text: Two theories explain the long time of action for LABAs. The first explained the long action in terms of a putative “exosite” or “exoceptor” distinct from the β-adrenoreceptor that long aliphatic tail of salmeterol binds to with high affinity. This allows the active saligenin head to angle on and off the receptor to activate it repeatedly. Formoterol does not have a long side chain like salmeterol to bind to the “exosite”, so this theory has been questioned. In 1994 Anderson. et al. introduced the plasmalemma diffusion microkinetic theory, explaining what happens to the β- agonist in the cell membrane lipid bilayer and in the aqueous biophase closest to the binding site of the β-adrenoceptor. It is postulated that the plasmalemma lipid bilayer of airway smooth muscles acts as a depot for β-adrenoceptor agonists. β-adrenoceptor agonists remain available to interact with the β-adrenoceptor active site after having partitioned into the lipid bilayer.