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Drug Notebook

Generic Name: dihydroergotamine

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D.H.E. 45, Dihydroergotamine Mesylate, Migranal
An antimigraine agent - treats Cluster Headache and Migraine
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FDA Alerts

  • Possible serious and/or life-threatening cerebral and/or peripheral ischemia when administered concomitantly with potent CYP3A4 inhibitors (see Interactions); concomitant use contraindicated.

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dihydroergotamine
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(dye hye droe er GOH ta meen)

Drug Interactions

Extensively metabolized, principally by CYP3A4. Inhibits CYP3A.

Drugs Affecting Hepatic Microsomal Enzymes

Potent CYP3A4 inhibitors: Potential pharmacokinetic interaction (increased serum dihydroergotamine concentrations); potentially fatal cerebral ischemia and/or ischemia of the extremities possible. Concomitant use with potent CYP3A4 inhibitors contraindicated.

Less-potent CYP3A4 inhibitors: Similar effects not reported to date; however, consider possibility of serious toxicity during concomitant use.

Specific Drugs and Foods

Drug or Food Interaction Comment
Antidepressants, SSRIs (e.g., fluoxetine, fluvoxamine, paroxetine, sertraline)

Weakness, hyperreflexia, and/or incoordination reported rarely with other 5-HT1 receptor agonists

Potential decrease in dihydroergotamine metabolism

 Use with caution
Antifungals, azole (e.g., fluconazole, itraconazole, ketoconazole)

Potent CYP3A4 inhibitors (e.g., itraconazole, ketoconazole): Inhibition of dihydroergotamine metabolism and increased risk of potentially fatal cerebral ischemia and/or ischemia of the extremities

Less potent CYP3A4 inhibitors (e.g., fluconazole): Potential decrease in dihydroergotamine metabolism

Concomitant use of potent CYP3A4 inhibitors contraindicated

Use less potent CYP3A4 inhibitors with caution

Clotrimazole Potential decrease in dihydroergotamine metabolism Use with caution
Ergot alkaloids (e.g., ergotamine, methysergide) Potential for excessive vasoconstriction Use within 24 hours contraindicated
Grapefruit juice Potential decrease in dihydroergotamine metabolism Use with caution
HIV protease inhibitors (e.g., ritonavir, nelfinavir, indinavir, saquinavir)

Potent CYP3A4 inhibitors (e.g., ritonavir, nelfinavir, indinavir): Inhibition of dihydroergotamine metabolism and increased risk of potentially fatal cerebral ischemia and/or ischemia of the extremities

Less potent CYP3A4 inhibitors (e.g., saquinavir): Potential decrease in dihydroergotamine metabolism

Concomitant use of potent CYP3a4 inhibitors contraindicated

Use less potent CYP3A4 inhibitors with caution

Macrolide antibiotics (e.g., erythromycin, clarithromycin, troleandomycin) Inhibition of dihydroergotamine metabolism; increased risk of potentially fatal cerebral ischemia and/or ischemia of the extremities Concomitant use contraindicated
Nefazodone Potential decrease in dihydroergotamine metabolism Use with caution
Nicotine Possible vasoconstriction and increased ischemic response Use with caution
Propranolol Potentiation of dihydroergotamine's vasoconstrictive action Use with caution
Serotonin (5-HT1) receptor agonists (e.g., sumatriptan) Additive vasoconstrictor effects Use within 24 hours contraindicated
Vasoconstrictors, peripheral or central Additive increases in BP Concomitant use contraindicated
Zileuton Potential decrease in dihydroergotamine metabolism Use with caution

Pharmacokinetics

Absorption

Bioavailability

Following oral administration, bioavailability is <1% because of first-pass metabolism.

Following intranasal administration, mean bioavailability is 32% relative to parenteral administration.

Absolute bioavailability for sub-Q and IM routes has not been determined, however, no difference was observed in bioavailability from IM and sub-Q doses.

Onset

Intranasal: About 30 minutes.

IM: 15–30 minutes.

IV: Variable, usually <5 minutes.

Duration

Intranasal: At least 4 hours.

Sub-Q or IV: Approximately 8 hours.

Distribution

Plasma Protein Binding

93%.

Elimination

Metabolism

Extensively metabolized in the liver to several metabolites; principal metabolite is pharmacologically active.

Metabolized by CYP3A4.

Elimination Route

Eliminated principally in feces (via bile) as metabolites; <10% of a dose is excreted in urine.

Half-life

Following intranasal administration: Biphasic; terminal half-life is approximately 10 hours.

Following IM or IV administration: Multi-exponential; terminal half-life is approximately 9 hours.

Stability

Storage

Intranasal

Solution

<25°C; do not refrigerate or freeze.

Parenteral

Injection

<25°C; do not refrigerate or freeze. Protect from light and heat.

Compatibility

Parenteral

Stable at pH 3.6–4.8. Increased degradation observed at pH <3.6; decreasing solubility occurs at pH >4.8.

Solution Compatibility

Compatible
Dextrose 5% in water
Sodium chloride 0.9%

Actions

  • A serotonin (5-hydroxytryptamine; 5-HT) type 1D receptor agonist. May ameliorate migraine through selective constriction of certain intracranial blood vessels, inhibition of neuropeptide release, and reduced transmission in trigeminal pathway.
  • Has greater α-adrenergic blocking activity but less vasoconstrictor activity than ergotamine.
  • Possesses oxytocic properties.

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Uses Dosage and Administration Cautions Drug Interactions Pharmacokinetics Stability Actions Advice to Patients Preparations
Related Learning
Centers
·As a Drug
Cluster Headaches
Migraine Headache
Migraine with Aura
Pain
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