The pharmacological effects of β~2~-adrenoceptor agonists are at least in part attributable to stimulation of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3′,5′-adenosine monophosphate (cyclic monophosphate). Increased cyclic AMP levels cause relaxation of bronchial smooth muscle. In vitro studies have shown that indacaterol, a long-acting β~2~-adrenergic agonist, has more than 24-fold greater agonist activity at β~2~-receptors compared to β~1~-receptors and 20-fold greater agonist activity compared to β~3~-receptors. When inhaled, indacaterol acts locally in the lung as a bronchodilator. Indacaterol is a partial agonist at the human β~2~-adrenergic receptor with nanomolar potency. In isolated human bronchus, indacaterol has a rapid onset of action and a long duration of action. Although β~2~-receptors are the predominant adrenergic receptors in bronchial smooth muscle and β~1~-receptors are the predominant receptors in the human heart, there are also β~2~-adrenergic receptors in the human heart comprising 10-50% of the total adrenergic receptors. The precise function of β~2~-adrenergic receptors in the heart is not known, but their presence raises the possibility that even highly selective β~2~-adrenergic agonists may have cardiac effects.