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1 , clinically relevant LTRAs (montelukast and zafirlukast).
2 h pathways were inhibited by montelukast and zafirlukast.
3 ing corticosteroid withdrawal facilitated by zafirlukast.
4 CysLT1-selective antagonists montelukast and zafirlukast.
5 nd remained higher 10 h after treatment with zafirlukast (2.7 versus 1.9 ppm; p = 0.09).
6                   Subjects were treated with zafirlukast (20 mg) or placebo on two treatment days 5 t
7 gonists MK-571, montelukast (Singulair(TM)), zafirlukast (Accolate(TM)), and pranlukast (Onon(TM)) ex
8 ntagonists, such as montelukast (Singulair), zafirlukast (Accolate) and pranlukast (Onon), are import
9        We report herein that montelukast and zafirlukast, acting in a concentration-dependent manner,
10                                              Zafirlukast also exhibited evidence of an anti-inflammat
11                      In registration trials, zafirlukast, an asthma medication, caused asymptomatic e
12        Comparable results were obtained with zafirlukast, an LTD4-receptor antagonist.
13                                         Both zafirlukast and montelukast have affinities that are app
14 h the CysLT receptor antagonists pranlukast, zafirlukast, and montelukast, have been introduced recen
15  CysLTR antagonists pranlukast, montelukast, zafirlukast, and pobilukast; the rank order potency was
16 ukotriene receptor antagonists, montelukast, zafirlukast, and pranlukast, and the 5-lipoxygenase inhi
17 te that both the cysLT1 receptor antagonist, zafirlukast, and the 5-LO inhibitor, zileuton, improve p
18                                              Zafirlukast antagonized LTD4-induced bronchoconstriction
19                                   In humans, zafirlukast antagonized the effects of exogenously admin
20                       A single 20-mg dose of zafirlukast attenuated SO2-induced bronchoconstriction.
21 ease of leukotrienes and that treatment with zafirlukast attenuates the bronchoconstrictor response.
22   PC8SRaw was significantly higher 2 h after zafirlukast compared with placebo (3.1 versus 1.5 ppm; p
23 rome developed while patients were receiving zafirlukast from 3 days to 4 months and from 3 days to 3
24 ast; the rank order potency was pranlukast = zafirlukast > montelukast > pobilukast.
25                              Minocycline and zafirlukast have been increasingly used, and were report
26 , no cases of severe hepatitis attributed to zafirlukast have been reported.
27                In clinical models of asthma, zafirlukast inhibited bronchospasm after allergen or exe
28                                              Zafirlukast is a potent leukotriene antagonist that rece
29                                              Zafirlukast is an orally active and selective cysteinyl
30                                              Zafirlukast is based on a lead compound that incorporate
31  from these clinical trials demonstrate that zafirlukast is effective and safe for the prophylactic t
32                           Patients receiving zafirlukast may develop severe liver injury and should b
33 rent CysLT(1) receptor-selective antagonists zafirlukast, montelukast, and MK-571 did not inhibit the
34 ed that cysLT, receptor antagonists, such as zafirlukast, montelukast, and pobilukast, are potent and
35 tment with either inhaled budesonide or oral zafirlukast over a one-year period.
36             An association was found between zafirlukast plasma concentrations and increases in PC8SR
37       Blood samples were collected to assess zafirlukast plasma concentrations versus effect.
38 als in patients with chronic, stable asthma, zafirlukast reduced asthma symptoms, decreased as-needed
39 -receptor antagonists such as montelukast or zafirlukast show good antiasthmatic activity over a wide
40          Collectively, the data suggest that zafirlukast therapy alters cellular infiltration and act
41                                        Daily zafirlukast therapy did not differ significantly from in
42                           Discontinuation of zafirlukast therapy in three patients, steroid therapy i
43  compared with intermittent therapy or daily zafirlukast therapy, daily budesonide therapy produced g
44 al syndrome improved with discontinuation of zafirlukast treatment and reinitiation of corticosteroid
45 osinophilia may have occurred independent of zafirlukast use or may have resulted from an allergic re
46  dose of the leukotriene receptor antagonist zafirlukast was assessed in a double-blind, placebo-cont
47                        The safety profile of zafirlukast was not clinically different from placebo.
48                                The effect of zafirlukast (Z) to alter the inflammatory response to se

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