Long-Acting Anticholinergic Therapy in Asthma Management

Long-acting anticholinergic agents have emerged as a vital component in the management of moderate to severe asthma, complementing established therapies such as inhaled corticosteroids and long-acting β2-agonists. By blocking muscarinic M3 receptors in airway smooth muscle, these agents reduce vagally mediated bronchoconstriction and mucus secretion. Clinical implementation of long-acting muscarinic antagonists (LAMAs) has been supported by robust evidence demonstrating improvements in lung function, symptom control and exacerbation rates across a broad spectrum of asthma phenotypes. Beyond bronchodilation, LAMAs modulate epithelial and immune cell function, attenuating acetylcholine-driven inflammation and airway remodelling. The favourable safety profile, ease of once-daily dosing and compatibility with combination inhalers have driven global uptake. Recent formulation advances—such as extrafine particle technology—enhance peripheral airway deposition, while single-molecule dual pharmacology constructs integrate anticholinergic and β2-agonist properties to maximise bronchoprotection. Long-acting anticholinergic therapy thus represents a strategic addition to personalised asthma care, addressing unmet clinical needs and reducing the burden of uncontrolled disease.

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Long-Acting Anticholinergic Therapy in Asthma Management publication trend

The graph below shows the total number of articles in long-acting anticholinergic therapy in asthma management across all publications each year (not limited to Nature Index journals).

Technical terms

Muscarinic Receptor: G protein-coupled receptor activated by acetylcholine, mediating airway smooth muscle contraction.

Anticholinergic: Agent that inhibits acetylcholine action at muscarinic receptors to induce bronchodilation.

Long-Acting Muscarinic Antagonist (LAMA): Anticholinergic with sustained receptor blockade, permitting once-daily dosing.

Inhaled Corticosteroid (ICS): Anti-inflammatory drug delivered directly to the airways to reduce mucosal inflammation.

Long-Acting β2-Agonist (LABA): Bronchodilator that stimulates β2-adrenergic receptors over an extended period.

Airway Remodelling: Structural changes in the bronchial wall including smooth muscle hypertrophy and subepithelial fibrosis.

Airway Hyperresponsiveness: Exaggerated bronchoconstrictive response to stimuli, characteristic of asthma.

References

1. The Bronchoprotective Effects of Dual Pharmacology, Muscarinic Receptor Antagonist and β2 Adrenergic Receptor Agonist Navafenterol in Human Small Airways. Cells (2023).
2. The effect of combining an inhaled corticosteroid and a long-acting muscarinic antagonist on human airway epithelial cells in vitro. Respiratory Research (2024).
3. Muscarinic receptor signaling in the pathophysiology of asthma and COPD. Respiratory Research (2006).
4. Determinants of response to inhaled extrafine triple therapy in asthma: analyses of TRIMARAN and TRIGGER. Respiratory Research (2020).
5. Pro-inflammatory mechanisms of muscarinic receptor stimulation in airway smooth muscle. Respiratory Research (2010).
6. Comparing LAMA with LABA and LTRA as add-on therapies in primary care asthma management. npj Primary Care Respiratory Medicine (2020).