SINGULAIR (montelukast) 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 large and small airways.^1,3,6 

Cysteinyl leukotrienes recruit important inflammatory cells, which produce proteins that 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.^5,7,9

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 trigger a second pathway of inflammation.¹⁰  It is important to note, however, that corticosteroids do not block the effects of cysteinyl leukotrienes in the airways of asthmatic patients.^9-11  Therefore, a treatment strategy targeting only steroid-sensitive mediators leaves the leukotriene pathway unchecked, potentially leading to continued inflammation and asthma symptoms.

SINGULAIR, when prescribed as the important partner to inhaled corticosteroids, represents a preferred treatment approach that targets dual pathways of inflammation. 

SINGULAIR as controller therapy provided substantial benefits to adult and pediatric patients with chronic asthma in clinical trials: 

• Improvement in key parameters of chronic airway inflammation ^12,13
     – reduction in airway and peripheral blood eosinophils
     – inhibition of EAR and LAR to antigen challenge
• Clinical control of asthma as reflected by ^14,15
     – improved respiratory function
     – control of asthma symptoms
     – reduced use of "as needed" beta₂ agonists
     – rapid onset of action (within the first day)
     – improved quality of life
• Additive effects to those of inhaled corticosteroids in clinical trials¹⁵
• Reduction in inhaled corticosteroid dose in patients requiring moderate
  to high doses of corticosteroids¹⁶
• Prevention of exercise-induced bronchoconstriction without development of tolerance over 8 weeks in a clinical study of patients with mild asthma¹⁷
• Effectiveness in aspirin-sensitive asthmatic patients
• Tolerability comparable to that of placebo
• Convenient once-daily bedtime dosing

• SINGULAIR improved day and nighttime symptoms^14,15
• SINGULAIR reduces asthma attacks¹⁵
• SINGULAIR in complementary therapy improved patients' quality of life (based on symptoms, activity limitation, emotional function, and environmental stimuli domains)¹⁸
• SINGULAIR relieved a broad range of asthma symptoms in children (cough, wheeze, trouble breathing, overnight symptoms)¹⁹
• SINGULAIR with an ICS provided better control of inflammation¹⁵by targeting the dual pathways