Raclopride is a substituted benzamide with high selectivity as an antagonist of dopamine D2 and D3 receptors[1]. The selectivity of Raclopride for dopamine receptors is determined by its respective Ki values, which are as follows: 1.8, 3.5, 2400, and 18000 nM for D2, D3, D4, and D1 receptors respectively. Raclopride is mainly used in the field of neurological disorders, including schizophrenia[2] and Parkinson's disease[3]. Raclopride can cross the blood-brain barrier and bind to dopamine receptors in the brain, so it is widely used in positron emission tomography (PET) imaging to study the distribution and density of dopamine receptors in the brain[4][5].
Raclopride (0.1, 0.3, or 0.6mg/kg) treatment exhibits a clear dose-dependent anti-aggressive effect, significantly inhibiting isolation-induced aggression in rats[6]. Raclopride (0.5mg/kg) can prevent the amphetamine-induced impairment in goal-directed action of C57BL6/J mice[7].
References:
[1]. Farde L, Pauli S, Hall H, et al. Stereoselective binding of 11C-raclopride in living human brain--a search for extrastriatal central D2-dopamine receptors by PET. Psychopharmacology (Berl). 1988;94(4):471-8. doi: 10.1007/BF00212840. PMID: 3131792.
[2]. Farde L, Wiesel FA, Stone-Elander S, et al. D2 dopamine receptors in neuroleptic-naive schizophrenic patients. A positron emission tomography study with [11C]raclopride. Arch Gen Psychiatry. 1990 Mar;47(3):213-9. doi: 10.1001/archpsyc.1990.01810150013003. PMID: 1968328.
[3]. Antonini A, Schwarz J, Oertel WH, et al. Long-term changes of striatal dopamine D2 receptors in patients with Parkinson's disease: a study with positron emission tomography and [11C]raclopride. Mov Disord. 1997 Jan;12(1):33-8. doi: 10.1002/mds.870120107. PMID: 8990051.
[4]. Schlaepfer TE, Pearlson GD, Wong DF, et al. PET study of competition between intravenous cocaine and [11C]raclopride at dopamine receptors in human subjects. Am J Psychiatry. 1997 Sep;154(9):1209-13. doi: 10.1176/ajp.154.9.1209. PMID: 9286178.
[5]. Roux GL, Jarray R, Guyot AC, et al. Proof-of-Concept Study of Drug Brain Permeability Between in Vivo Human Brain and an in Vitro iPSCs-Human Blood-Brain Barrier Model. Sci Rep. 2019 Nov 5;9(1):16310. doi: 10.1038/s41598-019-52213-6. PMID: 31690750; PMCID: PMC6831611.
[6]. Aguilar MA, Miñarro J, Pérez-Iranzo N, et al. Behavioral profile of raclopride in agonistic encounters between male mice. Pharmacol Biochem Behav. 1994 Mar;47(3):753-6. doi: 10.1016/0091-3057(94)90185-6. PMID: 7911581.
[7]. Conn KA, Alexander S, Burne THJ, et al. Antagonism of D2 receptors via raclopride ameliorates amphetamine-induced associative learning deficits in male mice. Behav Brain Res. 2023 Oct 2;454:114649. doi: 10.1016/j.bbr.2023.114649. Epub 2023 Aug 27. PMID: 37643667.
Raclopride是一种取代的苯甲酰胺，是具有高选择性的多巴胺D2 和D3受体拮抗剂 [1]。Raclopride对大脑多巴胺受体的选择性由其各自的Ki值表征决定，分别为：D2受体1.8nM，D3受体3.5nM，D4受体2400nM，D1受体18000nM。Raclopride主要用于神经系统疾病领域，包括精神分裂症[2]和帕金森病[3]。Raclopride能够穿过血脑屏障并结合大脑中的多巴胺受体，因此被广泛用于正电子发射断层扫描（PET）成像，以研究大脑中多巴胺受体的分布和密度[4]。
Raclopride（0.1、0.3或0.6mg/kg）处理显示出明显的剂量依赖性抗攻击效果，显著抑制了大鼠的隔离诱导攻击行为[5]。Raclopride（0.5mg/kg）处理可以预防C57BL6/J小鼠安非他明诱导的目标导向行为障碍[6]。