Medine.co.uk

Rizatriptan 5mg Orodispersible Tablets

Informations for option: Rizatriptan 5mg Orodispersible Tablets, show other option
Document: spc-doc_PL 04416-0935 change

SUMMARY OF PRODUCT CHARACTERISTICS

1 NAME OF THE MEDICINAL PRODUCT

Rizatriptan 5 mg Orodispersible Tablets

2 QUALITATIVE AND QUANTITATIVE COMPOSITION

Each orodispersible tablet contains 5 mg of rizatriptan (as rizatriptan benzoate) Excipient: each orodispersible tablet contains 2.8 mg of aspartame.

For a full list of excipients, see section 6.1.

3 PHARMACEUTICAL FORM

Orodispersible tablet

white to grey-white, round, flat tablet, debossed with “RZT” on one side, and “5” on the other side.

4 CLINICAL PARTICULARS

4.1 Therapeutic indications

Acute treatment of the headache phase of migraine attacks, with or without

aura.

4.2 Posology and method of administration

Rizatriptan orodispersible tablets should not be used prophylactically.

Rizatriptan orodispersible tablets need not be taken with liquid.

The tablet should be placed on the tongue, where it will dissolve and be swallowed with the saliva.

The orodispersible tablets can be used in situations in which liquids are not available, or to avoid the nausea and vomiting that may accompany the ingestion of tablets with liquids.

Adults 18 years of age and older

The recommended dose is 10 mg.

Redosing: doses should be separated by at least two hours; no more than two doses should be taken in any 24-hour period.

-for headache recurrence within 24 hours: if headache returns after relief of the initial attack, one further dose may be taken. The above dosing limits should be observed.

-after non-response: the effectiveness of a second dose for treatment of the same attack, when an initial dose is ineffective, has not been examined in controlled trials. Therefore, if a patient does not respond to the first dose, a second dose should not be taken for the same attack.

Clinical studies have shown that patients who do not respond to treatment of an attack are still likely to respond to treatment for subsequent attacks.

Some patients should receive a lower (5 mg) dose of rizatriptan, in particular the following patient groups:

-patients on propranolol. Administration of rizatriptan should be separated by at least two hours from administration of propranolol (See also section 4.5), -patients with mild or moderate renal insufficiency,

-patients with mild to moderate hepatic insufficiency.

Doses should be separated by at least two hours; no more than two doses should be taken in any 24-hour period.

Patients under 18 years of age

Rizatriptan orodispersible tablets are not recommended for use in patients below 18 years of age due to a lack of data on safety and efficacy.

Patients older than 65 years

The safety and effectiveness of rizatriptan in patients older than 65 years have not been systematically evaluated.

4.3 Contraindications

Hypersensitivity to rizatriptan or to any of the excipients.

Concurrent administration of monoamine oxidase (MAO) inhibitors or use within 2 weeks of discontinuation of MAO inhibitor therapy (see section 4.5).

Rizatriptan is contraindicated in patients with severe hepatic or severe renal insufficiency.

Rizatriptan is contraindicated in patients with a previous cerebrovascular accident (CVA) or transient ischaemic attack (TIA).

Moderately severe or severe hypertension, or untreated mild hypertension.

Established coronary artery disease, including ischaemic heart disease (angina pectoris, history of myocardial infarction, or documented silent ischaemia), signs and symptoms of ischaemic heart disease, or Prinzmetal's angina.

Peripheral vascular disease.

Concomitant use of rizatriptan and ergotamine, ergot derivatives (including methysergide), or other 5-HT1B/1D receptor agonists (see also section 4.5).

4.4 Special warnings and precautions for use

Rizatriptan should only be administered to patients in whom a clear diagnosis of migraine has been established. Rizatriptan should not be administered to patients with basilar or hemiplegic migraine.

Rizatriptan should not be used to treat 'atypical' headaches, i.e. those that might be associated with potentially serious medical conditions, (e.g. CVA, ruptured aneurysm) in which cerebrovascular vasoconstriction could be harmful.

