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In particular, the actions of adenosine (or methylxanthine antagonists) in the central nervous system, in the circulation, on immune cells, and on other tissues can be beneficial in certain disorders. Second, there exists a large number of ligands, which have been generated by introducing several modifications in the structure of the lead compounds (adenosine and methylxanthine), some of them highly specific. Four adenosine receptor subtypes (A<jats:sub>1<\/jats:sub>, A<jats:sub>2A<\/jats:sub>, A<jats:sub>2B<\/jats:sub>, and A<jats:sub>3<\/jats:sub>) have been cloned and pharmacologically characterized, all of which are G protein\u2010coupled receptors. Adenosine receptors can be distinguished according to their preferred mechanism of signal transduction: A<jats:sub>1<\/jats:sub> and A<jats:sub>3<\/jats:sub> receptors interact with pertussis toxin\u2010sensitive G proteins of the G<jats:sub>i<\/jats:sub> and G<jats:sub>o<\/jats:sub> family; the canonical signaling mechanism of the A<jats:sub>2A<\/jats:sub> and of the A<jats:sub>2B<\/jats:sub> receptors is stimulation of adenylyl cyclase <jats:italic>via<\/jats:italic> G<jats:sub>s<\/jats:sub> proteins. In addition to the coupling to adenylyl cyclase, all four subtypes may positively couple to phospholipase C <jats:italic>via<\/jats:italic> different G protein subunits. The development of new ligands, in particular, potent and selective antagonists, for all subtypes of adenosine receptors has so far been directed by traditional medicinal chemistry. The availability of genetic information promises to facilitate understanding of the drug\u2013receptor interaction leading to the rational design of a potentially therapeutically important class of drugs. Moreover, molecular modeling may further rationalize observed interactions between the receptors and their ligands. 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