Sumatriptan is an orally active 5-HT1 receptor agonist with IC50 values of 7.3nM, 9.3nM and 17.8nM for 5-HT1D, 5-HT1B and 5-HT1F receptors, respectively[1]. 5-HT1 receptor is a G-protein-coupled receptor subfamily that inhibits adenylyl cyclase and modulates serotonin-mediated neurotransmission[2]. Sumatriptan is usually used for migraine headache research[3].
In vitro, Sumatriptan(10pM-10μM; 20min) displaced [³H]-5-HT with an IC50 of 5.0nM and fully stimulated [35S]-GTPγS binding with an EC50 of 16nM in CHO cells stably expressing human 5-HT1D receptors[4]. Sumatriptan(10pM-10μM; 20min) inhibited forskolin-stimulated cAMP accumulation in HEK-293 cells expressing h5-HT1B receptors (IC50=20nM) and in C6-glioma cells expressing h5-HT1D receptors (IC50=2.6nM)[5].
In vivo, Sumatriptan (600μg/kg; i.p.) reversed nitroglycerin (NTG)-induced thermal and mechanical allodynia in male C57BL/6 mice, and restored withdrawal latencies and thresholds to baseline within 60min[6]. Sumatriptan (0.3mg/kg/day; i.p.; 28 days) reversed T9-10 clip-compression–induced mechanical and thermal allodynia, reduced spinal TNF-α, IL-1β and CGRP, and improved BBB locomotor scores in adult male Sprague-Dawley rats[7].
References:
[1] Peroutka SJ, McCarthy BG. Sumatriptan (GR 43175) interacts selectively with 5-HT1B and 5-HT1D binding sites. Eur J Pharmacol. 1989;163(1):133-136.
[2] Polter AM, Li X. 5-HT1A receptor-regulated signal transduction pathways in brain. Cell Signal. 2010;22(10):1406-1412.
[3] Dechant KL, Clissold SP. Sumatriptan. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the acute treatment of migraine and cluster headache. Drugs. 1992;43(5):776-798.
[4] Castro JL, Street LJ, Guiblin AR, et al. 3-[2-(Pyrrolidin-1-yl)ethyl]indoles and 3-[3-(piperidin-1-yl)propyl]indoles: agonists for the h5-HT1D receptor with high selectivity over the h5-HT1B subtype. J Med Chem. 1997;40(22):3497-3500.
[5] Lesage AS, Wouters R, Van Gompel P, et al. Agonistic properties of alniditan, sumatriptan and dihydroergotamine on human 5-HT1B and 5-HT1D receptors expressed in various mammalian cell lines. Br J Pharmacol. 1998;123(8):1655-1665.
[6] Bates EA, Nikai T, Brennan KC, et al. Sumatriptan alleviates nitroglycerin-induced mechanical and thermal allodynia in mice. Cephalalgia. 2010;30(2):170-178.
[7] Afshari K, Dehdashtian A, Haddad NS, et al. Sumatriptan improves the locomotor activity and neuropathic pain by modulating neuroinflammation in rat model of spinal cord injury. Neurol Res. 2021;43(1):29-39.
Sumatriptan是一种具有口服活性的5-HT1受体激动剂,对5-HT1D、5-HT1B和5-HT1F受体的IC50值分别为7.3nM、9.3nM和17.8nM[1]。5-HT1受体是一个G蛋白偶联受体亚家族,可抑制腺苷酸环化酶并调节血清素介导的神经传导[2]。Sumatriptan常用于偏头痛研究[3]。
在体外,Sumatriptan (10pM-10μM; 20分钟)在稳定表达人5-HT1D受体的CHO细胞中,置换[³H]-5-HT的IC50为5.0nM,完全刺激[35S]-GTPγS结合的EC50为16nM[4]。Sumatriptan(10pM-10μM;20分钟)在表达h5-HT1B受体的HEK-293细胞和表达h5-HT1D受体的C6胶质瘤细胞中抑制forskolin刺激的cAMP积聚的IC50分别为20nM和2.6nM[5]。
在体内,Sumatriptan(600μg/kg;腹腔注射)逆转了硝酸甘油(NTG)诱导的雄性C57BL/6小鼠的热和机械性痛觉过敏,并在60分钟内将撤退潜伏期和阈值恢复至基线水平[6]。在成年雄性Sprague-Dawley大鼠中,Sumatriptan(0.3mg/kg/天;腹腔注射;28天)逆转了T9-10夹压迫引起的机械和热性痛觉过敏,减少了脊髓中的TNF-α、IL-1β和CGRP,并改善了BBB运动评分[7]。
















