Naratriptan

Pharmaceuticals

Pharmaceuticals -> Listed in ZINC15

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

Pharmaceuticals

There is no specific antidote to naratriptan. Standard supportive treatment should be applied as required. If the patient presents with chest pain or other symptoms consistent with angina pectoris, ECG monitoring should be performed for evidence of ischemia. (L1712)

Three distinct pharmacological actions have been implicated in the antimigraine effect of the triptans: (1) stimulation of presynaptic 5-HT1D receptors, which serves to inhibit both dural vasodilation and inflammation; (2) direct inhibition of trigeminal nuclei cell excitability via 5-HT1B/1D receptor agonism in the brainstem and (3) vasoconstriction of meningeal, dural, cerebral or pial vessels as a result of vascular 5-HT1B receptor agonism.

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

naratriptan

DILI Negative

Oral

DOI:10.1016/j.drudis.2019.09.022

N02CC02

N - Nervous system

QN - Nervous system

Naratriptan is a selective agonist of serotonin (5-hydroxytryptamine; 5-HT) type 1B and 1D receptors. It is structurally and pharmacologically related to other selective 5-HT1B/1D receptor agonist. Naratriptan has only a weak affinity for 5-HT_1A, 5-HT_5A, and 5-HT₇ receptors and no significant affinity or pharmacological activity at 5-HT₂, 5-HT₃ or 5-HT₄ receptor subtypes or at alpha1-, alpha2-, or beta-adrenergic, dopamine1,; dopamine2; muscarinic, or benzodiazepine receptors. This action in humans correlates with the relief of migraine headache. In addition to causing vasoconstriction, experimental data from animal studies show that Naratriptan also activates 5-HT₁ receptors on peripheral terminals of the trigeminal nerve innervating cranial blood vessels, which may also contribute to the antimigrainous effect of Naratriptan in humans.

Three distinct pharmacological actions have been implicated in the antimigraine effect of the triptans: (1) stimulation of presynaptic 5-HT1D receptors, which serves to inhibit both dural vasodilation and inflammation; (2) direct inhibition of trigeminal nuclei cell excitability via 5-HT1B/1D receptor agonism in the brainstem and (3) vasoconstriction of meningeal, dural, cerebral or pial vessels as a result of vascular 5-HT1B receptor agonism.

Primarily hepatic. <i>In vitro,</i> naratriptan is metabolized by a wide range of cytochrome P450 isoenzymes into a number of inactive metabolites.

Primarily hepatic. <i>In vitro,</i> naratriptan is metabolized by a wide range of cytochrome P450 isoenzymes into a number of inactive metabolites. Half Life: 5-8 hours

QX3KXL1ZA2

NARATRIPTAN

Mechanisms of Action [MoA] - Serotonin 1b Receptor Agonists

Mechanisms of Action [MoA] - Serotonin 1d Receptor Agonists

Established Pharmacologic Class [EPC] - Serotonin-1b and Serotonin-1d Receptor Agonist

Naratriptan is a Serotonin-1b and Serotonin-1d Receptor Agonist. The mechanism of action of naratriptan is as a Serotonin 1b Receptor Agonist and Serotonin 1d Receptor Agonist.

Drugs used to cause constriction of the blood vessels.

Endogenous compounds and drugs that specifically stimulate SEROTONIN 5-HT1 RECEPTORS. Included under this heading are agonists for one or more of the specific 5-HT1 receptor subtypes.

Well absorbed (74% oral biovaility), absorption is rapid with peak plasma concentrations after 2-5 hours. The rate of absorption is slower during a migraine attack.

170 L

6.6 mL/min/kg

Use (kg; approx.) in Germany (2009): >10

For the acute treatment of migraine attacks with or without aura in adults.