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 umilast plus montelukast versus placebo plus montelukast.

4 resence or absence of the CysLT1R antagonist montelukast.

5 pack years tended to show more benefit with montelukast.

6 compared with 30.3% of subjects switched to montelukast.

7 lent doses of the CysLT1 receptor antagonist montelukast.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

23 Montelukast, a CysLT1 antagonist, completely inhibited L

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

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

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

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

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

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

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

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

32 85; percentage difference, -17%; P = .0026), montelukast (absolute difference, -0.74; percentage diff

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

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

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

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

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

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

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

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

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

42 Feverfew, montelukast and acupuncture have not proven effective.

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

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

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

46 Treatment with montelukast and loratadine inhibited the release of cyst

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 production that was significantly reduced by montelukast before treatment.

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

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

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

70 Montelukast, but not dexamethasone, reversed the establi

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

72 We evaluated whether montelukast conferred additive effects in patients with

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

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

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

76 icosteroid dexamethasone, or the combination montelukast + dexamethasone.

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

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

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

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

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

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

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

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

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

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

87 33% to 10.13%) increase from baseline in the montelukast group and a 3.58% (95% CI, 1.29% to 5.87%) i

88 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

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

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

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

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

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

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

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

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

97 Montelukast improved FEV1 over the first 20 minutes afte

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

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

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

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

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

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

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

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

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

107 Montelukast is a relatively large anionic inhibitor that

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

109 Montelukast is not an effective treatment for postinfect

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

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

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

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

114 , 2012, we randomly assigned 276 patients to montelukast (n=137) or placebo (n=139).

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

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

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

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

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

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

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

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

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

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

125 Montelukast originated from an early quinoline lead, whi

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

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

128 (23.0 +/- 2.5 vs. 15.5+/-2.4%) compared with montelukast (p < or = 0.001, all comparisons).

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

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

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

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

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

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

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

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

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

138 andidate genes contributes to variability in montelukast response.

139 5/5 ALOX5 promoter genotype might identify a montelukast-responsive subgroup.

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

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

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

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

144 Pretreatment with montelukast significantly protected against this reducti

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

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

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

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

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

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

151 obtain the desired chiral diol precursor of montelukast sodium.

152 a were available for nasal antihistamines or montelukast sodium.

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

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

155 At 12 weeks, montelukast therapy offered significantly greater protec

156 Montelukast therapy was also associated with a significa

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

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

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

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

161 Montelukast treatment induced significant reductions in

162 elukast treatment compared with placebo plus montelukast treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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