Rizatriptan can be associated with transient symptoms including chest pain and tightness which may be intense and involve the throat (see section 4.8). Where such symptoms are thought to indicate ischaemic heart disease, no further dose should be taken and appropriate evaluation should be carried out.

As with other 5-HT1B/1D receptor agonists, rizatriptan should not be given, without prior evaluation, to patients in whom unrecognized cardiac disease is likely or to patients at risk for coronary artery disease (CAD) [e.g. patients with hypertension, diabetics, smokers or users of nicotine substitution therapy, men over 40 years of age, postmenopausal women, patients with bundle branch block, and those with strong family history for CAD]. Cardiac evaluations may not identify every patient who has cardiac disease and, in very rare cases, serious cardiac events have occurred in patients without underlying cardiovascular disease when 5-HT1 agonists have been administered. Those in whom CAD is established should not be given rizatriptan (see section 4.3).

5-HT1B/1D receptor agonists have been associated with coronary vasospasm. In rare cases, myocardial ischaemia or infarction have been reported with 5-HT1B/1D receptor agonists including rizatriptan (see section 4.8).

Other 5-HT1B/1D agonists, (e.g. sumatriptan) should not be used concomitantly with rizatriptan (see also section 4.5).

Serotonin syndrome (including altered mental status, autonomic instability and neuromuscular abnormalities) has been reported following concomitant treatment with triptans and selective serotonin reuptake inhibitors (SSRIs) or serotonin noradrenaline reuptake inhibitors (SNRIs). These reactions can be severe. If concomitant treatment with rizatriptan and an SSRI or SNRI is clinically warranted, appropriate observation of the patient is advised, particularly during treatment initiation, with dose increases, or with addition of another serotonergic medicinal products (see section 4.5).

It is advised to wait at least six hours following use of rizatriptan before administering ergotamine-type medicinal products, (e.g. ergotamine, dihydroergotamine or methysergide). At least 24 hours should elapse after the administration of an ergotamine-containing preparation before rizatriptan is given. Although additive vasospastic effects were not observed in a clinical pharmacology study in which 16 healthy males received oral rizatriptan and parenteral ergotamine, such additive effects are theoretically possible, (see section 4.3).

Undesirable effects may be more common during concomitant use of triptans (5-HT1B/1D agonists) and herbal preparations containing St John’s wort (Hypericum perforatum).

Angioedema (e.g. facial oedema, tongue swelling and pharyngeal oedema) may occur in patients treated with triptans, among which is rizatriptan. If angioedema of the tongue or pharynx occurs, the patient should be placed under medical supervision until symptoms have resolved. Treatment should promptly be discontinued and replaced by an agent belonging to another class of drugs.

Phenylketonurics: Phenylketonuric patients should be informed that Rizatriptan orodispersible tablets contain aspartame (E 951), a source of phenylalanine. May be harmful for people with phenylketonuria.

The potential for interaction should be considered when rizatriptan is administered to patients taking CYP 2D6 substrates (see section 4.5).

Medication overuse headache (MOH)

Prolonged use of any painkiller for headaches can make them worse. If this situation is experienced or suspected, medical advice should be obtained and treatment should be discontinued. The diagnosis of MOH should be suspected in patients who have frequent or daily headaches despite (or because of) the regular use of headache medications.

4.5 Interaction with other medicinal products and other forms of interaction

Ergotamine, ergot derivatives (including methysergide), other 5 HT 1B/1D receptor agonists: Due to an additive effect, the concomitant use of rizatriptan and ergotamine, ergot derivatives (including methysergide), or other 5 HT 1B/1D receptor agonists (e.g. sumatriptan, zolmitriptan, naratriptan) increase the risk of coronary artery vasoconstriction and hypertensive effects. This combination is contraindicated (see also section 4.3).

Monoamine oxidase inhibitors: Rizatriptan is principally metabolized via monoamine oxidase, 'A' subtype (MAO-A). Plasma concentrations of rizatriptan and its active N-monodesmethyl metabolite were increased by concomitant administration of a selective, reversible MAO-A inhibitor. Similar or greater effects are expected with nonselective, reversible (e.g. linezolid) and irreversible MAO inhibitors. Due to a risk of coronary artery vasoconstriction and hypertensive episodes, administration of rizatriptan to patients taking inhibitors of MAO is contraindicated (see section 4.3).

