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The primary route of rizatriptan metabolism is via oxidative deamination by monoamine oxidase-AMAO-Ato the indole acetic acid metabolitewhich is not active at the 5-HT 1B1D receptorN-monodesmethyl-rizatriptana metabolite with activity similar to that of parent compound at the 5-HT 1B1D receptoris formed to a minor degreePlasma concentrations of N-monodesmethyl-rizatriptan are approximately 14of those of parent compoundand it is eliminated at a similar rateOther minor metabolitesthe N-oxidethe 6-hydroxy compound and the sulphate conjugate of the 6-hydroxy metabolite are not active at the 5-HT 1B1D receptorNone of these minor metabolites is pharmacologically active.

The primary route of rizatriptan metabolism is via oxidative deamination by monoamine oxidase-AMAO-Ato the indole acetic acid metabolitewhich is not active at the 5-HT 1B1D receptorN-monodesmethyl-rizatriptana metabolite with activity similar to that of parent compound at the 5-HT 1B1D receptoris formed to a minor degreePlasma concentrations of N-monodesmethyl-rizatriptan are approximately 14of those of parent compoundand it is eliminated at a similar rateOther minor metabolitesthe N-oxidethe 6-hydroxy compound and the sulphate conjugate of the 6-hydroxy metabolite are not active at the 5-HT 1B1D receptorNone of these minor metabolites is pharmacologically active.

For pediatric patientsAge 6 to 17 Yearsweighing 40 kg88 lbor moretaking propranololonly a single dose of RIZACT Tablets 5 mg is recommendedmaximum dose of 5 mg in a 24-hour periodRIZACT Tablets should not be prescribed to propranolol-treated pediatric patients who weigh less than 40 kg88 lb

The administration of rizatriptan with other 5-HT 1 agonistse.gsumatriptanzolmitriptannaratriptanhas not been evaluated in migraine patientsBecause their vasospastic effects may be additiveco-administration of rizatriptanand other 5-HT 1 agonists within 24 hours of each other is not recommended.

Current theories on the aetiology of migraine headache suggest that the symptoms are due to local cranial vasodilatation and/or to the release of vasoactive and pro-inflammatory peptides from sensory nerve endings in an activated trigeminal systemThe therapeutic activity of rizatriptan in migraine can most likely be attributed to agonist effects at 5-HT 1B/1D receptors on the extracerebralintracranial blood vesselswhich become dilated during a migraine attackand on nerve terminals in the trigeminal systemActivation of these receptors results in cranial vessel constrictioninhibition of neuropeptide release and reduced transmission in trigeminal pain pathways.

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