Formoterol and salmeterol are chemically distinct, highly selective beta-2-adrenoceptor agonists developed to provide sustained (12h+) relief of airway obstruction in diseases such as asthma. Despite their similar long duration of action, these drugs differ. Formoterol has a faster onset of action in both experimental and clinical tests than that of salmeterol. Salmeterol, but not formoterol, behaves as a beta-adrenoceptor antagonist in some experimental models due to its considerably weaker efficacy at the beta 2-adrenoceptor in vitro although their are no established clinical consequences of this antagonism. Both formoterol and salmeterol display a peculiar "reassertion" behaviour in isolated airway smooth muscle subjected to beta-adrenoceptor antagonism and then washed with antagonist-free buffer. Both formoterol and salmeterol are highly efficient inhibitors of a number of indices of acute inflammatory processes in cells and tissues of human or animal origin. However, neither of these drugs has a proven clinical anti-inflammatory effect in chronic asthma in humans. Surprisingly, recent biophysical studies of formoterol and salmeterol have provided strong evidence that their individual patterns of onset speed, duration of action and "reassertion" are due to a common drug-lipid membrane interaction rather than drug-adrenoceptor interactions. A membrane-drug diffusion microkinetic model is presented to describe these phenomena.