Disease relevance of Relpax

• CONCLUSION: Oral eletriptan (40 mg and 80 mg) is effective, safe, and tolerable in the acute treatment of migraine and yields a consistent response [1].
• Eletriptan for the short-term prophylaxis of cluster headache [2].
• The inhibitory actions of eletriptan on neurogenic inflammation in rat dura mater were also assessed [3].

High impact information on Relpax

• RESULTS: Eletriptan and sumatriptan induced concentration-dependent contractions of meningeal artery, coronary artery, and saphenous vein [4].
• BACKGROUND: Eletriptan is a potent and selective agonist at human recombinant 5HT1B/1D receptors, with efficacy in animal models that predict antimigraine activity [5].
• In healthy volunteers, the pharmacokinetics of eletriptan are characterized by linear and rapid oral absorption [5].
• Significantly more (P < or = 0.001) patients preferred rizatriptan 10-mg wafer [61.1%; 95% confidence interval (CI) 55.7, 66.3] to eletriptan 40-mg tablet (38.9%; 95% CI 33.7, 44.3) [6].
• Comparative efficacy of eletriptan vs. naratriptan in the acute treatment of migraine [7].

Chemical compound and disease context of Relpax

• OBJECTIVE: To compare the efficacy of oral eletriptan, 40 mg and 80 mg, and oral sumatriptan, 50 mg and 100 mg, in the acute treatment of migraine [1].
• The other new migraine drugs zolmitriptan, naratriptan, rizatriptan and eletriptan differ in their pharmacological profiles, which translates into minor differences in efficacy, headache recurrence and side-effects [8].
• Eletriptan is therefore a useful addition to the triptan family and a first-line treatment option in the acute management of migraine attacks [9].
• The objective of this study was to compare patient preference for rizatriptan 10-mg wafer vs. eletriptan 40-mg tablet for acute treatment of migraine [6].
• Effectiveness of eletriptan in acute migraine: primary care for Excedrin nonresponders [10].

Biological context of Relpax

• Female volunteers (n = 16) with a regular menstrual cycle (28 +/- 4 days) received a single oral dose of 80 mg eletriptan during each of the four cycle phases: phase 1 (menses), days 1 to 4; phase 2 (follicular), days 6 to 10; phase 3 (ovulatory), days 11 to 13; and phase 4 (luteal), days 21 to 24 [11].
• A linear PK/PD model, fitted to the data, predicted small, transient elevations in diastolic blood pressure following eletriptan doses > or = 60 mg [12].
• Characterisation of the 5-HT receptor binding profile of eletriptan and kinetics of [3H]eletriptan binding at human 5-HT1B and 5-HT1D receptors [13].
• In vitro pharmacology experiments showed that the 5-hydroxytryptamine (5-HT) type 1B and 1D receptor agonists, eletriptan, naratriptan, rizatriptan, sumatriptan, and zolmitriptan, induced vasoconstriction in the thoracic blood vessels from 38% to 57% of the patients [14].
• Eletriptan is metabolized through the cytochrome P450 3A4 system; therefore, it does have the potential for clinically significant drug interactions [15].

Anatomical context of Relpax

• METHODS: Ten patients (two men and eight women) without significant obstructive coronary artery disease were administered 3.33 microg/kg/min intravenous eletriptan after they were given a placebo infusion of 0.9% saline solution [16].
• Effects of eletriptan on the peptidergic innervation of the cerebral dura mater and trigeminal ganglion, and on the expression of c-fos and c-jun in the trigeminal complex of the rat in an experimental migraine model [17].
• It is concluded that eletriptan, acting on perikarya and both the peripheral and the central axon terminals of primary sensory neurons, exerts its antimigraine effect by an agonist action on 5-HT1B/1D receptors throughout the entire trigeminal system, probably by passing the blood-brain-barrier because of its lipophilic character [17].
• 1. Sumatriptan or eletriptan produced vasocontraction in common carotid artery (CCA) by stimulating 5HT(1B) receptors (see also Akin & Gurdal, this issue) [18].
• In all these respects, eletriptan acted in a similar way to sumatriptan, with the notable exception that eletriptan also blocked the stimulation-induced effects in the nucleus caudalis trigemini and the upper cervical spinal cord (trigeminal complex), whereas sumatriptan did not [17].

Associations of Relpax with other chemical compounds

• This was a randomized, double-blind study designed to evaluate the comparative efficacy and tolerability of the 40-mg dose of eletriptan and the 2.5-mg dose of naratriptan [7].
• When the relative importance of the treatment attributes was combined in a multiattribute decision model with meta-analysis data from controlled trials, almotriptan, eletriptan, and rizatriptan were significantly closer to the hypothetical ideal triptan than the reference product, sumatriptan 100 mg [19].
• Recently, a series of second-generation 5-HT1B/1D agonists (almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, and zolmitriptan) have been developed and are reviewed in this article [20].
• Contractions evoked by eletriptan were antagonised by the 5-HT1B/1D receptor antagonist GR125743 (N-[4-methoxy-3-(4-methyl piperazin-1-yl)phenyl]-3-methyl-4-(4-pyridyl)benzamide) with pA2 values of 9.1 in saphenous vein and 9.4 in basilar artery [21].
• Suppression by eletriptan of the activation of trigeminovascular sensory neurons by glyceryl trinitrate [22].

Gene context of Relpax

• Human hepatocytes in primary culture predict lack of cytochrome P-450 3A4 induction by eletriptan in vivo [23].
• Eletriptan metabolism by human hepatic CYP450 enzymes and transport by human P-glycoprotein [24].
• CYP2A6, a protein with minor pharmacological implication, also was induced by eletriptan and rifampicin in two cultures but was not detected in the others [23].
• Hemodynamic and coronary effects of intravenous eletriptan, a 5HT1B/1D-receptor agonist [16].
• Eletriptan also affected expression of CGRP in perikarya of trigeminal ganglion cells, insofar as the number of small nerve cells exhibiting a compact CGRP immunoreaction was decreased to one quarter of the original value [17].

Analytical, diagnostic and therapeutic context of Relpax

• CONCLUSIONS: Eletriptan, a 5HT1B/1D-agonist effective in migraine, causes no significant coronary artery constriction in patients without significant obstructive coronary artery disease [16].
• OBJECTIVE: To investigate the systemic, pulmonary, and coronary artery effects of eletriptan, a new 5HT1B/1D-agonist in patients undergoing cardiac catheterization [16].
• The results confirm previous meta-analyses that have suggested the superiority of eletriptan vs. naratriptan in the acute treatment of migraine [7].
• Headache relief occurred faster after eletriptan, with more patients at both doses reporting relief 30 min (P < 0.01) and 1 h (P < 0.0001) after treatment than after placebo [25].
• In this multicentre, open-label, two-period, crossover study, out-patients were randomly assigned to treat the first of two moderate to severe migraines with rizatriptan or eletriptan and the second with the alternate therapy [6].

References