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A new antileukotriene medication being tested

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It looks more powerful than Singulair becauses it addresses 2 leukotriene

receptors instead of one.

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Int Arch Allergy Immunol. 2011;155 Suppl 1:90-5. Epub 2011 Jun 1.

Effects of a cysteinyl leukotriene dual 1/2 receptor antagonist on

antigen-induced airway hypersensitivity and airway inflammation in a guinea pig

asthma model.

Muraki M, Imbe S, Santo H, Sato R, Sano H, Iwanaga T, Tohda Y.

Source

Department of Respiratory Medicine and Allergology, Nara Hospital, Kinki

University Faculty of Medicine, Ikoma, Japan. muraki@...

Abstract

BACKGROUND:

Little is known about the role of the cysteinyl leukotriene (cysLT) 2 receptor

in the pathophysiology of asthma. The aim of this study is to investigate the

effects of a cysLT1 receptor antagonist (montelukast) and a dual cysLT1/2

receptor antagonist (BAY-u9773) on airway hypersensitivity and airway

inflammation induced by antigen challenge in ovalbumin (OVA)-sensitized guinea

pigs.

METHODS:

Male Hartley guinea pigs sensitized with OVA were intraperitoneally administered

0.1, 1, or 10 mg/kg of montelukast or 0.1 mg/kg of BAY-u9773 and then challenged

with inhaled OVA. Airway reactivity to acetylcholine, inflammatory cells in

bronchoalveolar lavage (BAL) fluid, and eosinophil infiltration in airway walls

after OVA challenge were evaluated.

RESULTS:

Pretreatment with 1 or 10 mg/kg, but not 0.1 mg/kg, of montelukast significantly

suppressed airway hypersensitivity and eosinophil infiltration into the BAL

fluid. Moreover, 0.1 mg/kg of BAY-u9773 significantly suppressed the development

of these markers. The suppressive effects of BAY-u9773, although not

significantly different, trended toward being greater than those of montelukast.

Although all of the doses of montelukast tested and 0.1 mg/kg of BAY-u9773

significantly suppressed eosinophil infiltration in airway walls, the

suppressive effect of BAY-u9773 was significantly greater than that of 0.1 mg/kg

of montelukast.

CONCLUSION:

Signaling may contribute to the pathophysiology of asthma via the cysLT1/2

receptor.

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