Aclidinium

484.16162579

K17VY42F6C

DTXSID00223070

Very slightly soluble

Most common adverse reactions (≥3% incidence and greater than placebo) are headache, nasopharyngitis and cough.

Like other anticholinergic agents, aclidinium has not been linked to episodes of liver enzyme elevations or clinically apparent liver injury. A major reason for its safety may relate to the low systemic absorption and exposure associated with anticholinergic agents administered by inhaler.

Aclidinium bromide inhalation powder is indicated for the long-term, maintenance treatment of bronchospasm associated with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema.|FDA Label

Aclidinium is a synthetic anticholinergic agent that is used as an inhalant for treatment of acute bronchospasm due to chronic bronchitis or emphysema. Aclidinium has not been implicated in causing liver enzyme elevations or clinically apparent acute liver injury.

Anticholinergic Agents

Aclidinium does not prolong the QTc interval or have significant effects on cardiac rhythm.

Bioavailability, healthy subjects = 6%; T max, healthy subjects = 10 minutes; Time to steady state, healthy subjects = 2 days;|Intravenously administered radiolabelled aclidinium bromide was administered to healthy volunteers and was extensively metabolized with 1% excreted as unchanged aclidinium. Approximately 54% to 65% of the radioactivity was excreted in urine and 20% to 33% of the dose was excreted in feces. The combined results indicated that almost the entire aclidinium bromide dose was eliminated by hydrolysis. After dry powder inhalation, urinary excretion of aclidinium is about 0.09% of the dose.|Following IV administration, the volume of distribution is 300 L|Total clearance, IV dose, young healthy subjects = 170 L/h (inter-individual variability of 36%)

The major route of metabolism of aclidinium bromide is hydrolysis, which occurs both chemically and enzymatically by esterases in the plasma. Aclidinium bromide is rapidly and extensively hydrolyzed to its alcohol and dithienylglycolic acid derivatives, neither of which binds to muscarinic receptors and are pharmacologically inactive.

Plasma half-life = 2.4 minutes (indicating that aclidinium is very rapidly hydrolyzed in plasma into its two inactive metabolites and has a low chance of causing systemic side effects). Effective half-life = 5-8 hours.

Aclidinium is a long-acting, competitive, and reversible anticholinergic drug that is specific for the acetylcholine muscarinic receptors. It binds to all 5 muscarinic receptor subtypes to a similar affinity. Aclidinium's effects on the airways are mediated through the M3 receptor at the smooth muscle to cause bronchodilation. Prevention of acetylcholine-induced bronchoconstriction effects was dose-dependent and lasted longer than 24 hours.