Mechanism of action<unk>  is a long-acting, reversible antagonist at muscarinic receptors, with similar affinity to all five subtypes, but with a dissociation half-life from subtype M3 of 29.2 hours, or six times longer than that from M2. For comparison, M3 dissociation half-lives of the related drugs ipratropium and tiotropium are 0.47 hours and 62.2 hours, respectively. Its action at subtype M3 at the smooth muscle of the bronchioles is responsible for its desired effect: it reduces contraction of these muscles and improves the airflow. M2 affinity is the main reason for adverse effects at the heart. Pharmacokinetics About 30% of inhaled<unk>  are deposited in the lung. Its action there lasts for more than 24 hours. From the lung, it is absorbed into the bloodstream, reaching highest blood plasma concentrations after five minutes in healthy persons and after 10 to 15 minutes in COPD patients. The substance is quickly hydrolysed to the carboxylic acid and the alcohol, so that less than 5% of the inhaled dose are found unchanged in the plasma. Hydrolysis is both non-enzymatic and enzymatic, the latter mainly by butyrylcholinesterase. The acid metabolite has a plasma protein binding of 87%, and the alcohol of 15%. These metabolites are found to 65% in the urine and to 33% in the faeces. Elimination half-life is two to three hours. Unchanged<unk>  accounts for only 0.1% of the excreted dose.
Aclidinium bromide
Umeclidinium bromide
Chloropicrin
Tiratricol
Bifluranol
Hydrastine
Brinzolamide
Pirisudanol