1212932-15-4Relevant academic research and scientific papers
Enantioselective Access to Chiral Cyclic Sulfamidates Through Iridium-Catalyzed Asymmetric Hydrogenation
Liu, Yuanhua,Huang, Yi,Yi, Zhiyuan,Liu, Gongyi,Dong, Xiu-Qin,Zhang, Xumu
supporting information, p. 1582 - 1586 (2019/02/19)
The Iridium-catalyzed asymmetric hydrogenation of cyclic sulfamidate imines was successfully developed with N-methylated ZhaoPhos L2 as the ligand. A variety of chiral cyclic sulfamidates were obtained with excellent results (up to 99% yield, 99% ee). Furthermore, this asymmetric hydrogenation can be employed as the key reaction step to prepare the important intermediates in organic synthesis. (Figure presented.).
Difluorophenylglycinols as New Modulators of Proteolytic Processing of Amyloid Precursor Proteins
Chen, Chia-Yu,Liao, Yung-Feng,Chang, Ming-Yun,Hu, Ming-Kuan
, p. 161 - 173 (2014/03/21)
Synthesis and evaluation of difluorophenylglycinols as new modulators of proteolytic processing of the amyloid-β precursor proteins for Alzheimer's therapies were described. A range of N-substituted (R)- and (S)- difluorophenylglycinols, structured on the amino alcohol framework, were explored by incorporating the arylsulfonyl moieties and various N-substituents. Evans' chiral auxiliary strategy was employed for the asymmetric synthesis of these enantiomeric difluorophenylglycinols. Compounds with effects on the γ-secretase inhibition and ERK-mediated signaling pathways were evaluated on cell-based assays. Among them, N-cyclopropylmethyl derivatives R-12c and R-13c showed modest γ-secretase inhibition as well as ERK-dependent activation. A range of N-substituted (R)- and (S)-difluorophenylglycinols, structured on the amino alcohol framework, were explored by incorporating the arylsulfonyl moieties and various N-substituents. Compounds with effects on γ-secretase inhibition and ERK-mediated signaling pathways were evaluated on cell-based assays. The N-cyclopropylmethyl derivatives R-12c and R-13c showed modest γ-secretase inhibition and ERK-dependent activation.
