Imitrex Statdose Refill (sumatriptan succinate)

Dosage of sumatriptan succinate is expressed in terms of sumatriptan.

Although the effect of renal impairment on the pharmacokinetics of sumatriptan has not been evaluated, little clinical effect would be expected since the drug is largely inactivated metabolically.

The liver plays an important role in the presystemic clearance of orally administered sumatriptan. Accordingly, the bioavailability of sumatriptan following oral administration may be increased markedly in patients with liver disease. (See Pharmacokinetics: Elimination.) If oral sumatriptan therapy is considered in patients with hepatic impairment, the manufacturers state that the maximum single dose generally should not exceed 50 mg. Fixed-combination tablets containing sumatriptan 85 mg and naproxen sodium 500 mg should not be used in patients with hepatic impairment since sumatriptan dosage cannot be appropriately adjusted. Sumatriptan is contraindicated in patients with severe hepatic impairment.

Sumatriptan succinate is administered orally. The drug also can be administered parenterally but only by subcutaneous injection. Sumatriptan also can be administered intranasally. Sumatriptan should not be given IV because of the potential risk of inducing coronary vasospasm. (See Cautions: Precautions and Contraindications.) Sumatriptan has been administered as an iontophoretic transdermal system; however, the manufacturer voluntarily suspended marketing of the formulation because of reports of serious application site reactions. (See Cautions: Local Effects.)

The manufacturer states that tablets containing sumatriptan succinate in fixed combination with naproxen sodium may be administered without regard to meals. The fixed-combination tablets should not be split, crushed, or chewed.

Autoinjection devices are available for subcutaneous administration of sumatriptan to facilitate self-administration of the drug by patients for whom the commercially available doses of 4 or 6 mg are deemed appropriate. An injection pen is available for use with prefilled cartridges labeled as containing 4 or 6 mg of sumatriptan; the needles that accompany this device penetrate approximately 5-6 mm (1/4 inch). In addition, a prefilled, single-use injection pen labeled as containing 6 mg of sumatriptan (also with 1/4-inch projection of the needle following activation of the device) is available. Patients using these devices should be instructed to use injection sites with adequate skin and subcutaneous thickness to accommodate the length of the needle (e.g., lateral thigh, upper arm); care should be taken to avoid IM or IV administration. A prefilled needleless device for subcutaneous administration that is labeled as containing 6 mg of sumatriptan also is available; patients using this device should be instructed to use sites on the abdomen (avoiding the 2-inch area around the umbilicus) or thigh with adequate subcutaneous thickness to accommodate penetration of the injection solution into the subcutaneous space; use of administration sites on the upper arm should be avoided since the delivered dose may be suboptimal. Patients should be given adequate instructions by their clinician, as well as the written instructions supplied with the autoinjection device, before they self-administer sumatriptan injection for the first time.

The patient information provided by the manufacturer should be consulted for directions on intranasal administration of sumatriptan.

Consideration should be given to administering the initial dose of sumatriptan under medical supervision in patients with multiple risk factors for cardiovascular disease (e.g., postmenopausal women, men older than 40 years of age, smokers, patients with hypertension, hypercholesterolemia, obesity, diabetes mellitus, or a family history of coronary artery disease) but who have had a satisfactory cardiovascular evaluation. Electrocardiographic evaluation during the interval immediately after administration of sumatriptan should be considered in these patients since cardiac ischemia can occur in the absence of symptoms.

If a patient does not respond to the first dose of sumatriptan for a given attack, the diagnosis of migraine or cluster headache should be reconfirmed before administration of subsequent doses.

Although sumatriptan generally is effective at whatever stage of a migraine attack it is administered, it is advisable to initiate therapy with the drug as soon as possible after the onset of an attack so that the patient may experience maximum relief.

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Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

5-Ht1d Agonists/Ergot Alkaloids

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: The 5-HT1D agonists and ergot alkaloids can produce vasospastic reactions.

