SINGULAIR is a leukotriene receptor antagonist (LTRA), the first new class of anti-inflammatory agents to treat asthma in more than two decades.¹

Asthma
Asthma is a chronic inflammatory disease characterized by recurrent respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing.^2,3 The inflammatory cascade in asthma is initiated by exposure to allergens or other triggers, such as cold air and exercise.^2,4 The subsequent activation of inflammatory cells (eosinophils, mast cells, basophils, and macrophages) results in the release of inflammatory mediators, including cysteinyl leukotrienes,⁵ which mediate an important pathway of inflammation in the airways.^1,3,6

Cysteinyl leukotrienes recruit important inflammatory cells, which produce substances that can lead to epithelial cell damage and initiate further production and release of leukotrienes and other inflammatory mediators.Cysteinyl leukotrienes are known to cause changes in microvascular permeability, which lead to edema and swelling of the airway tissues. The effects of cysteinyl leukotrienes also mediate excess mucus production. Finally, the contractile effects of cysteinyl leukotrienes on the smooth muscle within airway walls mediate potent and sustained bronchoconstriction, up to 5000 times more potent than histamine.^5,7-10*

SINGULAIR binds with high affinity and selectivity to the type-1 cysteinyl leukotriene receptors (CysLT₁) found in the human airway and subsequently blocks the leukotriene pathway of inflammation.

Steroid-sensitive mediators represent a different pathway of inflammation.¹¹ It is important to note, however, that corticosteroids do not block the formation of cysteinyl leukotrienes in the airways of asthmatic patients.^9,11,12 Therefore, a treatment strategy targeting only steroid-sensitive mediators leaves the leukotriene pathway unchecked, potentially leading to continued inflammation and asthma symptoms.