Zolmitriptan

1.6

0.79

Breast Feeding; Lactation; Milk, Human; Serotonin Receptor Agonists; Serotonin 5-HT1 Receptor Agonists; Triptans; Vasoconstrictor Agents

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

159.7 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

160.6 Ų [M+H]+ [CCS Type: TW; Method: Major Mix IMS/Tof Calibration Kit (Waters)]

164.88 Ų [M+K]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

Warning

H302 (95.2%): Harmful if swallowed [Warning Acute toxicity, oral]

P260, P261, P264, P264+P265, P270, P271, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P308+P316, P319, P321, P330, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 21 reports by companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

There is no specific antidote to zolmitriptan. In cases of severe intoxication, intensive care procedures are recommended, including establishing and maintaining a patent airway, ensuring adequate oxygenation and ventilation, and monitoring and support of the cardiovascular system. (L1712)

Dysgeusia is the most commonly observed adverse effect of zolmitriptan in healthy individuals, with the nasal spray causing a more significant impact. This phenomenon is likely attributed to the method of drug administration through the nasal route. Additional minor adverse events reported with intranasal zolmitriptan usage include nasal passage irritation, dizziness, throat irritation, and fatigue. Furthermore, phase 1 trials of the Real Life Intranasal Zolmitriptan Exposure (REALIZE) study revealed that the encountered adverse effects did not result in participants discontinuing the medication.

N02CC03

N - Nervous system

QN - Nervous system

Zolmitriptan, like other triptans, is a serotonin (5-hydroxytryptamine; 5-HT) receptor agonist, with enhanced specificity for the 5-HT_1B and 5-HT_1D receptor subtypes. It is through the downstream effects of 5-HT_1B/1D activation that triptans are proposed to provide acute relief of migraines. Zolmitriptan is also a vasoconstrictor, leading to possible adverse cardiovascular effects such as myocardial ischemia/infarction, arrhythmias, cerebral and subarachnoid hemorrhage, stroke, gastrointestinal ischemia, and peripheral vasospastic reactions. In addition, chest/throat/neck/jaw pain, tightness, and/or pressure has been reported, along with the possibility of medication overuse headaches and serotonin syndrome. Patients with phenylketonuria should be advised that ZOMIG-ZMT contains phenylalanine.

Migraines are complex physiological events characterized by unilateral throbbing headaches combined with photophobia and other aversions to sensory input. Migraine attacks are generally divided into phases: the premonitory phase, which typically involves irritability, fatigue, yawning, and stiff neck; the headache phase, which lasts for between four and 72 hours; and the postdrome phase, which lasts for up to a day following resolution of pain and whose symptoms are similar to those of the premonitory phase. In addition, neurological deficits, collectively termed migraine aura, may precede the headache phase. The underlying pathophysiology of migraines is a matter of active research but involves both neurological and vascular components. The head pain associated with migraine is thought to be a consequence of activation of the nociceptive nerves comprising the trigeminocervical complex (TCC). Terminals of nociceptive nerves that innervate the dura matter release vasoactive peptides, such as calcitonin gene-related peptide (CGRP), resulting in cranial vasodilation. Finally, when present, migraine aura appears to correlate with a transient wave(s) of cortical depolarization, termed cortical spreading depression (CSD). Triptans, including zolmitriptan, are proposed to act in three ways. The main mechanism is through modulation of nociceptive nerve signalling in the central nervous system through 5-HT_1B/1D receptors throughout the TCC and associated areas of the brain. In addition, triptans can enhance vasoconstriction, both through direct 5-HT_1B-mediated dilation of cranial blood vessels, as well as through 5-HT_1D-mediated suppression of CGRP release. Although triptans are classically described solely in terms of their effects on 5-HT_1B/1D receptors, they also act as 5-HT_1F agonists as well. This 5-HT subtype is also found throughout the TCC, but is not present appreciably in cerebral vasculature; the significance of triptan-mediated 5-HT_1F activation is currently not well described. Additionally, CSD that initiates in the ipsilateral parietal region may exert its effects in a manner that relies on 5-HT_1B/1D receptor activation, suggesting that triptans may have some effect on CSD-mediated symptoms.