9/25/2023 0 Comments Tripter tript![]() ![]() Īlmotriptan: The absolute bioavailability of almotriptan tablets is about 70%, with peak plasma levels occurring 1 to 3 hours post-administration. Hence, it is unlikely that frovatriptan will affect the metabolism of co-administered drugs metabolized by these mechanisms. Renal clearance accounted for about 40% and 45% of total clearance in males and females. In addition, frovatriptan is not an inhibitor of human monoamine oxidase (MAO) enzymes of cytochrome P450. Approximately 14% of an oral rizatriptan dose is excreted in urine as unchanged, while 51% is excreted as indole acetic acid metabolite, proving substantial first-pass metabolism.įrovatriptan: The onset of action is delayed, but it has the longest half-life (approximately 26 hours) and the lower recurrence rate at 24 hours (7 to 25%). Frovatriptan is preferred in long-lasting attacks of migraine. The metabolite is not active at the 5-HT1B/1D receptor. Hence, rizatriptan seems the better option when attacks are severe with rapid onset but short-lasting. The primary route of rizatriptan metabolism is by MAO-A, which forms the indole acetic acid metabolite. For this reason, it has the highest recurrence rate at 24 hours (superior to placebo). Rizatriptan: Rizatriptan has the fastest onset of action among orally administered triptans (approximately 30 minutes) but with short elimination half-live (2 to 2.5 hours). Therefore, nasal sprays are an intermediate option for oral triptans and subcutaneous sumatriptan. In vitro studies on human microsomes suggest that sumatriptan is metabolized by the monoamine oxidase (MAO) enzyme, thus prone to serotonin syndrome when administered with other serotonergic drugs. The elimination half-life (t1/2) of sumatriptan is approximately 2.5 hours. Despite nasal sprays being faster than oral formulation, their effect is more temporary. Orally administered sumatriptan has a low bioavailability of around 15%, primarily due to pre-systemic metabolism and partly due to incomplete absorption. Sumatriptan: Sumatriptan is available as oral tablets, nasal spray, and subcutaneous injections. The pharmacokinetics of triptans vary widely between individuals and could be explained by the effect of P-glycoprotein efflux transporters, triptan-metabolizing enzymes (CYP450 and MAO), and drug bioavailability. When triptans bind to the neurogenic and central 5-HT1D receptors, they prevent the release of vasoactive neuropeptides by inhibiting trigeminal nerves' activation and blocking the transmission of pain signals to the brain. ![]() ![]() Triptan binding to the vascular 5-HT1B receptors leads to vasoconstriction of the cranial arteries, which painfully dilate during a migraine attack. Triptans act as antimigraine agents by selectively binding to the serotonin receptors 5-HT1B and 5-HT1D. Central mechanism: Inhibition of the release of vasoactive neuropeptides by trigeminal nerve innervating the intracranial vessels and dura mater. ![]()
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