Rizatriptan is reported to be a very effective acute migraine drug. It is reported to display high agonist activity at mainly the serotonin 5-HT1B and 5-HT1D receptor subtypes.
ChEBI: Rizatriptan is a member of tryptamines. It has a role as a serotonergic agonist, a vasoconstrictor agent and an anti-inflammatory drug. It is functionally related to a N,N-dimethyltryptamine.
Rizatriptan, approved in 1998, is a fast-acting triptan becauseof its moderate lipophilicity yet has a very shortelimination half-life similar to sumatriptan (i.e., like sumatriptan,it is mainly metabolized by MAO-A). The only advantagesof this drug when compared with sumatriptan arethat it has a slightly faster onset and that it has an orallydisintegrating tablet formulation which can be taken withoutwater.
5HT1
receptor agonist:
Acute treatment of migraine
Potentially hazardous interactions with other drugs
Antidepressants: increased risk of CNS excitation
with citalopram - avoid; risk of CNS toxicity
with MAOIs, moclobemide and linezolid - avoid
for 2 weeks after discontinuation of MAOI and
moclobemide; possibly increased serotonergic
effects with duloxetine and venlafaxine; increased
serotonergic effects with St John’s wort - avoid.
Dapoxetine: possible increased risk of serotonergic
effects - avoid for 2 weeks after stopping 5HT1
agonists.
Ergot alkaloids: increased risk of vasospasm - avoid.
Propranolol: rizatriptan levels increased, reduce dose
of rizatriptan to 5 mg (max 10 mg in 24 hours).
The main route of rizatriptan metabolism is via oxidative
deamination by monoamine oxidase-A (MAO-A)
to the indole acetic acid metabolite, which is not
pharmacologically active. N-monodesmethyl-rizatriptan,
a metabolite with activity similar to that of parent
compound, is formed to a minor degree, but does not
contribute significantly to the pharmacodynamic activity
of rizatriptan.
Less than 1% is excreted in the urine as active
N-monodesmethyl metabolite.
