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1 eta-adrenoceptor agonists, isoproterenol and salmeterol.
2 e not associated with the LOB in response to salmeterol.
3 steric binding site for larger drugs such as salmeterol.
4 be equivalent to those with the addition of salmeterol.
5 cells, which was enhanced by fluticasone and salmeterol.
6 thma treatment failure in patients receiving salmeterol.
7 se was partially inhibited by salbutamol and salmeterol.
8 choprotection at weeks 4 and 8 was seen with salmeterol.
9 gonist before and after chronic therapy with salmeterol.
10 ontributes to the long duration of action of salmeterol.
11 cations during the year before they received salmeterol.
12 ust 31, 1995, including 2, 708 recipients of salmeterol.
13 chronic dosing with formoterol compared with salmeterol.
14 fected the efficacy or duration of action of salmeterol.
15 on outcomes in response to tiotropium versus salmeterol.
20 numbered treatment packs containing inhaled salmeterol (100 mug twice daily) or a matching placebo.
21 h beta-agonists albuterol, isoproterenol, or salmeterol (100 nM to 10 muM) caused a significant ( app
23 of the selective beta2-adrenoceptor agonist salmeterol (15 microM) facilitated the excitatory field
24 reatment with a single inhalation of 100 mug salmeterol 30 min before bronchial segmental challenge.
25 and five patients with COPD received either salmeterol 42 microg twice daily, ipratropium bromide 36
26 0 microg twice per day; n = 54) or switch to salmeterol (42 microg twice per day; n = 54) or to place
28 -in period were randomized to treatment with salmeterol 50 microg combined with fluticasone propionat
29 to receive inhaled longacting beta2 agonist (salmeterol 50 microg twice a day) or placebo given in a
30 with fluticasone propionate (FP) 250 microg, salmeterol 50 microg, FP 250 microg, or placebo, each gi
31 ily tiotropium 5 mug or 2.5 mug, twice-daily salmeterol 50 mug, or placebo, while maintaining inhaled
34 tiotropium (at a dose of 18 mug once daily), salmeterol (50 mug twice daily), and the inhaled glucoco
35 ycopyrronium (50 mug) once daily or the LABA salmeterol (50 mug) plus the inhaled glucocorticoid flut
38 n cluster had best response with fluticasone/salmeterol (64% vs 23% 2.5x fluticasone and 13% fluticas
39 ifference 133 mL, 95% CI 105-161, p<0.0001), salmeterol (73 mL, 46-101, p<0.0001), or fluticasone alo
42 se asthma symptoms improve after addition of salmeterol, a substantial reduction (50%) in triamcinolo
43 ospectively evaluated the safety of the LABA salmeterol, added to fluticasone propionate, in a fixed-
44 ler monitors recorded fluticasone propionate/salmeterol adherence (covertly for non-IRF groups) and,
45 during the period examined: (1) fluticasone/salmeterol (Advair), (2) mometasone furoate (Asmanex), (
47 primary end point of trough FEV1 compared to salmeterol after 4 weeks of dosing in patients with mode
48 tyryl cyclic adenosine monophosphate (cAMP), salmeterol, albuterol, and isoproterenol in normal rat l
51 istered with a single inhaler, with placebo, salmeterol alone, or fluticasone propionate alone for a
53 the contribution of inhaled fluticasone and salmeterol, alone or combined, to the reversal of bronch
55 tive agonist site, it has been proposed that salmeterol also binds with very high affinity at a secon
58 g fluticasone twice daily (n=374), 50 microg salmeterol and 500 microg fluticasone twice daily (n=358
60 ticipants received high-dose fluticasone and salmeterol and continued other pre-study controller drug
64 Subsequently, we determined the effects of salmeterol and fluticasone propionate (FP) in seven ster
66 s, such as the beta(2)-adrenoceptor agonists salmeterol and formeterol, and the new anticholinergic t
67 terol has a 24 h duration of action, whereas salmeterol and formoterol require twice-daily administra
68 ion (indacaterol, two indacaterol analogues, salmeterol and formoterol) in monounsaturated model memb
69 ond cohort, B16Arg/Arg subjects treated with salmeterol and ICS concurrently (n = 8) had a lower A.M.
70 ly/Gly genotypes, combination treatment with salmeterol and inhaled corticosteroid improved airway fu
71 eness to methacholine did not differ between salmeterol and placebo in Arg/Arg participants (p=0.87).
