ライフサイエンスコーパス: montelukast

1 o; P < 0.01 for beclomethasone compared with montelukast).

2 o; P < 0.01 for beclomethasone compared with montelukast).

3 , of whom 77 473 individuals were exposed to montelukast.

4 reported in preclinical models with adjuvant montelukast.

5 g patients with allergic rhinitis exposed to montelukast.

6 umilast plus montelukast versus placebo plus montelukast.

7 resence or absence of the CysLT1R antagonist montelukast.

8 pack years tended to show more benefit with montelukast.

9 compared with 30.3% of subjects switched to montelukast.

10 lent doses of the CysLT1 receptor antagonist montelukast.

11 ntigen challenge in six animals treated with montelukast (0.15 mg/kg, intravenously) 30 minutes befor

12 is toxin IgG) and randomly assigned (1:1) to montelukast 10 mg daily or image-matched placebo for 2 w

13 mized crossover period to receive additional montelukast 10 mg daily or placebo for 3 weeks each.

14 ol 500/50 mug one inhalation twice daily and montelukast 10 mg/day.

15 te nasal spray (200 mug once daily), or oral montelukast (10 mg once daily) administered for 2 weeks

16 omly assigned to double-blind treatment with montelukast (10 mg once in the evening) or salmeterol (5

17 Subjects scored symptoms daily in 7 montelukast (10 mg, n = 6799), 9 desloratadine (5 mg, n

18 Montelukast, 10 mg once daily at bedtime; inhaled beclom

19 Participants were randomized 1:1 to receive montelukast, 10 mg once daily, or matched placebo for 14

20 rystal structures of P450 2C8 complexed with montelukast (2.8 A), troglitazone (2.7 A), felodipine (2

21 f beta2AR agonists (430,885 individuals) and montelukast (23,315 individuals) from July 1, 2005 to Ju

22 one (100 microg twice daily) (169 patients), montelukast (5 or 10 mg each night) (166 patients), or f

23 cebo run-in period, patients received either montelukast (5-mg chewable tablet) or matching-image pla

24 cough-specific quality of life improvement (montelukast: 5.2, 4.5-5.9; placebo: 5.9, 5.1-6.7; mean d

25 a placebo run-in period to receive 10 mg of montelukast (54 patients) or placebo (56 patients) once

26 ved standard therapy plus either intravenous montelukast (7 or 14 mg) or matching placebo.

27 study drug (99 [77%] of 129 participants on montelukast; 93 [72%] of 130 on placebo).

28 The patients received 10 mg of montelukast (98 patients) or placebo (124 patients) for

29 Montelukast, a CysLT1 antagonist, completely inhibited L

30 The effect of LTE4 was inhibited by montelukast, a CysLT1 antagonist.

31 In this study, we determined whether montelukast, a cysteinyl leukotriene 1 receptor antagoni

32 We investigated the effectiveness of montelukast, a cysteinyl leukotriene receptor antagonist

33 nduced diabetes mouse model, we administered montelukast, a leukotriene receptor antagonist, and diab

34 We aimed to assess whether montelukast, a leukotriene receptor antagonist, can impr

35 drug might provide benefit if combined with montelukast, a leukotriene receptor antagonist, in patie

36 We evaluated the ability of montelukast, a leukotriene-receptor antagonist, to prote

37 ung (4 months) and old (20 months) rats with montelukast, a marketed anti-asthmatic drug antagonizing

38 nance treatment strategy than treatment with montelukast, a single-mediator antagonist.

39 85; percentage difference, -17%; P = .0026), montelukast (absolute difference, -0.74; percentage diff

40 osinophilic gastroenteritis who responded to montelukast alone as a first line therapy.

41 eosinophilic gastroenteritis who responds to montelukast alone as a first line therapy.

42 f roflumilast with montelukast compared with montelukast alone improved lung function and asthma cont

43 dition of roflumilast and montelukast versus montelukast alone in patients with moderate-to-severe as

44 hidonic acid released by cPLA(2)alpha, using montelukast (an antagonist of the type 1 cysteinyl leuko

45 ologous molecule expressed on TH2 cells, and montelukast, an antagonist of cysteinyl leukotriene rece

46 Montelukast, an oral, once-daily leukotriene receptor an

47 ts actively smoking cigarettes, both 10 mg/d montelukast and 250 mug of fluticasone propionate twice

48 This study evaluates 10 mg/d montelukast and 250 mug of fluticasone propionate twice

49 dose were used by 39% of patients receiving montelukast and 33% receiving placebo.

