Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Josai International University, Chiba, Japan (K.Ma., N.M., K.T., S.H.); Department of Toxicology (K.Ma., M.N., T.S.) and Department of Pharmacology (K.Ma., M.N.), Hoshi University School of Pharmacy and Pharmaceutical Sciences, Tokyo, Japan; Department of Molecular Structure and Biological Function, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan (T.N., K.Mi., M.K., H.T.); and Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, New York (L.A.D.).
J Pharmacol Exp Ther. 2014 Mar;348(3):383-92. doi: 10.1124/jpet.113.208108. Epub 2013 Dec 17.
(E)-Methyl 2-((2S,3S,7aS,12bS)-3-ethyl-7a-hydroxy-8-methoxy-1,2,3,4,6,7,7a,12b-octahydroindolo[2,3-a]quinolizin-2-yl)-3-methoxyacrylate (7-hydroxymitragynine), a main active constituent of the traditional herbal medicine Mitragyna speciosa, is an indole alkaloid that is structurally different from morphine. 7-Hydroxymitragynine induces a potent antinociceptive effect on mouse acute pain through μ-opioid receptors. In this study, we developed dual-acting μ- and δ-opioid agonists MGM-15 and MGM-16 from 7-hydroxymitragynine for the treatment of acute and chronic pain. MGM-16 showed a higher potency than that of 7-hydroxymitragynine and MGM-15 in in vitro and in vivo assays. MGM-16 exhibited a high affinity for μ- and δ-opioid receptors, with K(i) values of 2.1 and 7.0 nM, respectively. MGM-16 showed μ- and δ-opioid full agonistic effects in a guanosine 5'-O-(3-[(35)S]thiotriphosphate) binding assay and in a functional test using electrically elicited guinea pig ileum and mouse vas deferens contractions. Systemic administration of MGM-16 produced antinociceptive effects in a mouse acute pain model and antiallodynic effects in a chronic pain model. The antinociceptive effect of MGM-16 was approximately 240 times more potent than that of morphine in a mouse tail-flick test, and its antiallodynic effect was approximately 100 times more potent than that of gabapentin in partial sciatic nerve-ligated mice, especially with oral administration. The antinociceptive effect of MGM-16 was completely and partially blocked by the μ-selective antagonist β-funaltrexamine hydrochloride (β-FNA) and by the δ-selective antagonist naltrindole, respectively, in a tail-flick test. The antiallodynic effect of MGM-16 was completely blocked by β-FNA and naltrindole in a neuropathic pain model. These findings suggest that MGM-16 could become a class of a compound with potential therapeutic utility for treating neuropathic pain.
(E)-甲基 2-((2S,3S,7aS,12bS)-3-乙基-7a-羟基-8-甲氧基-1,2,3,4,6,7,7a,12b-八氢吲哚并[2,3-a]喹啉嗪-2-基)-3-甲氧基丙烯酸酯(7-羟基育亨宾),一种传统草药美托拉宗的主要活性成分,是一种结构上不同于吗啡的吲哚生物碱。7-羟基育亨宾通过μ-阿片受体诱导小鼠急性疼痛产生强大的镇痛作用。在这项研究中,我们从 7-羟基育亨宾中开发出双重作用的μ-和 δ-阿片受体激动剂 MGM-15 和 MGM-16,用于治疗急性和慢性疼痛。MGM-16 在体外和体内试验中的效力均高于 7-羟基育亨宾和 MGM-15。MGM-16 对 μ-和 δ-阿片受体具有高亲和力,K(i) 值分别为 2.1 和 7.0 nM。MGM-16 在鸟嘌呤 5'-O-(3-[(35)S]三磷酸)结合测定和使用电刺激豚鼠回肠和小鼠输精管收缩的功能试验中表现出 μ-和 δ-阿片完全激动作用。MGM-16 全身给药可在小鼠急性疼痛模型中产生镇痛作用,并在慢性疼痛模型中产生抗痛觉过敏作用。在小鼠甩尾试验中,MGM-16 的镇痛作用比吗啡强约 240 倍,其抗痛觉过敏作用比加巴喷丁在部分坐骨神经结扎小鼠中强约 100 倍,特别是口服给药。MGM-16 在甩尾试验中的镇痛作用分别被 μ-选择性拮抗剂盐酸β-呋喃他胺(β-FNA)和 δ-选择性拮抗剂纳曲吲哚完全和部分阻断。MGM-16 在神经病理性疼痛模型中的抗痛觉过敏作用被β-FNA 和纳曲吲哚完全阻断。这些发现表明,MGM-16 可能成为一类具有治疗神经病理性疼痛潜力的化合物。