Ecopipam (SCH 39166) hydrobromide is a potent, selective and orally active antagonist of dopamine D1/D5 receptor, with K i s of 1.2 nM and 2.0 nM, respectively. Ecopipam hydrobromide shows more than 40-flod selectivity over D2, D4, 5-HT, and α2a receptor (K i =0.98, 5.52, 0.08, and 0.73 μM, respectively). Ecopipam hydrobromide can be used for the research of schizophrenia and obesity [1].
In Vivo, Ecopipam (10, mg/kg, oral administration) antagonizes Apomorphine-induced stereotypy in rats[4]. Ecopipam (5 and 10 μM, perfusion, 1 μL/min) reversibly and dose-dependently decreases acetylcholine release in the rat striatum[5].
In Vitro, Ecopipam (2 μM) hydrobromide completely abolishes the proconvulsive effect of Dopamine (10 μM) in isolated corticohippocampal formation[2].
References:
[1]. Wu WL, et al. Dopamine D1/D5 receptor antagonists with improved pharmacokinetics: design, synthesis, and biological evaluation of phenol bioisosteric analogues of benzazepine D1/D5 antagonists. J Med Chem. 2005 Feb 10;48(3):680-93.
[2]. Sharopov S, et al. Dopaminergic modulation of low-Mg²⁺-induced epileptiform activity in the intact hippocampus of the newborn mouse in vitro. J Neurosci Res. 2012 Oct;90(10):2020-33.
[3]. Satanove DJ, et al. Nicotine-induced enhancement of a sensory reinforcer in adult rats: antagonist pretreatment effects. Psychopharmacology (Berl). 2021 Feb;238(2):475-486.
[4]. R E Chipkin, et al. Pharmacological profile of SCH39166: a dopamine D1 selective benzonaphthazepine with potential antipsychotic activity. J Pharmacol Exp Ther. 1988 Dec;247(3):1093-102.
[5]. E Acquas, et al. Local application of SCH 39166 reversibly and dose-dependently decreases acetylcholine release in the rat striatum. Eur J Pharmacol. 1999 Nov 3;383(3):275-9.
In Vivo, Ecopipam (10, mg/kg, oral administration) antagonizes Apomorphine-induced stereotypy in rats[4]. Ecopipam (5 and 10 μM, perfusion, 1 μL/min) reversibly and dose-dependently decreases acetylcholine release in the rat striatum[5].
In Vitro, Ecopipam (2 μM) hydrobromide completely abolishes the proconvulsive effect of Dopamine (10 μM) in isolated corticohippocampal formation[2].
References:
[1]. Wu WL, et al. Dopamine D1/D5 receptor antagonists with improved pharmacokinetics: design, synthesis, and biological evaluation of phenol bioisosteric analogues of benzazepine D1/D5 antagonists. J Med Chem. 2005 Feb 10;48(3):680-93.
[2]. Sharopov S, et al. Dopaminergic modulation of low-Mg²⁺-induced epileptiform activity in the intact hippocampus of the newborn mouse in vitro. J Neurosci Res. 2012 Oct;90(10):2020-33.
[3]. Satanove DJ, et al. Nicotine-induced enhancement of a sensory reinforcer in adult rats: antagonist pretreatment effects. Psychopharmacology (Berl). 2021 Feb;238(2):475-486.
[4]. R E Chipkin, et al. Pharmacological profile of SCH39166: a dopamine D1 selective benzonaphthazepine with potential antipsychotic activity. J Pharmacol Exp Ther. 1988 Dec;247(3):1093-102.
[5]. E Acquas, et al. Local application of SCH 39166 reversibly and dose-dependently decreases acetylcholine release in the rat striatum. Eur J Pharmacol. 1999 Nov 3;383(3):275-9.