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Inhaled therapeutics in chronic obstructive pulmonary disease
Published in Anthony J. Hickey, Heidi M. Mansour, Inhalation Aerosols, 2019
Tejas Sinha, Paul Dejulio, Philip Diaz
Anticholinergic inhalational agents are a backbone of both COPD maintenance and rescue therapy. In fact, the use of anticholinergic agents can be traced back over two centuries; Datura Stramonium and other members of the nightshade family contain mixtures of muscarinic antagonists and were smoked for relief of asthma symptoms (30). Much progress has been made in the last century, initially with the isolation of atropine, followed by the development of inhaled ipratropium bromide with respiratory system selectivity, and finally the advent of LAMA therapy with specific subreceptor selectivity (31). The first LAMA agent commercially available was tiotropium bromide. Its preferential long-lasting binding to muscarinic receptor subtypes and ease of once daily use have been considered to be the primary reasons for its clinical success relative to its shorter-acting counterpart, ipratropium bromide (32,33). The efficacy of tiotropium was delineated in the UPLIFT trial, which demonstrated beneficial effects on respiratory symptoms, quality of life, lung function, and exacerbation rate (34). The success of tiotropium has led to the development of additional LAMAs, including glcopyrronium bromide, aclidinium bromide, and umeclidinum bromide with the aim of reproducing the similar clinical effects while also aspiring to concomitantly optimize safety, efficacy, and ease of use.
Aclidinium bromide and formoterol fumarate for the maintenance treatment of chronic obstructive pulmonary disease
Published in Expert Review of Clinical Pharmacology, 2020
Ryan Haley, Nita Gupta, Sanjay Sethi
Aclidinium bromide is a long-acting synthetic inhibitor of muscarinic receptors, with affinity for muscarinic receptor subtypes M1 through M5. The drug action on the M3 receptor subtype is critical in the treatment of COPD. M3 receptors are located on bronchial smooth muscle, submucosal glands, and on vascular endothelium in the lungs. Agonism of the M3 receptor leads to bronchoconstriction, mucus secretion, and vasodilation [11]. As a long-acting muscarinic antagonist (LAMA), aclidinium bromide blocks M3 receptors expressed in bronchial airways, leading to bronchodilation and decreased respiratory secretions [12].