Sarau H M, Griswold D E, Bush B, Potts W, Sandhu P, Lundberg D, Foley J J, Schmidt D B, Webb E F, Martin L D, Legos J J, Whitmore R G, Barone F C, Medhurst A D, Luttmann M A, Giardina G A, Hay D W
The Departments of Pulmonary Biology, SmithKline Beecham Pharmaceuticals, King of Prussia, Pennsylvania, USA.
J Pharmacol Exp Ther. 2000 Oct;295(1):373-81.
The pharmacological and pharmacokinetic profile of SB-222200 [(S)-(-)-N-(alpha-ethylbenzyl)-3-methyl-2-phenylquinoline-4-car boxami de], a human NK-3 receptor (hNK-3R) antagonist, was determined. SB-222200 inhibited (125)I-[MePhe(7)]neurokinin B (NKB) binding to Chinese hamster ovary (CHO) cell membranes stably expressing the hNK-3 receptor (CHO-hNK-3R) with a K(i) = 4.4 nM and antagonized NKB-induced Ca(2+) mobilization in HEK 293 cells stably expressing the hNK-3 receptor (HEK 293-hNK-3R) with an IC(50) = 18.4 nM. SB-222200 was selective for hNK-3 receptors compared with hNK-1 (K(i) > 100,000 nM) and hNK-2 receptors (K(i) = 250 nM). In HEK 293 cells transiently expressing murine NK-3 receptors (HEK 293-mNK-3R), SB-222200 inhibited binding of (125)I-[MePhe(7)]NKB (K(i) = 174 nM) and antagonized NKB (1 nM)-induced calcium mobilization (IC(50) = 265 nM). In mice oral administration of SB-222200 produced dose-dependent inhibition of behavioral responses induced by i.p. or intracerebral ventricular administration of the NK-3 receptor-selective agonist, senktide, with ED(50) values of approximately 5 mg/kg. SB-222200 effectively crossed the blood-brain barrier in the mouse and rat. The inhibitory effect of SB-222200 against senktide-induced behavioral responses in the mouse correlated significantly with brain, but not plasma, concentrations of the compound. Pharmacokinetic evaluation of SB-222200 in rat after oral administration (8 mg/kg) indicated sustained plasma concentrations (C(max) = about 400 ng/ml) and bioavailability of 46%. The preclinical profile of SB-222200, demonstrating high affinity, selectivity, reversibility, oral activity, and central nervous system penetration, suggests that it will be a useful tool compound to define the physiological and pathophysiological roles of NK-3 receptors, in particular in the central nervous system.
测定了人NK-3受体(hNK-3R)拮抗剂SB-222200 [(S)-(-)-N-(α-乙基苄基)-3-甲基-2-苯基喹啉-4-甲酰胺]的药理和药代动力学特征。SB-222200抑制(125)I-[MePhe(7)]神经激肽B(NKB)与稳定表达hNK-3受体的中国仓鼠卵巢(CHO)细胞膜(CHO-hNK-3R)的结合,其解离常数(K i)为4.4 nM,并拮抗NKB诱导的稳定表达hNK-3受体的HEK 293细胞(HEK 293-hNK-3R)中的Ca(2+)动员,半数抑制浓度(IC50)为18.4 nM。与hNK-1受体(K i>100,000 nM)和hNK-2受体(K i = 250 nM)相比,SB-222200对hNK-3受体具有选择性。在瞬时表达小鼠NK-3受体的HEK 293细胞(HEK 293-mNK-3R)中,SB-222200抑制(125)I-[MePhe(7)]NKB的结合(K i = 174 nM)并拮抗NKB(1 nM)诱导的钙动员(IC50 = 265 nM)。在小鼠中,口服SB-222200对腹腔注射或脑室内注射NK-3受体选择性激动剂senktide诱导的行为反应产生剂量依赖性抑制,半数有效剂量(ED50)值约为5 mg/kg。SB-222200在小鼠和大鼠中能有效穿过血脑屏障。SB-222200对小鼠中senktide诱导的行为反应的抑制作用与该化合物在脑中的浓度显著相关,而与血浆浓度无关。对大鼠口服给药(8 mg/kg)后SB-222200的药代动力学评估表明,其血浆浓度持续存在(Cmax =约400 ng/ml),生物利用度为46%。SB-222200的临床前特征表明其具有高亲和力、选择性、可逆性、口服活性和中枢神经系统渗透性,这表明它将是一种有用的工具化合物,可用于确定NK-3受体的生理和病理生理作用,特别是在中枢神经系统中的作用。