Drug Interactions
Metabolized principally by MAO-A isoenzyme in vitro.
Protein-bound Drugs
Effect on protein binding of other drugs has not been evaluated, but expected to be minor due to low-level protein binding of sumatriptan.
Specific Drugs
| Drug |
Interaction |
Comments |
| Acetaminophen |
Pretreatment with oral sumatriptan followed by acetaminophen affected rate, but not extent of acetaminophen absorption over 8 hours |
|
| Alcohol |
Administration of alcohol 30 minutes prior to oral sumatriptan did not affect sumatriptan pharmacokinetics |
|
| Amitriptyline |
Concomitant use did not affect sumatriptan efficacy |
|
| Antidepressants, SSRIs (e.g., citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline) and SNRIs (e.g., duloxetine, venlafaxine) |
Potentially life-threatening serotonin syndrome |
Observe carefully if used concomitantly, particularly during treatment initiation, dosage increases, or when another serotonergic agent is initiated |
| Ergot alkaloids (e.g., ergotamine, dihydroergotamine, methysergide) |
Additive vasospastic effects |
Use within 24 hours contraindicated |
| 5-HT1receptor agonists |
Additive vasospastic effects |
Use within 24 hours contraindicated |
| MAO inhibitors |
MAO-A inhibitors decrease sumatriptan clearance, resulting in substantially increased systemic exposure; no substantial effect on sumatriptan metabolism seen with an MAO-B inhibitor |
Use of nasal or oralsumatriptan within 2 weeks of MAO-A inhibitor contraindicated; although not generally recommended, if clinically warranted, sub-Q sumatriptan may be used concurrently with MAO-A inhibitors with appropriate dosage adjustment and careful monitoring |
| Propranolol |
Concomitant use did not affect sumatriptan efficacy; pretreatment with propranolol did not alter pharmacokinetics or pharmacodynamics of oral sumatriptan |
|
| Verapamil |
Concomitant use did not affect sumatriptan efficacy |
|
| Xylometazoline |
Topical application of xylometazoline to nasal mucosa 15 minutes prior to intranasal sumatriptan did not affect sumatriptan pharmacokinetics |
|
Pharmacokinetics
Absorption
Bioavailability
Absorbed rapidly after oral, intranasal, or sub-Q administration, with peak plasma concentrations attained within approximately 0.5–5 hours, 0.8–1.8 hours, or 5–20 minutes, respectively. Bioavailability after sub-Q administration averages 97% of that obtained with IV administration; bioavailability after oral or intranasal administration averages only about 15 or 17%, respectively, principally due to presystemic metabolism and in part due to incomplete absorption.
Oral absorption is not appreciably affected by gastric stasis that may occur during migraine attack, but time to peak concentration is prolonged by about 30 minutes; pharmacokinetics after sub-Q injection appear to be similar during migraine attacks and pain-free periods.
Special Populations
In patients with hepatic impairment, bioavailability after oral administration may be markedly increased. In a small study, AUC and peak plasma concentrations increased approximately 70% and time to peak plasma concentrations occurred 40 minutes earlier after oral administration compared with such values in healthy adults.
Onset
After oral administration, onset of relief of migraine symptoms generally occurs within 1–3 hours after single doses (25–100 mg), with maximum pain relief attained within 3–6 hours.
After intranasal administration, onset of headache relief occurs within 30 minutes following a 10-, 20-, or 40-mg dose.
After sub-Q administration, onset of pain relief usually occurs within 10–34 minutes in patients with moderate to severe migraine headache pain, with maximum relief attained within 1–2 hours; onset of pain relief generally occurs within 4–7 minutes in patients with cluster headache, with headache resolution shortly thereafter.
Food
Food does not appreciably affect oral bioavailability, but prolongs time to peak concentration.
Distribution
Extent
Rapidly and widely distributed into body tissues after sub-Q administration.
Distributed into human milk; only small amounts cross placenta by passive transport in vitro.
Plasma Protein Binding
Approximately 14–21%.
Elimination
Metabolism
Metabolized in the liver and possibly in the GI tract principally to inactive indole acetic acid metabolite and other minor metabolites; metabolized principally by MAO-A isoenzyme in vitro.
Elimination Route
After oral administration, excreted in urine (57–60%) and feces (37–40%); only 3 and 9% of dose is excreted as unchanged drug in urine and feces, respectively. After sub-Q administration, approximately 22 or 38–53% of dose is excreted in urine unchanged or as indole acetic acid metabolite, respectively; 0.6 and 3.3% of dose is excreted in feces as unchanged drug and indole acetic acid metabolite, respectively.
Half-life
1.5–2.6 hours.
Special Populations
In patients with renal impairment, pharmacokinetics not evaluated, but little clinical effect expected since drug is largely metabolized to an inactive metabolite.
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