Abstract
This article discusses a model to describe the effects of molecules that bind to a site on the receptor separate from that of the endogenous agonist to actively produce receptor signals (direct agonism). In addition, these molecules also modify the biological responses of the endogenous agonist (either potentiation or antagonism). The effects of such compounds in high-throughput screening assays are described as well as their effects on the dose-response curves to conventional agonists.
Key Words: :