73 fluticasone propionate and beta(2) agonists salmeterol and salbutamol on IL-6 production in BEAS-2B
75 dual and differential treatment responses to salmeterol and tiotropium and predictors of a positive r
76 f patients showed a differential response to salmeterol and tiotropium in terms of morning PEF (n = 9
77 ferential responses of asthmatic patients to salmeterol and tiotropium when added to an inhaled corti
78 roup) was randomly assigned to continue both salmeterol and triamcinolone for the remaining 16 weeks
79 riod, no significant differences between the salmeterol and triamcinolone groups were observed for co
80 inhaled combined long-acting beta2-agonist (salmeterol) and corticosteroid (fluticasone propionate)
81 /- 0.89 mm Hg (mean +/- SEM) at 30 min after salmeterol, and -3.45 +/- 0.92 mm Hg at 20 min after alb
82 patients received 18 mug tiotropium, 100 mug salmeterol, and 1000 mug fluticasone propionate daily fo
83 th tiotropium doses were similar to those of salmeterol, and all active compounds had good safety and
87 ts that the high affinity and selectivity of salmeterol are due to specific amino acids within the re
88 ior to the combination of beclomethasone and salmeterol as judged by protection against asthma treatm
89 d a randomized, double-blind trial comparing salmeterol at a dose of 50 microg plus fluticasone propi
91 , combination therapy with 100 microg FP and salmeterol augmented the action of FP on GR nuclear loca
93 biochemical evidence demonstrates that when salmeterol binds to the receptor, its hydrophobic arylox
95 maintained with long-term administration of salmeterol, but the length of time that the drug remains
98 onclusion, this study shows that fluticasone/salmeterol combination decreases extracellular matrix re
99 valents, was reduced to 64 +/- 9 microL with salmeterol compared with 119 +/- 51 microL in saline-tre
100 on of primary microglial-enriched cells with salmeterol could inhibit the inflammatory response induc
101 ination of the LTRA montelukast and the LABA salmeterol could provide an effective therapeutic strate
104 In addition to genotype, FEV1, response to salmeterol, degree of EIB, and exhaled nitric oxide (FE(
105 PEF, l/min) after 16 weeks of treatment with salmeterol (DeltaPEFsal) versus montelukast (DeltaPEFmon
106 r for both agonists demonstrated significant salmeterol desensitization, although it was reduced rela
107 nflammation and therapeutically administered salmeterol, dexamethasone, or the PP2A-activating drug (
109 rticosteroid treatment, chronic therapy with salmeterol does not result in tolerance to the bronchodi
110 +/- 4.1% bronchoprotection) after the first salmeterol dose, and 22.8 +/- 3.2% (18.9 +/- 11.5% bronc
112 moterol solution or 50 mug of large-particle salmeterol dry powder twice daily plus inhaled corticost
113 ction on guinea pig trachea, and longer than salmeterol duration of action in vivo, suitable for once
118 hat administration of extremely low doses of salmeterol exhibit potent neuroprotective effects by inh
119 icasone (F), (2) once daily fluticasone plus salmeterol (F + S), or (3) once daily oral montelukast (
121 horses/group) were treated with fluticasone, salmeterol, fluticasone/salmeterol, or with antigen avoi
122 indacaterol-glycopyrronium group than in the salmeterol-fluticasone group (0.98 vs. 1.19; rate ratio,
123 indacaterol-glycopyrronium group than in the salmeterol-fluticasone group (3.59 vs. 4.03; rate ratio,
124 time to the first exacerbation than did the salmeterol-fluticasone group (71 days [95% CI, 60 to 82]
125 indacaterol-glycopyrronium group than in the salmeterol-fluticasone group (hazard ratio, 0.78; 95% CI
128 terol-glycopyrronium was more effective than salmeterol-fluticasone in preventing COPD exacerbations
129 only noninferiority but also superiority to salmeterol-fluticasone in reducing the annual rate of al
130 effect of indacaterol-glycopyrronium versus salmeterol-fluticasone on the rate of COPD exacerbations
131 -acting beta2-agonist/inhaled corticosteroid salmeterol/fluticasone combination 50/500 mug in patient
132 glycopyrronium was significantly superior to salmeterol/fluticasone for the prevention of exacerbatio
133 ischarge from hospital patients were given a salmeterol/fluticasone inhaler with an INCA device attac
134 wk double-blind study to placebo (n = 73) or salmeterol/fluticasone propionate 50/500 microg (n = 67)
135 m provides superior or similar benefits over salmeterol/fluticasone regardless of blood eosinophil le
136 50 cells/mul subgroups, and at no cutoff was salmeterol/fluticasone superior to indacaterol/glycopyrr
137 f pneumonia was higher in patients receiving salmeterol/fluticasone than indacaterol/glycopyrronium i