50 By week 8, 67% of patients receiving montelukast and 46% of patients receiving salmeterol had

51 ] years; 35 446 female [47.7%]); 26 462 used montelukast and 47 829 used LABA.

52 Among 628 participants who received montelukast and 622 who received placebo, differences in

53 Feverfew, montelukast and acupuncture have not proven effective.

54 he evidence base for the association between montelukast and adverse neuropsychiatric outcomes is mix

55 study, the cysteinyl leukotriene antagonist montelukast and antihistamine loratadine or two matched

56 with MFNS and numerically greater than with montelukast and desloratadine for SAR.

57 ), and 39% (placebo); the difference between montelukast and fluticasone was not significant (P = .14

58 -1.20) among patients with asthma exposed to montelukast and insomnia (OR, 1.15; 95% CI, 1.05-1.27) a

59 antial differences were observed between the montelukast and LABA patients when analyzing the risk of

60 ncluded children aged 6 to 17 years who used montelukast and long-acting beta-agonists (LABA).

61 Treatment with montelukast and loratadine inhibited the release of cyst

62 or wheezing episodes between children in the montelukast and placebo groups (mean 2.0 [SD 2.6] vs 2.3

63 n baseline, 14.8% versus 3.6% for the pooled montelukast and placebo treatment groups, respectively;

64 atment over 14 weeks with the combination of montelukast and salmeterol to that with the combination

65 The combination of montelukast and salmeterol was inferior to the combinati

66 flow readings, there were four responders to montelukast and seven responders to placebo.

67 etermine whether the combination of the LTRA montelukast and the LABA salmeterol could provide an eff

68 ice, there was no association between use of montelukast and the risk of neuropsychiatric adverse eve

69 ically different, clinically relevant LTRAs (montelukast and zafirlukast).

70 We report herein that montelukast and zafirlukast, acting in a concentration-d

71 etected for the CysLT1-selective antagonists montelukast and zafirlukast.

72 rs, and that both pathways were inhibited by montelukast and zafirlukast.

73 core was -0.62 for beclomethasone, -0.41 for montelukast, and -0.17 for placebo (P < 0.001 for each a

74 EV1 was 13.1% with beclomethasone, 7.4% with montelukast, and 0.7% with placebo (P < 0.001 for each a

75 icantly decreased by etoposide as well as by montelukast, and a combination of etoposide and monteluk

76 receptor-selective antagonists zafirlukast, montelukast, and MK-571 did not inhibit the agonist-medi

77 include the leukotriene receptor antagonist montelukast, and other anti-allergy drugs such as mast c

78 verse associations between beta2AR agonists, montelukast, and PD.

79 , receptor antagonists, such as zafirlukast, montelukast, and pobilukast, are potent and selective an

80 l bronchodilator effect of salmeterol versus montelukast as an add-on therapy to ICS within 16 weeks

81 essfully treated and achieved remission with montelukast as an initial monotherapy.

82 ases treated with the leukotriene antagonist montelukast as an initial therapy or as a second line th

83 d cysteinyl-leukotriene receptor antagonist, montelukast, as well as between baseline and after follo

84 of the small airways to inhaled steroids or montelukast associates with better asthma control.

85 ellcome, Research Triangle Park, NC) or with montelukast at 10 mg once daily.

86 Distinct from montelukast, ATLa treatment led to marked reductions in

87 production that was significantly reduced by montelukast before treatment.

88 beclomethasone had a larger mean effect than montelukast, both drugs provided clinical benefit to pat

89 The effect of LTE(4) was inhibited by montelukast but not by the P2Y(12) antagonist methylthio

90 h saline-treated controls and was reduced by montelukast, but not dexamethasone, administration.

91 Montelukast, but not dexamethasone, reversed the establi

92 r in vitro model also revealed that adjuvant montelukast can reduce injury to proximal tubule cells t

93 eatment course by addition of cetirizine and montelukast compared to the control group (p < 0.025).

94 The combination of roflumilast with montelukast compared with montelukast alone improved lun

95 We evaluated whether montelukast conferred additive effects in patients with

96 Thus, in patients taking FP/SM or FP, montelukast conferred complimentary effects on surrogate

97 ti-interleukin-13 therapy, anti-IgE therapy, montelukast, cromolyn, and anti-TNF therapy.