CLINICAL EFFECTS: Concurrent therapy may produce additive vasospastic effects.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The US manufacturer states that sumatriptan should not be used within 24 hours of an ergotamine-containing or ergotamine-like medication (such as dihydroergotamine or methysergide).(1,2) The Australian(3) and UK(4,5) manufacturers state that 24 hours should elapse before sumatriptan is administered following an ergotamine-containing preparation and 6 hours should elapse before an ergotamine-containing preparation is administered following sumatriptan. The US manufacturer states that zolmitriptan should not be used within 24 hours of an ergotamine-containing or ergotamine-like medication.(6) The UK manufacturer states that zolmitriptan should not be used within 6 hours of an ergotamine-containing or ergotamine-like medication.(7) The The Australian manufacturer states that 24 hours should elapse before zolmitriptan is administered following an ergotamine-containing preparation and 6 hours should elapse before an ergotamine-containing medication is administered following zolmitriptan.(8) The US manufacturer states that the use of rizatriptan within 24 hours of an ergotamine-containing or ergot-type medication is contraindicated.(9) The US manufacturer states that the use of naratriptan within 24 hours of an ergotamine-containing or ergot-type medication is contraindicated.(10) The Australian manufacturer states that concurrent use of naratriptan and ergotamine or ergotamine derivatives is not recommended.(11) The US manufacturer states that the use of eletriptan within 24 hours of an ergotamine-containing or ergot-type medication is contraindicated.(12) The UK manufacturer states that the use of eletriptan within 24 hours of an ergotamine-containing or ergot-type medication is not recommended.(13)

DISCUSSION: Because of the theoretical risk of additive vasospastic effects, the US manufacturer states that the use of sumatriptan within 24 hours of an ergotamine-containing or ergotamine-like medication is contraindicated.(1,2) The Australian(3) and UK(4,5) manufacturer states that 24 hours should elapse before sumatriptan is administered following an ergotamine-containing preparation and 6 hours should elapse before an ergotamine-containing medication is administered following sumatriptan. Although the pharmacokinetics of zolmitriptan were not affected by ergotamine, the UK manufacturer of zolmitriptan recommends that 6 hours should elapse between the administration of zolmitriptan and an ergotamine preparation.(7) The US manufacturer of zolmitriptan states under contraindications that zolmitriptan should not be used within 24 hours of an ergotamine-containing or ergot-type medication.(6) The Australian manufacturer states that 24 hours should elapse before zolmitriptan is administered following an ergotamine-containing preparation and 6 hours should elapse before an ergotamine-containing medication is administered following zolmitriptan.(8) Because of the additive risk of prolonged vasospastic reactions, the manufacturers of rizatriptan(9) and naratriptan(10) in the US state that the use of ergotamine-containing or ergot-type medications and these agents is contraindicated. The Australian manufacturer states that concurrent use of naratriptan and ergotamine or ergotamine derivatives is not recommended.(11) Administration of oral ergotamine one and two hours after eletriptan resulted in additive increases in blood pressure.(13)

Selected 5-Ht1d Agonists/Mao Inhibitors

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: MAOIs inhibit the metabolism of rizatriptan,(1) sumatriptan,(2-9) and zolmitriptan.(10-11)

CLINICAL EFFECTS: Concurrent use of MAOIs may result in increased levels and effects of rizatriptan, sumatriptan or zolmitriptan.(1-11)

PREDISPOSING FACTORS: Patients with a history of cardiovascular disease, e.g., coronary artery disease (CAD), transient ischemic attack (TIA), stroke, cardiac conduction disorders or poorly controlled hypertension are not considered candidates for 5-HT1D agonist therapy and would be at greater risk for toxicity due to this interaction.

PATIENT MANAGEMENT: Concurrent administration of rizatriptan and a MAOI or administration of rizatriptan within two weeks of the discontinuation of a MAOI is contraindicated according to product labeling for rizatriptan.(1) Concurrent administration of sumatriptan and a MAOI or administration of sumatriptan within two weeks of the discontinuation of a MAOI is contraindicated according to the Australian, Canada, UK, and US product labeling for these agents.(2-9) Concurrent administration of zolmitriptan and a MAO-A inhibitor or the administration of zolmitriptan within two weeks of discontinuation of a MAO-A inhibitor is contraindicated according to US labeling.(10) The UK manufacturer states that a maximum of 7.5 mg of zolmitriptan should be administered within 24 hours of a MAO-A inhibitor.(11) Eletriptan and frovatriptan are not metabolized by MAO-A(12, 13) and may be an alternative in patients who require treatment with an MAO-A inhibitor.

