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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
5 nalyses were as follows: palonosetron versus granisetron: -0.01 (95% CI, -0.23 to 0.20; P = .72); add
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
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
19 cisplatin chemotherapy for single-dose oral granisetron (54.7%) and i.v. ondansetron (58.3%) (95% co
21 ropisetron (ICS 205-930) or 5-HT3 antagonist granisetron abolished luminal stimuli-evoked nodose neur
24 -other-residue periodicity of the effects on granisetron affinity strongly suggests that this region
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
29 both these and other substitutions, no [(3)H]granisetron binding could be detected, indicating a role
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
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
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
42 Premedication with the antiemetic Kytril (granisetron hydrochloride; SmithKline Beecham, Philadelp
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
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
51 Modeling and mutation studies suggest that granisetron plays its antagonist role by hindering the c
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)
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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