98 H(1)-antihistamines, montelukast, danazol, H(2)-antihistamines, pentoxifyllin

99 eatment with salmeterol (DeltaPEFsal) versus montelukast (DeltaPEFmon) was associated with the genoty

100 In the montelukast, desloratadine, and MFNS trials, TNSS overal

101 icosteroid dexamethasone, or the combination montelukast + dexamethasone.

102 apy in a hospital outpatient clinic setting, montelukast did not provide such additional benefit in p

103 th mild to moderate COVID-19, treatment with montelukast did not reduce duration of COVID-19 symptoms

104 Compared with placebo, addition of montelukast did not result in any significant change in

105 Our study suggests that montelukast during vancomycin therapy may be protective

106 rospect of lower PD incidence with high-dose montelukast exposure warrants further investigation, esp

107 ere 347, 336, and 336 patients randomized to montelukast, fluticasone, and placebo, respectively.

108 ukast (sequence AB) or placebo plus 10 mg of montelukast followed by 500 mug of roflumilast plus 10 m

109 mized to receive 500 mug of roflumilast plus montelukast followed by placebo plus 10 mg of montelukas

110 t; P < 0.01 for beclomethasone compared with montelukast for each end point).

111 for a potential role of the antiasthma drug montelukast for secondary prevention of cardiovascular d

112 These findings do not support the use of montelukast for the treatment of mild to moderate COVID-

113 The effectiveness of intermittent montelukast for wheeze in young children is unclear.

114 of rebound worsening of lung function in the montelukast group after the washout period.

115 s reported for 18 participants (2.9%) in the montelukast group and 18 (2.9%) in the placebo group (AH

116 nced serious adverse events (3 [0.5%] in the montelukast group and 2 [0.3%] in the placebo group).

117 percentage decrease in FEV1 was 57.2% in the montelukast group and 33.0% in the salmeterol group (P =

118 occurred in 108 patients, 32 patients in the montelukast group and 76 patients in the placebo group.

119 33% to 10.13%) increase from baseline in the montelukast group and a 3.58% (95% CI, 1.29% to 5.87%) i

120 FEV1 increased from 1.85 L to 2.01 L in the montelukast group and from 1.85 L to 1.93 L in the place

121 Sustained improvement occurred in the montelukast group at weeks 4 and 8; at these time points

122 y biomarkers were significantly lower in the montelukast group compared with the placebo group.

123 After 12 weeks of treatment, patients in the montelukast group were more likely to rate their asthma

124 igher in the placebo group compared with the montelukast Group.

125 ce in FEV1 response between the 7- and 14-mg montelukast groups.

126 order potency was pranlukast = zafirlukast > montelukast > pobilukast.

127 ater mean clinical benefit than montelukast, montelukast had a faster onset of action and a greater i

128 ndings indicated that compared with placebo, montelukast had a significant positive effect on remissi

129 Both zafirlukast and montelukast have affinities that are approximately two t

130 Leukotriene receptor antagonists such as montelukast have demonstrated efficacy in chronic asthma

131 tor antagonists pranlukast, zafirlukast, and montelukast, have been introduced recently as novel ther

132 Montelukast improved FEV1 over the first 20 minutes afte

133 Montelukast improves morning FEV1 in 6- to 14-year-old c

134 en patients were treated with cetirizine and montelukast in addition to conventional therapy, whereas

135 the steroid sparing effect of cetirizine and montelukast in addition to conventional treatment in MCN

136 We conclude that intravenous montelukast in addition to standard therapy causes rapid

137 ere x does not equal 5) modifies response to montelukast in adults, we stratified by this genotype.

138 inhibition of IL-13 by lebrikizumab, use of montelukast in asthmatic smokers, and a thorough review

139 tified in the evidence base on the safety of montelukast in observational studies.

140 e differential response to salmeterol versus montelukast in patients with chronic adult asthma.

141 The effect of montelukast in reducing symptom duration among outpatien

142 zing episodes were reduced in children given montelukast in the 5/5 stratum (2.0 [2.7] vs 2.4 [3.0];

143 vs 23% 2.5x fluticasone and 13% fluticasone/montelukast in the Best ADd-on Therapy Giving Effective

144 ndings show no clear benefit of intermittent montelukast in young children with wheeze.

