TABLE 1

Affinities of S33138 at multiple classes of dopamine receptor, 5-HT receptor, and AR

For procedural details, see Millan et al. (2000a,b, 2004a) and Newman-Tancredi et al. (2002). Data are means ± S.E.M. of pK_i values, based on three to four determinations, each performed in triplicate. S33138 displayed negligible (pK_i < 5.0) affinities for the following sites: histamine H₂; opiate μ, δ, and κ; adenosine (A₁, A₂ adenosine); angiotensin I; benzodiazepine; bradykinin B₂; calcitonin gene-related peptide; cannabinoid (CB₁, CB); cholecystokinin (A, B); choline uptake; endothelin (A, B); GABA (A, B); glutamate (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, N-methyl-d-aspartate); imidazoline (I₂); melatonin (MT₁, MT₂); neurokinin (NK₁, NK₂); neuropeptide Y (Y₁, Y₅); and nicotinic, prostanoid (thromboxane A₂/PGH₂), σ (1, 2), estrogen, progesterone, and testosterone receptors. It also showed low affinity (pK_i < 5.0) for Ca²⁺ channels (diltiazem site), Na⁺ channels (batrachotoxin site), and K⁺ channels (ATP, Ca²⁺ and voltage dependent) and for a variety of enzymes, including acetylcholinesterase, adenyl cyclase, cyclooxygenase 1, guanylyl cyclase, 5-lipoxygenase, monoamine oxydase A and B, nitric-oxide synthase, phospholipase A₂, phospholipase C, phosphodiesterase I and III, protein kinase C, and sodium-potassium ATPase.