Suzuki Yoshiko, Funakoshi Takeo, Chaki Shigeyuki, Kawashima Naoya, Ogawa Shin, Kumagai Toshihito, Nakazato Atsurou, Komurasaki Toshi, Okuyama Shigeru
Molecular Biology Laboratory, Taisho Pharmaceutical Co., Ltd., 1-403 Yoshino-cho, Saitama-shi, Saitama, 330-8530, Japan.
Life Sci. 2002 Oct 18;71(22):2603-15. doi: 10.1016/s0024-3205(02)02085-4.
Atypical antipsychotic properties of 4-(4-fluorobenzylidene)-1-[2-[5-(4-fluorophenyl)-1H-pyrazol-4-yl]ethyl] piperidine (NRA0161) were investigated by in vitro receptor affinities, in vivo receptor occupancies and findings were compared with those of risperidone and haloperidol in rodent behavioral studies. In in vitro receptor binding studies, NRA0161 has a high affinity for human cloned dopamine D(4) and 5-HT(2A) receptor with Ki values of 1.00 and 2.52 nM, respectively. NRA0161 had a relatively high affinity for the alpha(1) adrenoceptor (Ki; 10.44 nM) and a low affinity for the dopamine D(2) receptor (Ki; 95.80 nM). In in vivo receptor binding studies, NRA0161 highly occupied the 5-HT(2A) receptor in rat frontal cortex. In contrast, NRA0161 did not occupy the striatal D(2) receptor. In behavioral studies, NRA0161, risperidone and haloperidol antagonized the locomotor hyperactivity in mice, as induced by methamphetamine (MAP). At a higher dosage, NRA0161, risperidone and haloperidol dose-dependently antagonized the MAP-induced stereotyped behavior in mice and NRA0161 dose-dependently and significantly induced catalepsy in rats. The ED(50) value in inhibiting the MAP-induced locomotor hyperactivity was 30 times lower than that inhibiting the MAP-induced stereotyped behavior and 50 times lower than that which induced catalepsy. These findings suggest that NRA0161 may have atypical antipsychotic activities yet without producing extrapyramidal side effects.
通过体外受体亲和力和体内受体占有率研究了4-(4-氟亚苄基)-1-[2-[5-(4-氟苯基)-1H-吡唑-4-基]乙基]哌啶(NRA0161)的非典型抗精神病特性,并在啮齿动物行为学研究中将结果与利培酮和氟哌啶醇进行了比较。在体外受体结合研究中,NRA0161对人克隆多巴胺D(4)和5-HT(2A)受体具有高亲和力,其Ki值分别为1.00和2.52 nM。NRA0161对α(1)肾上腺素能受体具有相对较高的亲和力(Ki;10.44 nM),对多巴胺D(2)受体具有低亲和力(Ki;95.80 nM)。在体内受体结合研究中,NRA0161高度占据大鼠额叶皮质中的5-HT(2A)受体。相比之下,NRA0161不占据纹状体D(2)受体。在行为学研究中,NRA0161、利培酮和氟哌啶醇拮抗了由甲基苯丙胺(MAP)诱导的小鼠运动亢进。在较高剂量下,NRA0161、利培酮和氟哌啶醇剂量依赖性地拮抗了MAP诱导的小鼠刻板行为,并且NRA0161剂量依赖性地并显著地诱导了大鼠僵住症。抑制MAP诱导的运动亢进的ED(50)值比抑制MAP诱导的刻板行为的ED(50)值低30倍,比诱导僵住症的ED(50)值低50倍。这些发现表明NRA0161可能具有非典型抗精神病活性,但不会产生锥体外系副作用。