145 and owing to the anti-leukotrienes effect of montelukast, in the present clinical trial, we aimed to

146 Spontaneous reports have indicated that montelukast increases the risk of neuropsychiatric adver

147 Montelukast inhibited the diabetes-induced capillary and

148 s of adverse neuropsychiatric outcomes after montelukast initiation.

149 mendations are impossible for mycophenolate, montelukast, intravenous immunoglobulins, and systemic g

150 Montelukast is a relatively large anionic inhibitor that

151 We aimed to assess whether intermittent montelukast is better than placebo for treatment of whee

152 Montelukast is not an effective treatment for postinfect

153 s salmeterol (F + S), or (3) once daily oral montelukast (M).

154 Montelukast may be an effective treatment for eosinophil

155 life occurred in both groups after 2 weeks (montelukast: mean 2.7, 95% CI 2.2-3.3; placebo: 3.6, 2.9

156 ed the effect of the antiinflammatory agents montelukast (ML) and fluticasone propionate (FP) on Qaw

157 oenteritis and was successfully treated with montelukast monotherapy.

158 one had a greater mean clinical benefit than montelukast, montelukast had a faster onset of action an

159 ect of the cysteinyl-LT receptor antagonist (montelukast [MT]) on ligature-induced experimental perio

160 Patients receiving montelukast (n = 110) were compared with controls (n = 3

161 , 2012, we randomly assigned 276 patients to montelukast (n=137) or placebo (n=139).

162 e randomly assigned 1358 children to receive montelukast (n=669) or placebo (n=677).

163 ntelukast, n=3; placebo, n=5), and headache (montelukast, n=2; placebo, n=6).

164 placebo, n=2), gastrointestinal disturbance (montelukast, n=3; placebo, n=5), and headache (monteluka

165 ts reported were increased mucus production (montelukast, n=6; placebo, n=2), gastrointestinal distur

166 role of the leukotriene receptor antagonist montelukast on future risk of incident and recurrent myo

167 ical trial, we aimed to assess the effect of montelukast on remission maintenance in patients with ul

168 cription for leukotriene receptor antagonist montelukast or control medication.

169 cells because inhibition of cysLT action by montelukast or cysLT synthesis by MK886, an inhibitor of

170 oblet cell metaplasia were reduced by either montelukast or dexamethasone alone.

171 d intranasal OVA periodically Days 14-73 and montelukast or dexamethasone or placebo from Days 73-163

172 ged 15 to 64 years at index prescription for montelukast or for control prescription who had a histor

173 schedule (size ten), to receive intermittent montelukast or placebo given by parents at each wheeze e

174 ith leukotriene-receptor antagonists such as montelukast or zafirlukast show good antiasthmatic activ

175 ere independently associated with AKI, while montelukast (OR, 0.26; 95% CI, .06-.77; P = .03) and mal

176 Montelukast originated from an early quinoline lead, whi

177 eceive a step-down treatment with once-daily montelukast (our primary hypothesis) or once-daily fluti

178 er of exacerbations (0 vs. 11) compared with montelukast (p < 0.001).

179 (23.0 +/- 2.5 vs. 15.5+/-2.4%) compared with montelukast (p < or = 0.001, all comparisons).

180 control over 6 months of treatment was 45% (montelukast, P < .05 vs placebo), 49% (fluticasone, P <

181 ated with double dose ICS (PUFFIN) or add-on montelukast (PACT).

182 , 310 neuropsychiatric adverse events in the montelukast patients and 566 events in the LABA patients

183 Using ADAS-6 as the primary end point in the montelukast pivotal trials would have significantly redu

184 he clinically prescribed receptor antagonist montelukast prevented their activation by active mast ce

185 Long-term administration of montelukast provided consistent inhibition of exercise-i

186 ared with placebo, once-daily treatment with montelukast provided significant protection against exer

187 matics, and the CysLT(1) receptor antagonist Montelukast reduced exosome-induced IL-8 secretion.

188 antigen challenge and that pretreatment with montelukast reduces this impairment.

189 sed asthma control; however, patients taking montelukast remained free of symptoms on 78.7% of treatm

190 rse event rates (21 (15%) of 137 patients on montelukast reported one or more adverse events; 31 (22%

191 andidate genes contributes to variability in montelukast response.