Beta-blockers: Plasma concentrations of rizatriptan may be increased by concomitant administration of propranolol. This increase is most probably due to first-pass metabolic interaction between the two active substances, since MAO-A plays a role in the metabolism of both rizatriptan and propranolol. This interaction leads to a mean increase in AUC and Cmax of 70-80%. In patients receiving propranolol, the 5 mg dose of rizatriptan should be used (see section 4.2).

In a drug-interaction study, nadolol and metoprolol did not alter plasma concentrations of rizatriptan.

Selective Serotonin Reuptake Inhibitors (SSRIs) /Serotonin Norepinephrine Reuptake Inhibitors (SNRIs) and Serotonin Syndrome: There have been reports describing patients with symptoms compatible with serotonin syndrome (including altered mental status, autonomic instability and neuromuscular abnormalities) following the use of selective serotonin reuptake inhibitors (SSRIs) or serotonin noradrenaline reuptake inhibitors (SNRIs) and triptans (see section 4.4).

In vitro studies indicate that rizatriptan inhibits cytochrome P450 2D6 (CYP 2D6). Clinical interaction data are not available. The potential for interaction should be considered when rizatriptan is administered to patients taking CYP 2D6 substrates.

4.6 Pregnancy and lactation

Use during pregnancy

The safety of rizatriptan for use in human pregnancy has not been established. Animal studies do not indicate harmful effects at dose levels that exceed therapeutic dose levels with respect to the development of the embryo or fetus, or the course of gestation, parturition and postnatal development. Because animal reproductive and developmental studies are not always predictive of human response, Rizatriptan should be used during pregnancy only if clearly needed.

Use during lactation

Studies in rats indicated that very high milk transfer of rizatriptan occurred. Transient, very slight decreases in preweaning pup body weights were observed only when the mother's systemic exposure was well in excess of the maximum exposure levels for humans. No data exist in humans.

Therefore, caution should be exercised when administering rizatriptan to women who are breast-feeding. Infant exposure should be minimized by avoiding breast-feeding for 24 hours after treatment.

4.7 Effects on ability to drive and use machines

Migraine or treatment with rizatriptan may cause somnolence in some patients. Dizziness has also been reported in some patients receiving rizatriptan. Patients should, therefore, evaluate their ability to perform complex tasks during migraine attacks and after administration of rizatriptan.

4.8 Undesirable effects

Rizatriptan was evaluated in over 3600 patients for up to one year in controlled clinical studies. The most common side effects evaluated in clinical studies were dizziness, somnolence, and asthenia/fatigue.

The following side effects have been evaluated in clinical studies and/or reported in post-marketing experience:

Very common 1/10); common 1/100, < 1/10); uncommon 1/1,000, < 1/100); rare (> 1/10,000, < 1/1,000); very rare (< 1/10,000), not known (cannot be estimated from the available data)

Immune system disorders

Not known: hypersensitivity reaction, anaphylaxis/anaphylactoid reaction Psychiatric disorders

Uncommon: disorientation, insomnia, nervousness Nervous system disorders

Common: dizziness, somnolence, paresthesia, headache, hypesthesia, decreased mental acuity, tremor Uncommon: ataxia, vertigo

Rare: syncope, dysgeusia/bad taste, serotonin syndrome Not known: seizure

Eye disorders Uncommon: blurred vision

Cardiac disorders

Common: palpitation, tachycardia

Rare: myocardial ischaemia or infarction, cerebrovascular accident. Most of these adverse reactions have been reported in patients with risk factors predictive of coronary artery disease.

