1190882-47-3Relevant academic research and scientific papers
Rhodium catalyzed selective hydroaminomethylation of biorenewable eugenol under aqueous biphasic condition
Jagtap, Samadhan A.,Gowalkar, Shilpa P.,Monflier, Eric,Ponchel, Anne,Bhanage, Bhalchandra M.
, p. 108 - 116 (2018)
This work reports a highly regioselective hydroaminomethylation of eugenol, anethole and estragole with piperidine in aqueous medium. This catalytic system was composed of rhodium complexes stabilized by trisulfonated triphenylphosphine (TPPTS) and of a native or chemically modified cyclodextrins. Various cyclodextrins such as α-cyclodextrins (α-CD), β-cyclodextrin (β-CD), γ-cyclodextrin (γ-CD), 2-hydroxy-propyl β-cyclodextrin (hp-β-CD) and RAndomly MEthylated β-cyclodextrin (RAME-β-CD) have been tested. The effect of different parameters such as syngas pressure, time, temperature, catalyst precursor/loading and the ratio of Metal/Ligand/Cyclodextrin were also investigated. The addition of cyclodextrins as a mass transfer agent remarkably increased the rate reaction and the selectivity of linear amines, specially in the case of RAME-β-CD. So, the Rh/TPPTS/RAME-β-CD as a catalyst exhibited high conversion (92%) and selectivity (79.2%) towards the linear amine as major product under mild conditions. Finally, the catalytic system was recycled up to five times without a significant loss in activity and selectivity.
Structural determinants for histamine H1 affinity, hERG affinity and QTc prolongation in a series of terfenadine analogs
Aslanian, Robert,Piwinski, John J.,Zhu, Xiaohong,Priestley, Tony,Sorota, Steve,Du, Xiao-Yi,Zhang, Xue-Song,McLeod, Robbie L.,West, Robert E.,Williams, Shirley M.,Hey, John A.
supporting information; experimental part, p. 5043 - 5047 (2010/03/31)
In the late 1980's reports linking the non-sedating antihistamines terfenadine and astemizole with torsades de pointes, a form of ventricular tachyarrhythmia that can degenerate into ventricular fibrillation and sudden death, appeared in the clinical literature. A substantial body of evidence demonstrates that the arrhythmogenic effect of these cardiotoxic antihistamines, as well as a number of structurally related compounds, results from prolongation of the QT interval due to suppression of specific delayed rectifier ventricular K+ currents via blockade of the hERG-IKr channel. In order to better understand the structural requirements for hERG and H1 binding for terfenadine, a series of analogs of terfenadine has been prepared and studied in both in vitro and in vivo hERG and H1 assays.
