AMERGE
Pronunciation: NAR-a-trip-tan (a-MERJ)

What it is5-HT1B/1D agonist; acute migraine.
Why this oneIts slower onset and longer action produce fewer recurrences, fitting gradual or prolonged attacks.
What limits itIt is too slow for a fast-peaking attack. Coronary vasospasm precludes use in ischemic disease; adjust for renal impairment.
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| FDA dosing | Population | Start | Target | Max |
|---|---|---|---|---|
| Acute migraine | Adults | 1 mg or 2.5 mg PRN | 1 mg or 2.5 mg | 5 mg / 24 h |
Renal Mild-moderate: start 1 mg, max 2.5 mg/24 h; contraindicated in severe (CLcr <15 mL/min)
Hepatic Mild-moderate (Child-Pugh A/B): start 1 mg, max 2.5 mg/24 h; contraindicated in severe (Child-Pugh C)
May repeat once after 4 h; not to exceed 5 mg in any 24-h period
Available strengths
Pregnancy No adequate human data; animal developmental toxicity (embryolethality, fetal abnormalities)
Lactation No human data; present in rat milk
Generic entry2010
NO BOXED WARNINGS
Principal riskSlow onset; coronary vasospasm
Legacy pregnancy categoryUnknown / historical label unavailable
Defining liabilityAgent-specific vascular, serotonergic or hepatic risks; acute overdose is usually limited outside ergot or cardiovascular agents.
This drug is routinely called serotonergic. By Gillman’s human-effect criteria it does not raise serotonin in the synapse.
Triptan receptor agonism is not a mechanistic serotonin-toxicity interaction with SRIs.
Gillman’s four human testsA measurable SERT affinity that fails all four is not clinical serotonicity.
Non-elevating action5-HT1B/1D agonist
Evidence confidenceHigh
Background: what serotonicity is · what is and is not an SRI · what counts as a relevant MAOI.