Not known: arrhythmia, bradycardia

Vascular disorders

Common: hot flushes/flashes

Uncommon: hypertension

Not known: peripheral vascular ischaemia

Respiratory, thoracic and mediastinal disorders Common: pharyngeal discomfort, dyspnoea Rare: wheezing

Gastrointestinal disorders

Common: nausea, dry mouth, vomiting, diarrhoea Uncommon: thirst, dyspepsia Not known: ischaemic colitis

Skin and subcutaneous tissue disorders Common: flushing, sweating Uncommon: pruritus, urticaria

Rare: angioedema (e.g. facial oedema, tongue swelling, pharyngeal oedema), rash, toxic epidermal necrolysis (for angioedema see also section 4.4)

Musculoskeletal and connective tissue disorders Common: regional heaviness

Uncommon: neck pain, regional tightness, stiffness, muscle weakness.

Rare: facial pain Not known: myalgia

General disorders and administration site conditions Common: asthenia/fatigue, pain in abdomen or chest

Investigations

Not known: ECG abnormalities

4.9 Overdose

Rizatriptan 40 mg (administered as either a single dose or as two doses with a 2-hour interdose interval) was generally well tolerated in over 300 patients; dizziness and somnolence were the most common drug-related adverse effects.

In a clinical pharmacology study in which 12 subjects received rizatriptan, at total cumulative doses of 80 mg (given within four hours), two subjects experienced syncope and/or bradycardia. One subject, a female aged 29 years, developed vomiting, bradycardia, and dizziness beginning three hours after receiving a total of 80 mg rizatriptan (administered over two hours). A third degree AV block, responsive to atropine, was observed an hour after the onset of the other symptoms. The second subject, a 25 year old male, experienced transient dizziness, syncope, incontinence, and a 5-second systolic pause (on ECG monitor) immediately after a painful venipuncture. The venipuncture occurred two hours after the subject had received a total of 80 mg rizatriptan (administered over four hours).

In addition, based on the pharmacology of rizatriptan, hypertension or other more serious cardiovascular symptoms could occur after overdosage. Gastrointestinal decontamination (e.g. gastric lavage followed by activated charcoal) should be considered in patients suspected of an overdose with rizatriptan. Clinical and electrocardiographic monitoring should be continued for at least 12 hours, even if clinical symptoms are not observed.

The effects of haemo- or peritoneal dialysis on serum concentrations of rizatriptan are unknown

5 PHARMACOLOGICAL PROPERTIES

5.1 Pharmacodynamic properties

Pharmacotherapeutic group: antimigraine. preparations; Selective serotonin (5-HT1) agonist.

ATC code: N02C C04

Mechanism of action:

Rizatriptan binds selectively with high affinity to human 5-HT1B and 5-HT1D receptors and has little or no effect or pharmacological activity at 5-HT2, 5-HT3; adrenergic alpha1, alpha2 or beta; D1, D2, dopaminergic, histaminergic H1; muscarinic; or benzodiazepine receptors.

The therapeutic activity of rizatriptan in treating migraine headache may be attributed to its agonist effects at 5-HT1B and 5-HT1D receptors on the extracerebral intracranial blood vessels that are thought to become dilated during an attack and on the trigeminal sensory nerves that innervate them. Activation of these 5-HT1B and 5-HT1D receptors may result in constriction of pain-producing intracranial blood vessels and inhibition of neuropeptide release that leads to decreased inflammation in sensitive tissues and reduced central trigeminal pain signal transmission.

Pharmacodynamic effects:

The efficacy of rizatriptan orodispersible tablets in the acute treatment of migraine attacks was established in two multicentre, randomised, placebo-controlled trials that were similar in design to the trials of rizatriptan tablets. In one study (n=311), by two hours post-dosing, relief rates in patients treated with rizatriptan orodispersible tablets were approximately 66% for rizatriptan 5 mg and 10 mg, compared to 47% in the placebo group. In a larger study (n=547), by two hours post-dosing, relief rates were 59% in patients treated with rizatriptan orodispersible tablets 5 mg, and 74% after 10 mg, compared to 28% in the placebo group. Rizatriptan orodispersible tablets also relieved the disability, nausea, photophobia, and phonophobia which accompanied the migraine episodes. A significant effect on pain relief was observed as early as 30 minutes post-dosing in one of the two clinical trials for the 10 mg dose (see also section 5.2).

Based on studies with the tablet, rizatriptan remains effective in treating menstrual migraine, i.e. migraine that occurs within 3 days before or after the onset of menses.