DISCUSSION: Rizatriptan is metabolized by the 'A' subtype of monoamine oxidase. In a study with 12 subjects, the concurrent administration of rizatriptan (10 mg) with moclobemide (450 mg daily, a selective, reversible MAO-A inhibitor) resulted in increases in the rizatriptan area-under-curve (AUC) and maximum concentration (Cmax) by 119% and 41%, respectively. The AUC of the active metabolite, N-monodesmethyl rizatriptan, increased over 400%. Plasma concentrations of rizatriptan may be increased by selective MAO-A inhibitors or by nonselective MAO-A and MAO-B inhibitors, although the interaction is expected to be greater with selective MAO-A inhibitors. The manufacturer also states that no interaction is expected with selective MAO-B inhibitors.(1) Sumatriptan oral bioavailability is approximately 15%, primarily due to presystemic clearance by MAO-A in the gut and liver. A small study found an approximately 7-fold increase in systemic sumatriptan exposure when an MAO-A inhibitor was given prior to a 25 mg oral dose of sumatriptan.(4) In another study, pretreatment with an MAO-A inhibitor prior to administration of injectable sumatriptan resulted in a 2-fold increase in sumatriptan AUC and a 40% increase in elimination half-life.(8) Pretreatment with a MAO-B inhibitor did not produce any significant changes in sumatriptan pharmacokinetics. The effect of a MAOI on nasal sumatriptan systemic absorption is expected to be less than that seen with oral sumatriptan but greater than that seen with injectable sumatriptan.(6) Administration of moclobemide, a MAO-A inhibitor, for one week (150 mg twice daily) resulted in a 25% increase in zolmitriptan AUC and a three-fold increase in Cmax and AUC for zolmitriptan's active N-desmethyl metabolite.(10,11) Administration of selegiline for one week at a dosage of 10 mg daily had no effect on the pharmacokinetics of zolmitriptan or its metabolite.(10) At daily doses of 10 mg, selegiline is primarily a selective MAO-B inhibitor; however, at higher doses, selegiline is capable of inhibiting MAO-A. Hypertensive reactions to the addition of either tyramine or a sympathomimetic to recommended dosages of selegiline have been reported.(14) Therefore, patients receiving selegiline at dosages of greater than 10 mg daily should be considered to be receiving a MAO-A inhibitor. It would also be prudent to monitor patients receiving selegiline at recommended dosages for this interaction. Methylene blue, when administered intravenously, has been shown to reach sufficient concentrations to be a potent inhibitor of MAO-A.(15) Metaxalone is a weak inhibitor of MAO.(17,18) One or more of the drug pairs linked to this monograph have been included in a list of interactions that should be considered "high-priority" for inclusion and should not be inactivated in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology.

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Selected 5-Ht1d Agonists/Linezolid

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Monoamine oxidase inhibitors (MAOIs) inhibit the metabolism of rizatriptan,(1) sumatriptan,(2-9) and zolmitriptan.(10) Linezolid is a weak, reversible, nonselective MAOI.(12)

CLINICAL EFFECTS: Concurrent use of linezolid may result in increased levels and effects of rizatriptan, sumatriptan or zolmitriptan.(1-11)

PREDISPOSING FACTORS: Patients with a history of cardiovascular disease, e.g. coronary artery disease (CAD), transient ischemic attack (TIA), stroke, cardiac conduction disorders or poorly controlled hypertension, are not considered candidates for 5-HT1D agonist therapy and would be at greater risk for toxicity due to this interaction.

