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      Imidafenacin, An Orally Active Muscarinic Receptor Antagonist, Improves Pulmonary Function In Patients With Chronic Obstructive Pulmonary Disease: A Multicenter, Randomized, Double-Blind, Placebo-Controlled 3×3 Crossover Phase II Trial

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          Abstract

          Background

          Although long-acting muscarinic receptor antagonists are central to the management of chronic obstructive pulmonary disease (COPD), inhaled medicines may have technical difficulty in some patients and adherence barriers.

          Methods

          A multicenter, randomized, double-blind, placebo-controlled 3×3 crossover Phase II trial was performed to evaluate the efficacy and safety of oral administration of the antimuscarinic agent imidafenacin in patients with COPD. Twenty-seven male COPD patients with % forced expiratory volume in 1 s (FEV 1) ≥30% and <80% predicted were randomized to single oral dose of imidafenacin 0.1 mg, imidafenacin 0.2 mg, or placebo.

          Results

          Maximum change in FEV 1 with both doses of imidafenacin significantly improved from baseline to 24 hrs after administration when compared with a placebo. Area under the curve in FEV 1 during 24 hrs after administration with 0.2 mg, but not 0.1 mg dose, was significantly improved when compared with a placebo, and the improvement was significantly based on dose-dependent manners. Plasma imidafenacin level was positively correlated with change in FEV 1. All subjects with both doses of imidafenacin completed without moderate nor severe adverse events.

          Conclusion

          A single oral dose of imidafenacin 0.1 mg or imidafenacin 0.2 mg may contribute to the improvement of pulmonary function with excellent safety and tolerability in patients with COPD.

          Trial registration

          JapicCTI-121760 (Japan Pharmaceutical Information Center – Clinical Trials Information [JapicCTI]; http://www.clinicaltrials.jp/user/cteSearch_e.jsp).

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          Most cited references 25

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          Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study.

           Patricia Kiley,  R Kanner,  P Enright … (1994)
          To determine whether a program incorporating smoking intervention and use of an inhaled bronchodilator can slow the rate of decline in forced expiratory volume in 1 second (FEV1) in smokers aged 35 to 60 years who have mild obstructive pulmonary disease. Randomized clinical trial. Participants randomized with equal probability to one of the following groups: (1) smoking intervention plus bronchodilator, (2) smoking intervention plus placebo, or (3) no intervention. Ten clinical centers in the United States and Canada. A total of 5887 male and female smokers, aged 35 to 60 years, with spirometric signs of early chronic obstructive pulmonary disease. Smoking intervention: intensive 12-session smoking cessation program combining behavior modification and use of nicotine gum, with continuing 5-year maintenance program to minimize relapse. Bronchodilator: ipratropium bromide prescribed three times daily (two puffs per time) from a metered-dose inhaler. Rate of change and cumulative change in FEV1 over a 5-year period. Participants in the two smoking intervention groups showed significantly smaller declines in FEV1 than did those in the control group. Most of this difference occurred during the first year following entry into the study and was attributable to smoking cessation, with those who achieved sustained smoking cessation experiencing the largest benefit. The small noncumulative benefit associated with use of the active bronchodilator vanished after the bronchodilator was discontinued at the end of the study. An aggressive smoking intervention program significantly reduces the age-related decline in FEV1 in middle-aged smokers with mild airways obstruction. Use of an inhaled anticholinergic bronchodilator results in a relatively small improvement in FEV1 that appears to be reversed after the drug is discontinued. Use of the bronchodilator did not influence the long-term decline of FEV1.
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            New anti-inflammatory targets for chronic obstructive pulmonary disease.

             Peter Barnes (2013)
            Chronic obstructive pulmonary disease (COPD) is associated with chronic inflammation of the peripheral airways and lung parenchyma, which leads to progressive obstruction of the airways. Current management with long-acting bronchodilators does not reduce disease progression, and there are no treatments that effectively suppress chronic inflammation in COPD. An increased understanding of the inflammatory processes that are involved in the pathophysiology of COPD has identified several new therapeutic targets. This Review discusses some of the most promising of these targets, including new antioxidants, kinase inhibitors and drugs that target cellular senescence, microbial colonization, epigenetic regulation of inflammatory gene expression and corticosteroid resistance.
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              Tiotropium (Spiriva): mechanistical considerations and clinical profile in obstructive lung disease.

