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 -methoxybenzylamine hydrochloride (R-467), a
phenylalkylamine,
are thought to activate CaSR by allost
12 that the structure-affinity relationships of
phenylalkylamines as 5-HT(2A) ligands now be reinvestiga
13 al basis for binding of dihydropyridines and
phenylalkylamines at their distinct receptor sites on Ca
14 By using a
phenylalkylamine azido derivative, a 75-kDa carrot membr
15 ate that there are important determinants of
phenylalkylamine binding in both the S6 segments and the
16 Recent studies of the
phenylalkylamine binding site in the alpha1C subunit of
17 We have extended this analysis of the
phenylalkylamine binding site to amino acid residues in
18 In contrast, the
phenylalkylamine Br-verapamil binds in the central cavit
19 y weakly sensitive to 1,4-dihydropyridine or
phenylalkylamine Ca2+ channel blockers and is not potent
20 The
phenylalkylamine compound, NPS 568, identified as a posi
21 In this study, two novel
phenylalkylamine compounds, NPS 467 and NPS 568, were ex
22 We discovered that certain
phenylalkylamine compounds, typified by NPS R-568 and it
23 The
phenylalkylamine D600 (2 microM) reduced release at all
24 The
phenylalkylamines (-)-
D888, verapamil, and D600, cause v
25 it one of the most potent hallucinogen-like
phenylalkylamine derivatives reported to date.
26 Calcium channel blockers of the
phenylalkylamine family and bepridil specifically inhibi
27 of tryptamine ligands and the 5-position of
phenylalkylamine ligands.
28 Compounds, such as the
phenylalkylamines NPS 568 and AMG 073, act as agonists o
29 els participate in dihydropyridine (DHP) and
phenylalkylamine (
PAA) binding.
30 Verapamil is a prototypical
phenylalkylamine (
PAA), and it was the first calcium cha
31 The
phenylalkylamine,
particularly the phenylethylamine, moi
32 nnels, as do the dihydropyridines (DHPs) and
phenylalkylamines (
PAs), but it has unique properties th
33 A model of the
phenylalkylamine receptor site at the interface between
34 To study the effects of mutations in the
phenylalkylamine receptor site on block by these drugs,
35 ffects on the kinetics of block by all three
phenylalkylamines require larger molecular changes, perh
36 Phenylalkylamines such as 1-(4-bromo-2, 5-dimethoxypheny
37 Phenylalkylamines such as NPS R-568 are allosteric modul
38 pine, the benzothiazepine diltiazem, and the
phenylalkylamine verapamil all prevented restraint-induc
39 , which is inhibited by dihydropyridines and
phenylalkylamines with nanomolar affinity in a state-dep