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1 ar for cisatracurium and (+)-tubocurarine or metocurine.
2 n experiments with the curariform antagonist metocurine.
3                                     However, metocurine and atracurium could potentiate the responses
4                           The interaction of metocurine and atracurium with acetylcholine at fetal-ty
5 hypothesis was tested for the pair of agents metocurine and gallamine by determining the ability of a
6 sults are consistent with the idea that both metocurine and gallamine have a high affinity for the sa
7 ular blocking agents (atracurium, gallamine, metocurine, and pancuronium) to act as competitive antag
8 amine to block the partial agonist action of metocurine at fetal-type receptors was tested as well an
9 t despite their similar structures, d-TC and metocurine bind in distinctly different orientations to
10 juxtapose one of two quaternary nitrogens in metocurine but are remote from the equivalent quaternary
11 minant docking orientation for both d-TC and metocurine, but unexpectedly, the bound orientations dif
12 111K, and epsilon L109K decrease affinity of metocurine by up to 3 orders of magnitude but only sligh
13 orientations of each antagonist; the flatter metocurine fits into a pocket formed principally by the
14 competitive antagonists (+)-tubocurarine and metocurine for adult mouse receptors is known.
15 ns of Trp-53 and Gln-55 closely approach the metocurine scaffold but not that of d-TC.
16                                              Metocurine shifted the apparent IC(50) of (+)-tubocurari
17 curare derivatives d-tubocurarine (d-TC) and metocurine to AChBP using computational methods, mutagen
18 urarine (d-TC) and its methylated derivative metocurine using mutagenesis, ligand binding measurement
19 farther away from the equivalent nitrogen in metocurine, whereas, at the opposing interface, side cha

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