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To check whether such a delayed effect is also present for other oral antimigraine drugs, we hand\u2010searched the literature for publications on RCTs reporting efficacy. Two triptans, 3 nonsteroidal anti\u2010inflammatory drugs (NSAIDs), a triptan combined with an NSAID and a calcitonin gene\u2013related peptide receptor antagonist were evaluated for their therapeutic gain with determination of time to maximum effect (E<jats:sub>max<\/jats:sub>). E<jats:sub>max<\/jats:sub> was compared with known T<jats:sub>max<\/jats:sub> from pharmacokinetic studies to estimate the delay to pain\u2010free. The delay in therapeutic gain varied from 1\u20132\u00a0hours for zolmitriptan 5\u00a0mg to 7\u00a0hours for naproxen 500\u00a0mg. An increase in effect from 2 to 4\u00a0hours was observed after eletriptan 40\u00a0mg, frovatriptan 2.5\u00a0mg and lasmiditan 200\u00a0mg, and after rizatriptan 10\u00a0mg (T<jats:sub>max<\/jats:sub>\u00a0=\u00a01\u00a0h) from 1 to 2\u00a0hours. This strongly indicates a general delay of effect in oral antimigraine drugs. A review of 5 possible effects of triptans on the trigemino\u2010vascular system did not yield a simple explanation for the delay. In addition, E<jats:sub>max<\/jats:sub> for triptans probably depends partly on the rise in plasma levels and not only on its maximum. The most likely explanation for the delay in effect is that a complex <jats:italic>antimigraine system<\/jats:italic> with more than 1 site of action is involved.<\/jats:p>","DOI":"10.1111\/bcp.14090","type":"journal-article","created":{"date-parts":[[2019,8,7]],"date-time":"2019-08-07T00:34:38Z","timestamp":1565138078000},"page":"2487-2498","source":"Crossref","is-referenced-by-count":8,"title":["Why is the therapeutic effect of acute antimigraine drugs delayed? 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