The mammalian tachykinins are a group of neuropeptides that include substance P, neurokinin A (NKA; also known as tachykinin precursor 1) and neurokinin B (NKB; also known as tachykinin 3). These tachykinins are widely distributed in the central nervous system (CNS) but they have distinct expression patterns. The biological actions of substance P, NKA and NKB are mediated via the activation of G protein-coupled seven-transmembrane domain receptors (GPCR-A9) designated as tachykinin receptor 1 (TACR1; also known as the NK1 receptor), TACR2 (also known as the NK2 receptor) and TACR3 (also known as the NK3 receptor), respectively. Both NK1 and NK3 receptors are widely distributed in the CNS, whereas the NK2 receptor is found in the smooth muscle of the gastrointestinal, respiratory and urinary tracts, but it has also been located in discrete regions of the rodent CNS. The development of drugs interacting with NK receptors has focused predominantly on the treatment of social anxiety disorders (SAD). Unfortunately, clinical trials with several NK1 antagonists showed inconsistent or no positive results for the treatment of SAD[1].