Showell H J, Pettipher E R, Cheng J B, Breslow R, Conklyn M J, Farrell C A, Hingorani G P, Salter E D, Hackman B C, Wimberly D J
Department of Immunology and Infectious Diseases, Pfizer Inc, Groton, Connecticut, USA.
J Pharmacol Exp Ther. 1995 Apr;273(1):176-84.
CP-105696, (+)-1-(3S,4R)-[3-(4-phenyl-benzyl)-4-hydroxy-chroman-7-yl] cyclopentane carboxylic acid, is a structurally novel, selective and potent leukotriene B4 (LTB4) receptor antagonist. In vitro, CP-105696 inhibited [3H]LTB4 (0.3 nM) binding to high-affinity LTB4 receptors on human neutrophils with an IC50 value of 8.42 +/- 0.26 nM. Scatchard analyses of [3H]LTB4 binding to these high-affinity receptors indicated that CP-105696 acted as a noncompetitive antagonist. CP-105696 inhibited human neutrophil chemotaxis mediated by LTB4 (5 nM) in a noncompetitive manner with an IC50 value of 5.0 +/- 2.0 nM. Scatchard analyses of [3H]LTB4 binding to low-affinity receptors on neutrophils indicated that CP-105696 acted as a competitive antagonist at this receptor, and inhibition of LTB4-mediated CD11b upregulation on human neutrophils was competitively inhibited by CP-105696 (pA2 = 8.03 +/- 0.19). CP-105696 at 10 microM did not inhibit either human neutrophil chemotaxis or CD11b upregulation mediated through alternate (i.e., C5a, IL-8, PAF) G-protein coupled chemotactic factor receptors. In isolated human monocytes, LTB4 (5 nM)-mediated Ca++ mobilization was inhibited by CP-105696 with an IC50 value of 940 +/- 70 nM. In vivo, after oral administration, CP-105696 blocked neutrophil and eosinophil infiltration in cavine dermis mediated by either LTB4 or arachidonic acid with ED50 values of 0.3 +/- 0.1 mg/kg. 12(R)-Hydroxyeicosatetraenoic acid-mediated neutrophil infiltration was blocked by 76.4 +/- 14.8% at 3 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)
CP - 105696,(+)-1-(3S,4R)-[3-(4 - 苯基 - 苄基)-4 - 羟基 - 色满 - 7 - 基]环戊烷羧酸,是一种结构新颖、具有选择性且强效的白三烯B4(LTB4)受体拮抗剂。在体外,CP - 105696抑制[3H]LTB4(0.3 nM)与人中性粒细胞上高亲和力LTB4受体的结合,IC50值为8.42±0.26 nM。对[3H]LTB4与这些高亲和力受体结合的Scatchard分析表明,CP - 105696作为非竞争性拮抗剂起作用。CP - 105696以非竞争性方式抑制由LTB4(5 nM)介导的人中性粒细胞趋化作用,IC50值为5.0±2.0 nM。对[3H]LTB4与中性粒细胞上低亲和力受体结合的Scatchard分析表明,CP - 105696在该受体处作为竞争性拮抗剂起作用,并且CP - 105696竞争性抑制LTB4介导的人中性粒细胞上CD11b上调(pA2 = 8.03±0.19)。10 microM的CP - 105696既不抑制通过替代的(即C5a、IL - 8、PAF)G蛋白偶联趋化因子受体介导的人中性粒细胞趋化作用,也不抑制CD11b上调。在分离的人单核细胞中,CP - 105696抑制LTB4(5 nM)介导的Ca++动员,IC50值为940±70 nM。在体内,口服给药后,CP - 105696阻断由LTB4或花生四烯酸介导的豚鼠真皮中中性粒细胞和嗜酸性粒细胞浸润,ED50值为0.3±0.1 mg/kg。在3 mg/kg剂量下,12(R)-羟基二十碳四烯酸介导的中性粒细胞浸润被阻断76.4±14.8%。(摘要截短于250字)