139 AW264.7 and THP-1 cells were pretreated with salmeterol, followed by PgLPS, and monitored for product
143 pium was also noninferior to the addition of salmeterol for all assessed outcomes and increased the p
146 significantly (p </= 0.001) greater with the salmeterol/FP combination product (0.48 L) than with pla
147 g of fluticasone propionate and 50 microg of salmeterol [FSC]) administered twice daily through the D
148 g (1.33, 1.03-1.72; p=0.031) groups, and the salmeterol group (1.46, 1.13-1.89; p=0.0039), than in th
149 Adverse events were less frequent in the salmeterol group (55 vs. 70; OR, 0.63; 95% CI, 0.39-0.99
150 m 2.5 mug group, and 196 mL (158-234) in the salmeterol group (all p<0.0001); difference in trough FE
151 ), the tiotropium 2.5 mug group (n=520), the salmeterol group (n=541), or the placebo group (n=523);
153 ebo-minus group was assigned and half of the salmeterol group (salmeterol-minus group) was randomly a
155 208 patients, 27 patients in the fluticasone-salmeterol group and 21 in the fluticasone-alone group h
156 al of 265 patients (8.5%) in the fluticasone-salmeterol group and 309 (10.0%) in the fluticasone-alon
157 36 events in 34 patients in the fluticasone-salmeterol group and 38 events in 33 patients in the flu
159 xacerbation was 21% lower in the fluticasone-salmeterol group than in the fluticasone-only group (haz
160 ious asthma-related event in the fluticasone-salmeterol group was 1.03 (95% confidence interval [CI],
161 ors, incidence rates of severe asthma in the salmeterol group were not elevated for emergency care (r
162 up, 15.2% in the placebo group, 13.5% in the salmeterol group, and 16.0% in the fluticasone group.
163 480 of 5834 patients (8%) in the fluticasone-salmeterol group, as compared with 597 of 5845 patients
167 ng montelukast and 46% of patients receiving salmeterol had a maximal percentage decrease in FEV1 of
168 is study, the authors sought to determine if salmeterol had a similar inhibitory effect on the inflam
170 switched to treatment with fluticasone plus salmeterol had treatment failure, as compared with 30.3%
171 onstriction) with fluticasone propionate and salmeterol in a combination product was a more effective
172 n this trial involving children with asthma, salmeterol in a fixed-dose combination with fluticasone
175 greater improvements with formoterol versus salmeterol in all IOS outcomes and FEF25-75, but not FEV
176 evaluate the risk of administering the LABA salmeterol in combination with an inhaled glucocorticoid
178 may have an impaired therapeutic response to salmeterol in either the absence or presence of concurre
180 ects of long-acting beta2AR agonists such as salmeterol in rodent models of Parkinson's disease.
181 yl ring of the aralkyloxyalkyl side chain of salmeterol in the beta 2AR binding site, we designed and
183 ference at 60 minutes between formoterol and salmeterol in total airway resistance at 5 Hz, 7.50% (95
184 treated with the selective beta2-AR agonist, salmeterol, in the presence of osteogenic medium showed
185 desensitization, we examined the kinetics of salmeterol-induced cAMP accumulation (0-30 minutes) in h
186 roid, two during double-blind treatment with salmeterol/inhaled corticosteroid, and one during double
193 Combination therapy with theophylline or salmeterol may allow clinicians to minimize the dose of
194 nflammation by PgLPS, suggesting that use of salmeterol may be an effective treatment in inhibiting o
195 ptor kinase/arrestin and protein kinase A in salmeterol-mediated desensitization through bioluminesce
197 e occurred in 46.3% (95% CI, 34%-59%) of the salmeterol-minus group 8 weeks after triamcinolone thera
198 95% confidence interval [CI], 2%-15%) of the salmeterol-minus group 8 weeks after triamcinolone treat
199 f the triamcinolone elimination phase in the salmeterol-minus group was 4.3 (2.0-9.2) compared with t
200 s assigned and half of the salmeterol group (salmeterol-minus group) was randomly assigned to reduce
202 doses of triamcinolone cannot be switched to salmeterol monotherapy without risk of clinically signif
203 asthma-related deaths was obtained from the Salmeterol Multi-center Asthma Research Trial (SMART).
206 flow (PEF; p = 0.005) in B16Arg/Arg subjects(salmeterol, n = 12; placebo, n = 5) as compared with B16
208 Seven Arg/Arg participants (placebo, n=5; salmeterol, n=2) and six Gly/Gly participants (placebo,
211 he effect of the long-acting beta(2)-agonist salmeterol on airway inflammation induced by segmental a
212 of Indacaterol Glycopyronium vs Fluticasone Salmeterol on COPD Exacerbations) study, which compared
213 the effects of treatment with tiotropium or salmeterol on exacerbations in 7376 patients with COPD.
