Revefenacin for the treatment of chronic obstructive pulmonary disease

ABSTRACT

Introduction: Acetylcholine is the predominant parasympathetic neurotransmitter in the airways, and plays a key role in the pathophysiology of chronic obstructive pulmonary disease (COPD). Muscarinic receptors are found in smooth muscle cells and submucosal glands. Binding of acetylcholine to muscarinic receptors could trigger bronchoconstriction. Muscarinic antagonists prevent acetylcholine from binding to its receptors and produce bronchodilation. Revefenacin is the first once-daily dosed nebulized long-acting muscarinic antagonist indicated for the maintenance treatment of patients with COPD.

Areas covered: In this paper, the chemical properties, mechanism of action, pharmacokinetics, clinical efficacy and safety of Revefenacin was introduced, and the evolution of muscarinic antagonists is also briefly described.

Expert commentary: Revefenacin is a new M₃ muscarinic receptor antagonist, which could prevent acetylcholine from binding with the muscarinic receptor, making bronchodilation and relieving COPD symptoms. Revefenacin has a rapid onset of action, and the curative effect is to maintain a long time. Clinical trials showed that Revefenacin could significantly increase forced expiratory volume in 1 s (FEV₁) in patients with COPD and improve their quality of life. The recommended dose of Revefenacin inhalation solution is 175 μg once daily. Adverse reactions were mild and the drug was well tolerated.

KEYWORDS:

• Chronic obstructive pulmonary disease
• forced expiratory volume in 1 s
• long-acting muscarinic antagonists
• muscarinic receptor
• revefenacin

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer Disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.