PATIENT MANAGEMENT: Concurrent administration of rizatriptan and a MAOI or administration of rizatriptan within two weeks of the discontinuation of a MAOI is contraindicated according to product labeling for rizatriptan.(1) Concurrent administration of sumatriptan and a MAOI within two weeks of the discontinuation of a MAOI is contraindicated according to the Australian, Canada, UK, and US product labeling for these agents.(2-9) Concurrent administration of zolmitriptan and a MAO-A Inhibitor or the administration of zolmitriptan within two weeks of discontinuation of a MAO-A Inhibitor is contraindicated according to US labeling.(10) The UK manufacturer states that a maximum of 7.5 mg of zolmitriptan should be administered within 24 hours of a MAO-A inhibitor.(11) The manufacturer of linezolid does not contraindicated the use of 5-HT1D agonists but states that they should not be coadministered unless clinically appropriate and patients are carefully observed for signs and symptoms of serotonin syndrome.(12) Eletriptan and frovatriptan are not metabolized by MAO-A(13,14) and may be an alternative in patients who require treatment with linezolid.

DISCUSSION: The combination of linezolid and 5-HT1D agonists has not been studied. Other MAOIs have been reported to interact with 5-HT1D agonists. Rizatriptan is metabolized by the 'A' subtype of monoamine oxidase. In a study with 12 subjects, the concurrent administration of rizatriptan (10 mg) with moclobemide (450 mg daily, a selective, reversible MAO-A inhibitor) resulted in increases in the rizatriptan area-under-curve (AUC) and maximum concentration (Cmax) by 119% and 41%, respectively. The AUC of the active metabolite, N-monodesmethyl rizatriptan, increased over 400%. Plasma concentrations of rizatriptan may be increased by selective MAO-A inhibitors or by nonselective MAO-A&B inhibitors, although the interaction is expected to be greater with selective MAO-A inhibitors. The manufacturer also states that no interaction is expected with selective MAO-B inhibitors.(1) Sumatriptan oral bioavailability is approximately 15%, primarily due to presystemic clearance by MAO-A in the gut and liver. A small study found an approximately 7-fold increase in systemic sumatriptan exposure when an MAO-A inhibitor was given prior to a 25 mg oral dose of sumatriptan.(4) In another study, pretreatment with an MAO-A inhibitor prior to administration of injectable sumatriptan resulted in a 2-fold increase in sumatriptan AUC and a 40% increase in elimination half-life.(8) Pretreatment with a MAO-B inhibitor did not produce any significant changes in sumatriptan pharmacokinetics. The effect of a MAOI on nasal sumatriptan systemic absorption is expected to be less than that seen with oral sumatriptan but greater than that seen with injectable sumatriptan.(6) Administration of moclobemide, a MAO-A inhibitor, for one week (150 mg twice daily) resulted in a 25% increase in zolmitriptan AUC and a three-fold increase in Cmax and AUC for zolmitriptan's active N-desmethyl metabolite.(10,11)

Moderate Interaction: Assess the risk to the patient and take action as needed.

Selected 5-Ht1d Agonists/Rasagiline

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Rasagiline may inhibit the monamine oxidase-A (MAO-A) mediated metabolism of rizatriptan,(2) sumatriptan,(3-10) and zolmitriptan.(11-12) At concentrations associated with recommended doses of 0.5 mg to 1 mg daily, rasagiline has a high specificity for MAO-B. Mild hepatic impairment, concomitant use of strong CYP1A2 inhibitors, or use of higher than recommended doses may substantially increase rasagiline systemic exposure and could result in MAO-A inhibition.

CLINICAL EFFECTS: Systemic concentrations of rizatriptan, sumatriptan or zolmitriptan may be increased.(2-12)

PREDISPOSING FACTORS: Rasagiline concentration may be increased 2-fold or more in patients also receiving a strong CYP1A2 inhibitor (e.g. ciprofloxacin, fluvoxamine).(1) Rasagiline plasma concentrations are higher in patients with any degree of hepatic impairment. Rasagiline should not be used in patients with moderate or severe hepatic impairment.(1) Patients with a history of cardiovascular disease, e.g. coronary artery disease (CAD), transient ischemic attack (TIA), stroke, cardiac conduction disorders or poorly controlled hypertension, are not considered candidates for 5-HT1D agonist therapy and would be at greater risk for toxicity due to this interaction.

PATIENT MANAGEMENT: Evaluate patient for predisposing risk factors, e.g. concomitant use with CYP1A2 inhibitors, cardiovascular disease, and hepatic impairment. Patients with mild hepatic impairment or receiving concurrent therapy with a CYP1A2 inhibitor (e.g. ciprofloxacin, fluvoxamine) should be receiving a maximum rasagiline dose of 0.5 mg daily.

