Garcia-Ladona F J, Cox B F
Department of Molecular Biology, Neuroscience Research, Abbott GmbH and Co. KG, P.O. Box 210805, D-67008 Ludwigshafen, Germany.
CNS Drug Rev. 2003 Summer;9(2):141-58. doi: 10.1111/j.1527-3458.2003.tb00246.x.
BP 897 is a potent (K(i) = 0.92 nM) dopamine D(3) receptor compound developed for the treatment of cocaine abuse and craving. BP 897 has a high selectivity for the dopamine D(3) versus D(2) receptors (70-fold) and a moderate affinity for 5-HT(1A) receptors, (K(i) = 84 nM), adrenergic-alpha(1) (K(i) = 60 nM) and -alpha(2) adrenoceptors (K(i) = 83 nM). BP 897 displays significant intrinsic activity at the human dopamine D(3) receptor by decreasing forskolin-stimulated cAMP levels and by stimulating mitogenesis of dopamine D(3)-expressing NG108-15 cells. Although these findings suggest that BP 897 is a partial agonist, recent studies in Chinese Hamster Ovary (CHO) cells with expressed dopamine D(3) receptors demonstrated that BP 897 is devoid of any intrinsic activity but potently inhibits dopamine agonist effects (pIC(50) = 9.43 and 9.51) in agonist-induced acidification rate or increase of GTPgammaS binding, respectively. In addition, BP 897 inhibits in vivo (EC(50) = 1.1 mg/kg, i.v.) agonist-induced decrease of firing rate of dopaminergic neurons in the substantia nigra. It has been clearly shown that BP 897, 1 mg/kg, i.p., reduces cocaine-seeking behavior in rats, without producing reinforcement on its own. In rhesus monkeys, BP 897 is not self-administered (up to 30 microg/kg, i.v.) but reduces cocaine self-administration. The potential usefulness of BP 897 in the treatment of drug-seeking behavior is further supported by its effects in drug conditioning models. Although BP 897 reduces L-DOPA-induced dyskinesia in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys, it provokes a return of parkinsonian symptoms. At high doses BP 897 has been reported to produce catalepsy in rats. Pharmacokinetic and toxicological data have not yet been published. These interesting preclinical findings with BP 897 provide additional validation for dopamine D(3) receptor as a therapeutic target for the treatment of cocaine abuse and its associated central nervous system (CNS) disorders. BP 897 recently entered phase II clinical studies.
BP 897是一种强效(Ki = 0.92 nM)的多巴胺D3受体化合物,开发用于治疗可卡因成瘾和渴望。BP 897对多巴胺D3受体与D2受体具有高选择性(70倍),对5-HT1A受体(Ki = 84 nM)、肾上腺素α1(Ki = 60 nM)和α2肾上腺素受体(Ki = 83 nM)具有中等亲和力。BP 897通过降低福斯高林刺激的cAMP水平和刺激表达多巴胺D3的NG108-15细胞的有丝分裂,在人多巴胺D3受体上显示出显著的内在活性。尽管这些发现表明BP 897是一种部分激动剂,但最近在中国仓鼠卵巢(CHO)细胞中对表达的多巴胺D3受体的研究表明,BP 897没有任何内在活性,但分别在激动剂诱导的酸化率或GTPγS结合增加方面有效抑制多巴胺激动剂的作用(pIC50 = 9.43和9.51)。此外,BP 897在体内抑制(EC50 = 1.1 mg/kg,静脉注射)激动剂诱导的黑质多巴胺能神经元放电率降低。已经清楚地表明,1 mg/kg腹腔注射的BP 897可减少大鼠的觅药行为,且自身不会产生强化作用。在恒河猴中,BP 897不会自我给药(高达30 μg/kg,静脉注射),但可减少可卡因的自我给药。BP 897在药物条件模型中的作用进一步支持了其在治疗觅药行为方面的潜在用途。尽管BP 897可减少1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)处理的猴子中左旋多巴诱导的运动障碍,但它会引发帕金森症状的复发。据报道,高剂量的BP 897会在大鼠中产生僵住症。药代动力学和毒理学数据尚未公布。这些关于BP 897有趣的临床前研究结果为多巴胺D3受体作为治疗可卡因成瘾及其相关中枢神经系统(CNS)疾病的治疗靶点提供了额外的验证。BP 897最近进入了II期临床研究。