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SANDOZ NARATRIPTAN is a brand name for Naratriptan, supplied as a tablet. The medicine, its uses, side effects and dosage are the same regardless of brand.
Used for: AND CLINICAL USE........................................................................... 3 CONTRAINDICATIONS ............................................................................................... 4 WARNINGS AND PRECAUTIONS .............................................................................. 5…
Verbatim from this product's HC label. Tap a section to expand.
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Hepatic Impairment:
Hepatic disease/functional impairment causes prolongation of the half-life of orally administered naratriptan tablets. Consequently, if treatment is deemed advisable in the presence of hepatic impairment, a maximum single dose of 1 mg* should be administered.
No more than a total of 2 mg should be taken in any 24 hour period (see ACTION AND CLINICAL PHARMACOLOGY). Administration of Sandoz Naratriptan tablets in patients with severe hepatic impairment (Child-Pugh grade C) is contraindicated (see CONTRAINDICATIONS).
* Sandoz Naratriptan is not available as 1 mg strength.
Hypertension:
Sandoz Naratriptan should not be used in patients with uncontrolled or severe hypertension. Patients with mild to moderate controlled hypertension should be treated cautiously at the lowest effective dose. OVERDOSAGE For management of suspected drug overdose, contact your regional Poison Control Centre immediately.
In clinical studies, numerous patients (N=222) and healthy subjects (N=196) have received naratriptan tablets (naratriptan hydrochloride) at doses of 5-25 mg. In the majority of cases, no serious adverse events were reported. 5 mg dose experienced ischemic ECG changes which were likely due to coronary vasospasm.
This event was not associated with a serious clinical outcome. A patient who was mildly hypertensive experienced a significant increase in blood pressure (baseline value of 150/98 to 204/144 mmHg at 225 minutes) beginning 30 minutes after the administration of a 10 mg dose (4 times the maximum recommended single dose).
The event resolved with antihypertensive treatment. Administration of 25 mg (10 times the maximum recommended single dose) in one healthy male subject increased blood pressure from 120/67 mmHg pretreatment up to 191/113 mmHg at approximately 6 hours postdose and resulted in adverse events including lightheadedness, tension in the neck, tiredness, and loss of coordination.
Blood pressure returned to near baseline by 8 hours after dosing without any pharmacological intervention. The elimination half-life of naratriptan is about 5 to 8 hours (see ACTION AND CLINICAL PHARMACOLOGY), and therefore monitoring of patients after overdose with Sandoz Naratriptan should continue for at least 24 hours or longer if symptoms or signs persist.
Not medical advice. Always read the patient information leaflet and follow your prescriber or pharmacist.
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Standard supportive treatment should be applied as required. If the patient presents with chest pain or other symptoms consistent with angina pectoris, electrocardiogram monitoring should be performed for evidence of ischemia. g. nitroglycerin or other coronary artery vasodilators) should be administered as required.
It is unknown what effect hemodialysis or peritoneal dialysis has on the serum Sandoz Naratriptan Page 17 of 31 concentrations of naratriptan. ACTION AND CLINICAL PHARMACOLOGY Mechanism of Action Naratriptan has been demonstrated to be a selective agonist for a vascular 5- hydroxytryptamine1 receptor subtype (probably a member of the 5-HT1B/1D family) with little or no binding affinity for 5-HT2/3 receptor subtypes, alpha1-, alpha2-, or beta- adrenergic; dopamine1; dopamine2; muscarinic; or benzodiazepine receptors.
Naratriptan did not exhibit agonist or antagonist activity in ex vivo assays of 5-HT4 and 5-HT7 receptor- mediated activities. The therapeutic activity of naratriptan tablet in migraine is generally attributed to its agonist activity at 5-HT1B/5-HT1D receptors.
Two current theories have been proposed to explain the efficacy of 5-HT1 receptor agonists in migraine. One theory suggests that activation of 5-HT1 receptors located on intracranial blood vessels, including those on the arteriovenous anastomoses, leads to vasoconstriction, which is believed to be correlated with the relief of migraine headache.
The other hypothesis suggests that activation of 5-HT1 receptors on perivascular fibres of the trigeminal system results in the inhibition of pro-inflammatory neuropeptide release. These theories are not mutually exclusive.
Pharmacokinetics Absorption:
Naratriptan is well absorbed, with 74% oral bioavailability in females and 63% in males. After oral administration, the absorption is rapid and peak concentrations are obtained in 2 to 5 hours. 5 mg treatment during a non-migraine period.
During a migraine attack, absorption is slower, although exposure (AUC) and elimination half-life are not significantly affected. 39) * Values quoted are arithmetic mean (standard deviation) Cmax : Maximum concentrations tmax : Time to maximum concentrations CI/F : Apparent clearance t1/2 : Elimination half-life AUC: Area under the curve of concentration vs time extrapolated to infinity Plasma levels of naratriptan increase in a dose-proportional manner consistent with linear pharmacokinetics over a 1 to 10 mg dose range.
The absorption and elimination are Sandoz Naratriptan Page 18 of 31 independent of the dose. Administration with food does not appreciably influence the pharmacokinetics of naratriptan. Repeat administration of naratriptan tablets (up to 10 mg once daily for 5 days) does not result in drug accumulation.
Distribution:
According to a population pharmacokinetics estimate, naratriptan is distributed into a volume of approximately 261 L. Plasma protein binding is low (29%).
Metabolism:
In vitro, naratriptan is metabolized by a wide range of cytochrome P450 isoenzymes into a number of inactive metabolites. Naratriptan is a poor inhibitor of […]