192 5/5 ALOX5 promoter genotype might identify a montelukast-responsive subgroup.

193 A switch to montelukast results in an increased rate of treatment fa

194 their effects on Th2 cells are mediated by a montelukast-sensitive receptor.

195 ontelukast followed by placebo plus 10 mg of montelukast (sequence AB) or placebo plus 10 mg of monte

196 owed by 500 mug of roflumilast plus 10 mg of montelukast (sequence BA).

197 nifestations; fluticasone, azithromycin, and montelukast should be used for bronchiolitis obliterans

198 Montelukast should only be used for AR if there has been

199 Pretreatment with montelukast significantly protected against this reducti

200 eukotriene(1) (CysLT(1)) receptor antagonist montelukast significantly reduced the airway eosinophil

201 LT(1) receptor-selective antagonists MK-571, montelukast (Singulair(TM)), zafirlukast (Accolate(TM)),

202 vair), (2) mometasone furoate (Asmanex), (3) montelukast (Singulair), and (4) budesonide/formoterol (

203 The CysLT1-selective antagonists, such as montelukast (Singulair), zafirlukast (Accolate) and pran

204 oids and additional therapy were given 10 mg montelukast sodium for 14 days in an outpatient clinic s

205 Montelukast sodium hydrate also rescues the inhibitory e

206 Among the top hits obtained, montelukast sodium hydrate binds to Nsp1 with a binding

207 We, therefore, propose montelukast sodium hydrate can be used as a lead molecul

208 A formal synthesis of the antiasthma drug montelukast sodium is described, wherein the key chiral

209 obtain the desired chiral diol precursor of montelukast sodium.

210 a were available for nasal antihistamines or montelukast sodium.

211 Patients treated with montelukast tended to receive less beta-agonists and hav

212 nyl leukotriene (CysLT)1 receptor antagonist montelukast, the corticosteroid dexamethasone, or the co

213 In patients exposed to montelukast, the odds ratio [OR] for any incident neurop

214 At 12 weeks, montelukast therapy offered significantly greater protec

215 Montelukast therapy was also associated with a significa

216 l intervention study for 16 weeks with daily montelukast therapy.

217 Compared with FP/SM run-in, adding montelukast to FP/SM was better (p < 0.05) than placebo

218 equired to evaluate whether these effects of montelukast translate into clinical benefits.

219 levels were observed during roflumilast plus montelukast treatment compared with placebo plus montelu

220 Montelukast treatment induced significant reductions in

221 ential adverse mental health symptoms during montelukast treatment, particularly in individuals with

222 elukast treatment compared with placebo plus montelukast treatment.

223 In contrast to these findings, montelukast use was associated with a lower risk for rec

224 alyses revealed a significant association of montelukast use with a lower risk for recurrent myocardi

225 atios (HRs) did not reveal an association of montelukast use with incident events.

226 ndertaken to examine the association between montelukast use, beta2-adrenoreceptor (beta2AR) agonist

227 ts were 2.39 per 100 patient-years among the montelukast users and 2.41 per 100 patient-years among t

228 lower PD incidence was noted among high-dose montelukast users when restricted to PD registered as th

229 differential responses to salmeterol versus montelukast using the participants of the J-Blossom stud

230 of action of the addition of roflumilast and montelukast versus montelukast alone in patients with mo

231 nt difference of 100 mL for roflumilast plus montelukast versus placebo plus montelukast.

232 om baseline in the placebo group (P<.001 for montelukast vs placebo).

233 The purpose of the study was to ascertain if montelukast was associated with a reduction in the preva

234 The bronchoprotective effect of montelukast was maintained throughout 8 weeks of study.

235 telukast, and a combination of etoposide and montelukast was significantly more effective in inhibiti

236 The tolerability profile for montelukast was similar to that observed for placebo, an

237 The combination of FP plus montelukast was superior to FP/SM for inflammatory marke

238 Overall, use of beta2AR agonists and montelukast were not related to PD incidence.

239 UC patients on high-dose corticosteroid and montelukast were recruited.

240 combinations are Ponatinib, Rilpivirine, and Montelukast, which together, reversed the toxic effects

241 ally distinct CysLTR antagonists pranlukast, montelukast, zafirlukast, and pobilukast; the rank order

242 The leukotriene receptor antagonists, montelukast, zafirlukast, and pranlukast, and the 5-lipo