ライフサイエンスコーパス: phenylalkylamine

1 lpha 1c subunit disrupted block by all three phenylalkylamines.

2 ethoxy groups in prototypical hallucinogenic phenylalkylamines 1 and 2.

3 The synthesis of the adamantane phenylalkylamines 2a-d, 3a-c, and 4a-e is described.

4 2+ channels, we systematically characterized phenylalkylamine and benzothiazepine inhibition of three

5 These bind to the dihydropyridine, phenylalkylamine and benzothiazepine sites respectively.

6 ng of the channel and use-dependent block by phenylalkylamines and benzothiazepines and provide evide

7 dependent Ca(2+) channel activation, whereas phenylalkylamines and benzothiazepines are used primaril

8 n applied to understand the actions of these phenylalkylamines and their mechanisms of action.

9 Verapamil (a phenylalkylamine) and diltiazem (a benzothiazepine) were

10 Verapamil is a potent phenylalkylamine antihypertensive believed to exert its

11 (LSD), psilocybin, and substituted N-benzyl phenylalkylamines are widely used recreationally with ps

12 -methoxybenzylamine hydrochloride (R-467), a phenylalkylamine, are thought to activate CaSR by allost

13 that the structure-affinity relationships of phenylalkylamines as 5-HT(2A) ligands now be reinvestiga

14 al basis for binding of dihydropyridines and phenylalkylamines at their distinct receptor sites on Ca

15 By using a phenylalkylamine azido derivative, a 75-kDa carrot membr

16 ate that there are important determinants of phenylalkylamine binding in both the S6 segments and the

17 Recent studies of the phenylalkylamine binding site in the alpha1C subunit of

18 We have extended this analysis of the phenylalkylamine binding site to amino acid residues in

19 In contrast, the phenylalkylamine Br-verapamil binds in the central cavit

20 y weakly sensitive to 1,4-dihydropyridine or phenylalkylamine Ca2+ channel blockers and is not potent

21 The phenylalkylamine compound, NPS 568, identified as a posi

22 In this study, two novel phenylalkylamine compounds, NPS 467 and NPS 568, were ex

23 We discovered that certain phenylalkylamine compounds, typified by NPS R-568 and it

24 The phenylalkylamine D600 (2 microM) reduced release at all

25 The phenylalkylamines (-)-D888, verapamil, and D600, cause v

26 it one of the most potent hallucinogen-like phenylalkylamine derivatives reported to date.

27 Calcium channel blockers of the phenylalkylamine family and bepridil specifically inhibi

28 of tryptamine ligands and the 5-position of phenylalkylamine ligands.

29 Compounds, such as the phenylalkylamines NPS 568 and AMG 073, act as agonists o

30 els participate in dihydropyridine (DHP) and phenylalkylamine (PAA) binding.

31 Verapamil is a prototypical phenylalkylamine (PAA), and it was the first calcium cha

32 pyridines (DHP), benzothiazepines (BTZ), and phenylalkylamines (PAA), many of which have been used fo

33 The phenylalkylamine, particularly the phenylethylamine, moi

34 nnels, as do the dihydropyridines (DHPs) and phenylalkylamines (PAs), but it has unique properties th

35 A model of the phenylalkylamine receptor site at the interface between

36 To study the effects of mutations in the phenylalkylamine receptor site on block by these drugs,

37 ffects on the kinetics of block by all three phenylalkylamines require larger molecular changes, perh

38 Phenylalkylamines such as 1-(4-bromo-2, 5-dimethoxypheny

39 Phenylalkylamines such as NPS R-568 are allosteric modul

40 pine, the benzothiazepine diltiazem, and the phenylalkylamine verapamil all prevented restraint-induc

41 , which is inhibited by dihydropyridines and phenylalkylamines with nanomolar affinity in a state-dep