217 ticosteroid arms (fluticasone propionate and salmeterol or fluticasone furoate and vilanterol); a con
220 e statistically significantly increased with salmeterol (OR, 1.7 [CI, 1.1 to 2.7]) and formoterol (OR
221 relative to baseline over that with placebo, salmeterol, or FP at Day 1, Week 1, and Week 12 (p </= 0
223 ed with fluticasone, salmeterol, fluticasone/salmeterol, or with antigen avoidance for 12 weeks.
225 s) or once-daily fluticasone propionate plus salmeterol (our secondary hypothesis) has not yet been d
230 The other half of the salmeterol group (salmeterol-plus group) was randomly assigned to continue
234 m (10 minutes) or long-term (2 and 14 hours) salmeterol pretreatments, we found that salmeterol progr
235 urs) salmeterol pretreatments, we found that salmeterol progressively depressed isoproterenol stimula
236 s (epinephrine, terbutaline, metaproterenol, salmeterol, propranolol, alprenolol, bisoprolol, ICI 118
237 Systemic or intranasal administration of salmeterol protected against the development of allergen
239 ents and, after adjusting for baseline risk, salmeterol recipients did not have a greater risk than t
240 th recipients of other beta-agonists, future salmeterol recipients had higher rates of asthma hospita
241 RET demonstrated a much reduced efficacy for salmeterol recruitment of arrestin to beta2AR relative t
248 with an inhaled long-acting beta(2)-agonist, salmeterol (S), to treat the inflammatory and bronchocon
249 the double mutant beta2-H296K-K305D, reduced salmeterol's affinity by 275-fold, to within 4-fold of t
250 5) had the largest single effect by reducing salmeterol's affinity for the beta2-adrenoceptor by 31-f
253 desensitization, demonstrating that although salmeterol shows weak efficacy for adenylyl cyclase acti
258 ffects of fluticasone propionate (FP) and of salmeterol (SM), on the response of well-differentiated
259 ntermediate strengths, such as albuterol and salmeterol, stimulate GRK site phosphorylations that are
260 better exacerbation outcomes in response to salmeterol than Gly16Gly and Arg16Gly genotypes, suggest
261 es higher when participants were assigned to salmeterol than when assigned to placebo (p<0.0001).
262 r when participants were assigned to receive salmeterol than when assigned to receive placebo (p<0.00
263 r when participants were assigned to receive salmeterol than when assigned to receive placebo (p<0.00
264 re significantly greater with tiotropium and salmeterol than with placebo and were similar in both st
266 s with severe COPD receiving tiotropium plus salmeterol, the risk of moderate or severe exacerbations
272 eeks with the combination of montelukast and salmeterol to that with the combination of beclomethason
274 ter increased to only 180 +/- 30 microL with salmeterol treatment, compared with 296 +/- 65 microL in
275 ne Modifier Corticosteroid or Corticosteroid-Salmeterol) trial of the American Lung Association Airwa
276 erformed less well for patients treated with salmeterol/triamcinolone during the entire study duratio
277 07], respectively, for patients treated with salmeterol/triamcinolone during the first half of the SL
278 acebo-controlled study with either 50 microg salmeterol twice daily (n=372), 500 microg fluticasone t
279 izations); the hazard ratio with fluticasone-salmeterol versus fluticasone alone was 1.28 (95% confid
280 ce the differential bronchodilator effect of salmeterol versus montelukast as an add-on therapy to IC
281 in determining the differential response to salmeterol versus montelukast in patients with chronic a
282 GER4 could explain differential responses to salmeterol versus montelukast using the participants of
284 hort, compared with placebo, the addition of salmeterol was associated with a 51.4 L/min lower A.M. p
286 g16Gly polymorphism on treatment response to salmeterol was dependent on the use of inhaled corticost
293 orticoid fluticasone and the beta(2)-agonist salmeterol, whereas MCP-1 inhibition was post-transcript
295 ects were randomized to regular therapy with salmeterol while simultaneously discontinuing ICS therap
296 ompared the acute effects on gas exchange of salmeterol with those of albuterol and the anticholinerg
297 sed the prebronchodilator FEV1 more than did salmeterol, with a difference of 0.11 liters (P=0.003).
298 n be switched to once-daily fluticasone plus salmeterol without increased rates of treatment failure.
299 icasone propionate (FP) 100 mug, FP 500 mug, salmeterol xinafoate (SLM) 50 mug, and combination FP 10
300 her placebo (placebo-minus group, n = 21) or salmeterol xinafoate, 42 microg twice per day (n = 154)
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