               B Disse,  T J Witek,  Peter G. Speck … (1998)
              Inhaled antimuscarinics, often called anticholinergics in clinical medicine, are established as first line bronchodilators in COPD. Tiotropium has been developed as a new generation antimuscarinic following ipratropium. Tiotropium is a specific, highly potent antimuscarinic, demonstrating very slow dissociation from muscarinic receptors. Dissociation from M2-receptors is faster than from M3 or M1, which in functional in vitro studies, appeared as kinetic receptor subtype selectivity of M3 and M1 over M2. The high potency and slow receptor dissociation found its clinical correlate in significant and long lasting bronchodilatation and bronchoprotection in patients with COPD and asthma. In asthma, protection against methacholine challenge exceeded the study period of 48 hours. In COPD, bronchodilatation of about 80% of the plateau was demonstrated after the first dose. Following chronic once daily inhalation for 28 days, the improvement in pulmonary function was sustained and there was a further increase in peak effects, but more importantly a rising baseline, achieving steady state within 2 weeks. Tiotropium achieves very stable long lasting effects with comparatively low variation of bronchodilatation between peak and trough (the level before the next administration). Stable 24 hour effectiveness profiles the compound as the first once daily bronchodilator. Clinical correlates of kinetic receptor subtype selective blockade remain to be shown. Plasma levels of tiotropium at trough are in the low pg/ml range and are unlikely to explain the sustained effectiveness in the airways. Slow dissociation from muscarinic receptors is likely to be responsible for the long duration of action.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Chron Obstruct Pulmon Dis
                Journal ID (iso-abbrev): Int J Chron Obstruct Pulmon Dis
                Journal ID (publisher-id): COPD
                Journal ID (pmc): copd
                Title: International Journal of Chronic Obstructive Pulmonary Disease
                Publisher: Dove
                ISSN (Print): 1176-9106
                ISSN (Electronic): 1178-2005
                Publication date (Electronic): 19 September 2019
                Publication date Collection: 2019
                Volume: 14
                Pages: 2175-2184
                Affiliations
                [1 ]Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University , Kagoshima 890-8520, Japan
                [2 ]Division of Respirology, Neurology, and Rheumatology, Department of Medicine, Kurume University School of Medicine , Kurume 830-0011, Japan
                [3 ]Nagata Hospital , Yanagawa 832-0059, Japan
                [4 ]Department of Respiratory Medicine, Tohoku University, Graduate School of Medicine , Sendai 980-8574, Japan
                [5 ]Kirigaoka Tsuda Hospital , Kitakyushu 802-0052 Japan
                [6 ]Division of Respiratory Medicine, National Hospital Organization Fukuoka-Higashi Medical Center , Koga 811-3195, Japan
                [7 ]Division of Respiratory Medicine, Kyushu Central Hospital of the Mutual Aid Association of Public School Teachers , Fukuoka 815-8588, Japan
                [8 ]Division of Respiratory Medicine, National Hospital Organization Fukuoka Hospital , Fukuoka 811-1394, Japan
                [9 ]Division of Respiratory Medicine, Oita Nakamura Hospital , Oita 870-0022, Japan
                [10 ]ONO Pharmaceutical Co. Ltd ., Osaka 541-8564, Japan
                Author notes
                Correspondence: Hiromasa Inoue Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University , 8-35-1 Sakuragaoka, Kagoshima890-8520, JapanTel +81 99 275 6481Fax +81 99 275 6482 Email inoue-pulm@umin.net
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 223002
                DOI: 10.2147/COPD.S223002
                PMC ID: 6757323
                Copyright statement: © 2019 Machida et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 5, Tables: 3, References: 32, Pages: 10
                Categories
                Subject: Original Research

                Data availability:

                ScienceOpen disciplines: Respiratory medicine

                Keywords: copd, anti-cholinergic, bronchodilator, imidafenacin, lung function

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