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1 nd binding affinity was measured using [(3)H]granisetron.
2 ) by the selective 5-HT3 receptor antagonist granisetron.
3 d, however, was unaffected by treatment with granisetron (0.5 mg kg-1) indicating that endogenous 5-H
4  abolished by the 5-HT3 receptor antagonist, granisetron (0.5 mg kg-1).
5 nalyses were as follows: palonosetron versus granisetron: -0.01 (95% CI, -0.23 to 0.20; P = .72); add
6              The 5-HT(3) receptor antagonist granisetron (1 microM) and the 5-HT(4) receptor antagoni
7                        All patients received granisetron 10 microg/kg and dexamethasone 20 mg intrave
8 ceiving cisplatin, all the patients received granisetron (10 microg per kilogram of body weight intra
9 ) (n = number randomized; number evaluable): granisetron (10 microg/kg intravenously) pre-cisplatin f
10                        All patients received granisetron (10 mug/kg intravenously) and dexamethasone
11 y on day 1 and 80 mg orally on days 2 to 4), granisetron (2 mg orally on days 1 to 4), and dexamethas
12  orally on days 2 to 3) or matching placebo, granisetron (2 mg orally on days 1 to 4), and dexamethas
13                   All patients also received granisetron (2 mg orally) and dexamethasone (20 mg orall
14 thasone according to the package insert) and granisetron (2 mg orally) on days 2-3.
15                             Single-dose oral granisetron (2 mg) and I.V. ondansetron (32 mg) resulted
16                        A single oral dose of granisetron (2 mg) resulted in equivalent levels of anti
17 were normal levels of specific surface [(3)H]granisetron ([(3)H]BRL-43694) binding sites.
18                These effects were blocked by granisetron (5-HT3 antagonist) and were absent from TPH1
19  cisplatin chemotherapy for single-dose oral granisetron (54.7%) and i.v. ondansetron (58.3%) (95% co
20  was used to re-evaluate the interactions of granisetron, a 5-HT(3A)R antagonist.
21 ropisetron (ICS 205-930) or 5-HT3 antagonist granisetron abolished luminal stimuli-evoked nodose neur
22                                         Oral granisetron, administered as a single 2-mg dose, provide
23                           On the other hand, granisetron affinity is reduced by substitutions at Trp-
24 -other-residue periodicity of the effects on granisetron affinity strongly suggests that this region
25                    Y143F and Y153F decreased granisetron affinity to the same extent as Y143A and Y15
26 ed to one of three treatments in addition to granisetron and dexamethasone: 400 mg of an oral trisubs
27 acebo on days 2 to 5 (group I) (n = 90; 90); granisetron and MK-869 (400 mg PO [by mouth]) pre-cispla
28                     The 5-HT(3) antagonists, granisetron and ondansetron, are useful in combating the
29 both these and other substitutions, no [(3)H]granisetron binding could be detected, indicating a role
30             Nimodipine neither displaced [3H]granisetron binding nor affected its displacement by dil
31 etween verapamil and either [3H]mCPBG or [3H]granisetron binding was not competitive.
32     Mutation H185A resulted in no detectable granisetron binding, while D189A resulted in a 22-fold r
33  of the 5HT3R for the antagonists curare and granisetron but has little effect on the affinity for th
34 lowed the identification of positions on the granisetron core that might be used as attachment points
35                    Some of these substituted granisetron derivatives showed low nanomolar binding aff
36 sis and biological characterization of novel granisetron derivatives that are antagonists of the huma
37 h prochlorperazine on days 2 and 3; group 2: granisetron + dexamethasone on day 1 with prochlorperazi
38 creened for 5-HT(3) R affinity using a [(3)H]granisetron displacement assay.
39 ions of patients remained nausea-free in the granisetron group (55.4%) and the ondansetron group (59%
40  complete control of emesis was 61.2% in the granisetron group and 67.1% in the ondansetron group (95
41                             Palonosetron and granisetron have similar effects on DN.
42    Premedication with the antiemetic Kytril (granisetron hydrochloride; SmithKline Beecham, Philadelp
43                                   Docking of granisetron identified two possible binding modes, inclu
44   Two energetically similar conformations of granisetron in the binding site were obtained from the d
45 with the model in which the indazole ring of granisetron interacts with Arg92 and the tropane ring in
46           In one model, the indazole ring of granisetron is near Trp90 and the tropane ring is near A
47       5-HT receptor antagonists (SDZ205-557, granisetron, methysergide) failed to inhibit serotonin-i
48 rapy, were randomized to receive either oral granisetron (n = 542) or I.V. ondansetron (n = 543).
49 uld be improved by using palonosetron versus granisetron on day 1 (group 1 v group 2); by adding dexa
50                                  Dolasetron, granisetron, ondansetron, palonosetron, and tropisetron
51   Modeling and mutation studies suggest that granisetron plays its antagonist role by hindering the c
52           Moreover, combining L-754,030 with granisetron plus dexamethasone improves the prevention o
53  More patients who received ondonsetron than granisetron reported dizziness (9.6% v 5.4%, respectivel
54 nd cardiopulmonary afferent stimulation, and granisetron significantly attenuated this cardiopulmonar
55 re randomized to receive either 2 mg of oral granisetron tablets 1 hour before chemotherapy (n = 534)
56                    Docking of the antagonist granisetron was carried out using a Lamarckian genetic a
57 hen an antagonist of the 5-HT3 receptor, [3H]granisetron, was used as the radioligand.
58 effectiveness and safety of single-dose oral granisetron were compared with intravenous (I.V.) ondans
59 5-HT3 receptor As subunit, [3H]mCPBG and [3H]granisetron were displaced by (+)-verapamil, (-)-verapam

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