DISCUSSION: Triptan interaction studies with other MAO inhibitors: Rizatriptan is metabolized by the 'A' subtype of monoamine oxidase. In a study with 12 subjects, the concurrent administration of rizatriptan (10 mg) with moclobemide (450 mg daily, a selective, reversible MAO-A inhibitor) resulted in increases in the rizatriptan area-under-curve (AUC) and maximum concentration (Cmax) by 119% and 41%, respectively. The AUC of the active metabolite, N-monodesmethyl rizatriptan, increased over 400%. Plasma concentrations of rizatriptan may be increased by selective MAO-A inhibitors or by nonselective MAO-A&B inhibitors, although the interaction is expected to be greater with selective MAO-A inhibitors. The manufacturer also states that no interaction is expected with selective MAO-B inhibitors.(2) Sumatriptan oral bioavailability is approximately 15%, primarily due to presystemic clearance by MAO-A in the gut and liver. A small study found an approximately 7-fold increase in systemic sumatriptan exposure when an MAO-A inhibitor was given prior to a 25 mg oral dose of sumatriptan.(5) In another study, pretreatment with an MAO-A inhibitor prior to administration of injectable sumatriptan resulted in a 2-fold increase in sumatriptan AUC and a 40% increase in elimination half-life.(9) Pretreatment with a MAO-B inhibitor did not produce any significant changes in sumatriptan pharmacokinetics. The effect of a MAOI on nasal sumatriptan systemic absorption is expected to be less than that seen with oral sumatriptan but greater than that seen with injectable sumatriptan.(6) Administration of moclobemide, a MAO-A inhibitor, for one week (150 mg twice daily) resulted in a 25% increase in zolmitriptan AUC and a three-fold increase in Cmax and AUC for zolmitriptan's active N-desmethyl metabolite.(11,12) Administration of selegiline for one week at a dosage of 10 mg daily had no effect on the pharmacokinetics of zolmitriptan or its metabolite.(11) At daily doses of 10 mg, selegiline is primarily a selective MAO-B inhibitor; however, at higher doses, selegiline is capable of inhibiting MAO-A. Hypertensive reactions to the addition of either tyramine or a sympathomimetic to recommended dosages of selegiline have been reported.(15) Therefore, patients receiving selegiline at dosages of greater than 10 mg daily should be considered to be receiving a MAO-A inhibitor. It would also be prudent to monitor patients receiving selegiline at recommended dosages for this interaction.

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• Acute myocardial infarction
• Angina
• Cerebral ischemia
• Cerebrovascular accident
• Coronary artery disease
• Hemiplegic migraine
• Ischemic bowel disease
• Myocardial ischemia
• Peripheral vascular disease
• Prinzmetal angina
• Serotonin syndrome
• Severe uncontrolled hypertension

• Tachyarrhythmia

• Seizure disorder

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Rare or Very Rare

• Abdominal pain with cramps
• Acquired dystonia
• Acute myocardial infarction
• Anaphylaxis
• Angioedema
• Bronchospastic pulmonary disease
• Cerebrovascular accident
• Chest pain
• Chest tightness
• Coronary artery spasm
• Dysphagia
• Hypersensitivity drug reaction
• Hypertension
• Hypotension
• Intracerebral hemorrhage
• Ischemic bowel disease
• Myocardial ischemia
• Peripheral ischemia
• Raynaud's phenomenon
• Seizure disorder
• Serotonin syndrome
• Splenic infarction
• Subarachnoid intracranial hemorrhage
• Ventricular fibrillation
• Ventricular tachycardia
• Vision impairment

More Frequent

• Dizziness
• Dysgeusia
• Flushing
• Hypoesthesia
• Injection site sequelae
• Nasal passage irritation
• Nausea
• Paresthesia
• Sensation of warmth
• Stinging of skin
• Vertigo
• Vomiting

Less Frequent

• Drowsy
• Dysesthesia
• Hyperhidrosis
• Muscle weakness
• Myalgia
• Neck stiffness

Rare or Very Rare

• Anticholinergic toxicity
• Cramps
• Fatigue
• Jaw pain
• Medication overuse headache
• Mouth irritation
• Muscle rigidity
• Nasal pain
• Palpitations
• Sinusitis
• Sore tongue
• Symptoms of anxiety
• Tremor
• Visual changes

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There are no adequate and well-controlled studies evaluating the use of sumatriptan in pregnant women. Although a causal relationship to the drug has not been definitely established, agenesis of the corpus callosum has been reported in an infant whose mother received oral sumatriptan at week 4 and 6 of pregnancy. Sumatriptan should be used during pregnancy only if the potential benefit justifies the risk to the fetus.

