Zileuton is used in chronic asthma but differs from montelukast in its mechanism because zileuton:

• A Blocks CysLT1 receptors on bronchial smooth muscle preventing leukotriene-induced bronchoconstriction
• B Inhibits 5-lipoxygenase, blocking synthesis of all leukotrienes including LTB4 and CysLTs upstream ✓
• C Inhibits 15-lipoxygenase, preventing lipoxin synthesis and resolving airway inflammation
• D Blocks COX-2 selectively reducing prostaglandin-mediated bronchodilator prostaglandin E2

Explanation

Zileuton inhibits 5-lipoxygenase (5-LOX), the enzyme that converts arachidonic acid to 5-HPETE and then to LTA4, the common precursor of all leukotrienes (LTB4, LTC4, LTD4, LTE4). This blocks synthesis of all leukotrienes including chemotactic LTB4 (neutrophil recruitment) and cysteinyl leukotrienes (bronchoconstriction, mucus secretion). Montelukast/zafirlukast block only CysLT1 receptors (downstream), missing LTB4 effects. Option C (15-LOX) produces lipoxins and anti-inflammatory mediators — not zileuton's mechanism.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.