Ecopipam (SCH 39166) hydrochloride is a highly potent, selective, and orally active antagonist of dopamine D1/D5 receptors. It exhibits impressive binding affinities, with Ki values of 1.2 nM and 2.0 nM for D1 and D5 receptors, respectively. Ecopipam hydrochloride demonstrates remarkable selectivity, displaying over 40-fold selectivity compared to D2, D4, 5-HT, and α2a receptors, with Ki values of 0.98 μM, 5.52 μM, 0.08 μM, and 0.73 μM, respectively. Its application extends to various areas of research, including schizophrenia, cocaine addiction, and obesity [1] [3].

D5 receptor:2.0 nM (Ki), 5-HT receptor:80 nM (Ki), D1 receptor:1.2 nM (Ki), α2A-adrenoceptor:731 nM (Ki), D 4 Receptor:5520 nM (Ki), D 2 Receptor:980 nM (Ki)

Ecopipam hydrochloride (2 μM) entirely eliminates the proconvulsive impact of Dopamine (10 μM) in isolated corticohippocampal formations [2].

Ecopipam hydrochloride, administered in varying dosages and methods, demonstrates potent effects in modulating behavior and neurotransmitter release in rat models. At doses ranging from 0.003 to 0.3 mg/kg, a single subcutaneous (s.c.) injection of Ecopipam significantly inhibits the Nicotine-induced enhancement of sensory reinforcement in adult rats [3]. When administered orally at 10 mg/kg, Ecopipam counteracts the stereotypical behaviors induced by Apomorphine [4]. Furthermore, through perfusion at concentrations of 5 and 10 μM (1 μL/min), Ecopipam effectively and reversibly diminishes the release of acetylcholine in the rat striatum in a dose-dependent manner [5]. In experiments involving young adult Long-Evans rats injected with Nicotine, doses of Ecopipam were methodologically varied (0.003, 0.01, 0.03, 0.1, 0.3 mg/kg), administered subcutaneously 20 minutes before nicotine exposure (0.1 mg/kg), revealing a dose-dependent reduction in lever pressing, indicative of both active and inactive lever interactions.