Sumatriptan has been associated with fetal abnormalities and embryo and fetal mortality in animals. Embryolethality was noted in pregnant rabbits given IV sumatriptan throughout the period of organogenesis in daily doses at or close to those producing maternal toxicity, representing systemic exposures less than the maximum recommended daily subcutaneous dosage in humans of 12 mg (on a mg/m2 basis). The mechanism of the embryolethality is not known. This effect was not seen in pregnant rats given IV sumatriptan throughout organogenesis at dosages representing approximately 10 times the maximum recommended daily subcutaneous human dosage of 12 mg (on a mg/m2 basis) or in pregnant rats given subcutaneous sumatriptan prior to and throughout pregnancy. In pregnant rabbits, oral sumatriptan dosages of 100 mg/kg daily (representing 18 times the maximum single human oral dose of 100 mg on a mg/m2 basis) throughout the period of organogenesis produced embryolethality and maternotoxicity; these effects were not observed at oral sumatriptan dosages of 50 mg/kg daily. No fetal effects were observed in rats receiving 50 mg/kg daily (representing 5 times the maximum single oral human dose of 100 mg on a mg/m2 basis).

Sumatriptan has been shown to be teratogenic in pregnant rats given long-term oral sumatriptan dosages of 500 mg/kg daily (representing 50 times the maximum single human oral dose of 100 mg on a mg/m2 basis); an increased incidence of a syndrome of malformations (short tail/short body and vertebral disorganization) was observed in these animals. Sumatriptan was associated with an increased incidence of cervicothoracic vascular defects and skeletal abnormalities in fetuses of rabbits receiving oral dosages greater than 15 mg/kg daily (representing 3 times the maximum single human oral dose of 100 mg on a mg/m2 basis); these effects were not observed at lower dosages. Blood vessel abnormalities (cervicothoracic and umbilical) occurred in offspring of pregnant rats given oral dosages of 250 mg/kg daily or greater (representing 25 times the maximum single human oral dose of 100 mg on a mg/m2 basis); these effects were not observed at oral dosages of approximately 60 mg/kg daily or less (representing 6 times the maximum single human oral dose of 100 mg on a mg/m2 basis). In a study in rats dosed daily with subcutaneous sumatriptan prior to and throughout pregnancy, there was no evidence of teratogenicity.

Oral sumatriptan produced a decrease in pup survival between birth and postnatal day 4 when administered to pregnant rats at dosages of 250 mg/kg daily or higher (representing 25 times the maximum single human oral dose of 100 mg on a mg/m2 basis) during the period of organogenesis; pups were not affected when dams were given 60 mg/kg daily (representing 6 times the maximum single human dose of 100 mg on a mg/m2 basis). In rats given oral dosages of 1000 mg/kg daily (representing 100 times the maximum single human oral dose of 100 mg on a mg/m2 basis) from gestational day 17 through postnatal day 21, decreased pup survival was found at postnatal days 2, 4, and 20; pups were not affected when dams were given 100 mg/kg of sumatriptan daily.

Sumatriptan is distributed into breast milk following administration of the drug to lactating animals or nursing women. (See Pharmacokinetics: Distribution.) Some manufacturers state that caution is advised when sumatriptan is administered to nursing women. It has been suggested that exposure of the infant to the limited amount of drug distributed into milk following a single 6-mg subcutaneous dose could be minimized by expressing and discarding all milk for 8 hours after the dose. The manufacturers recommend minimizing infant exposure to sumatriptan by avoiding breast-feeding for 12 hours after receiving the drug as oral tablets or nasal spray.

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