Zolmitriptan (311C90) selectively binds to and activates serotonin (5-HT) 1B receptors expressed in intracranial arteries and 5-HT 1D receptors located on peripheral trigeminal sensory nerve terminals in the meninges and central terminals in brainstem sensory nuclei. Zolmitriptan is a member of the triptan class of agents with anti-migraine properties. Receptor binding results in constriction of cranial vessels, reduction of vessel pulsation and inhibition of nociceptive transmission, thereby providing relief of migraine headaches. Zolmitriptan may also relieve migraine headaches by inhibition of pro-inflammatory neuropeptide release.

5-HT1B receptor:5.01 nM (Ki), 5-HT1F receptor:63.09 nM (Ki), 5-HT1D receptor:0.63 nM (Ki)

Zolmitriptan 在灵长类动物的基底动脉和人类的心外膜冠状动脉环中产生浓度依赖性收缩。在转染的CHO-K1细胞膜中，Zolmitriptan 在人类重组5-HT1D（原5-HT1D alpha）和5-HT1B（原5-HT1D beta）受体上显示出高亲和力。[1] Zolmitriptan 在表达重组人类5-HT(1B)受体的C6胶质瘤细胞中使I(K)浓度依赖性增加（最大增幅16.3%），其pD(2)值为7.03。在表达克隆人类5-HT(1B)受体的C6细胞中，当EGTA (5 mM)被包含在贴片管内时，可以阻止由Zolmitriptan引起的I(K)增加。[2]

Zolmitriptan（3-30 mg/kg，静脉注射）在单侧三叉神经节电刺激前十分钟给药，可引起剂量依赖性地抑制麻醉豚鼠同侧硬脑膜内的[125I]-白蛋白渗出。[1] Zolmitriptan（10-1000 mg/kg，静脉注射）选择性降低动静脉吻合支（AVA）的通透性，最大降低92.5%。该化合物还可适度降低额外脑通透性（最大降低23.9%，30 mg/kg，静脉注射），但不影响脑部通透性。Zolmitriptan（1-30 mg/kg，静脉注射）引起剂量依赖性降低麻醉猫耳部微血管通透性（降低15%至60%），与颈动脉通透性减少呈现相似的趋势。[3] Zolmitriptan在老鼠身上呈现行为特异性抗攻击效果，并同样有效减少由酒精增高的攻击性。[4]