactions via chelation therapy holds considerable promise as a therapeutic strategy. Tetrahydrosalens such as H2L1-5 have a significant affinity for metal ions, and thus should be able to compete with the Aβ peptide for Cu, Zn, and Fe in the brain. This activity was assayed in vitrovia a turbidity assay; H2L1 and H2L 3 were found to attenuate Aβ1-40 aggregation after exposure to Cu2+ and Zn2+. In addition, H 2L1-5 were determined to be potent antioxidants on the basis of an in vitro antioxidant assay. GL1-5 were prepared as metal binding prodrugs; glycosylation is intended to prevent systemic metal binding, improve solubility, and enhance brain uptake. Enzymatic (β-glucosidase) deprotection of the carbohydrate moieties was facile, with the exception of GL4, demonstrating the general feasibility of this prodrug approach. Finally, a representative prodrug, GL3, was determined to be non-toxic over a large concentration range in a cell viability assay.