Rizatriptan orodispersible tablets enable migraine patients to treat their migraine attacks without having to swallow liquids. This may allow patients to administer their medicinal product earlier, for example, when liquids are not available, and to avoid possible worsening of gastrointestinal symptoms by swallowing liquids.

5.2 Pharmacokinetic properties

Absorption

Rizatriptan is rapidly and completely absorbed following oral administration.

The mean oral bioavailability of the orodispersible tablets is approximately 40-45%, and mean peak plasma concentrations (Cmax) are reached in approximately 1.6-2.5 hours (Tmax). The time to maximum plasma concentration following administration of rizatriptan as the orodispersible formulation is delayed by 30-60 minutes relative to the tablet.

Effect of food: The effect of food on the absorption of rizatriptan from the orodispersible tablets has not been studied. For the rizatriptan tablets, Tmax is delayed by approximately 1 hour when the tablets are administered in the fed state. A further delay in the absorption of rizatriptan may occur when the orodispersible tablets are administered after meals.

Distribution

Rizatriptan is minimally bound (14%) to plasma proteins. The volume of distribution is approximately 140 litres in male subjects, and 110 litres in female subjects.

Biotransformation

The primary 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 at the 5-HT1B/1D receptor, is formed to a minor degree, but does not contribute significantly to the pharmacodynamic activity of rizatriptan. Plasma concentrations of N-monodesmethyl-rizatriptan are approximately 14% of those of parent compound, and it is eliminated at a similar rate. Other minor metabolites include the N-oxide, the 6-hydroxy compound, and the sulphate conjugate of the 6-hydroxy metabolite. None of these minor metabolites is pharmacologically active. Following oral administration of 14C-labelled rizatriptan, rizatriptan accounts for about 17% of circulating plasma radioactivity.

Elimination

Following intravenous administration, AUC in men increases proportionally and in women near-proportionally with the dose over a dose range of 10-60 mcg/kg. Following oral administration, AUC increases near-proportionally with the dose over a dose range of 2.5-10 mg. The plasma half-life of rizatriptan in males and females averages 2-3 hours. The plasma clearance of rizatriptan averages about 1,000-1,500 ml/min in males and about 900-1,100 ml/min in females; about 20-30% of this is renal clearance. Following an oral dose of 14C-labelled rizatriptan, about 80% of the radioactivity is excreted in urine, and about 10% of the dose is excreted in faeces. This shows that the metabolites are excreted primarily via the kidneys.

Consistent with its first pass metabolism, approximately 14% of an oral dose is excreted in urine as unchanged rizatriptan while 51% is excreted as indole acetic acid metabolite. No more than 1% is excreted in urine as the active N monodesmethyl metabolite.

If rizatriptan is administered according to the maximum dosage regimen, no accumulation of the active substance in the plasma occurs from day to day.

Characteristics in patients

The following data are based on studies with the rizatriptan tablet.

Patients with a migraine attack: A migraine attack does not affect the pharmacokinetics of rizatriptan.

Gender: The AUC of rizatriptan (10 mg orally) was about 25% lower in males as compared to females, Cmax was 11% lower, and Tmax occurred at approximately the same time. This apparent pharmacokinetic difference was of no clinical significance.

Elderly: The plasma concentrations of rizatriptan observed in elderly subjects (age range 65 to 77 years) after tablet administration were similar to those observed in young adults.

Hepatic impairment (Child-Pugh's score 5-6): Following oral tablet administration in patients with hepatic impairment caused by mild alcoholic cirrhosis of the liver, plasma concentrations of rizatriptan were similar to those seen in young male and female subjects. A significant increase in AUC (50%) and Cmax (25%) was observed in patients with moderate hepatic impairment (Child Pugh's score 7). Pharmacokinetics were not studied in patients with Child Pugh's score>7 (severe hepatic impairment).

Renal impairment: In patients with renal impairment (creatinine clearance 10-60 ml/min/1.73 m2), the AUC of rizatriptan after tablet administration was not significantly different from that in healthy subjects. In haemodialysis patients (creatinine clearance <10 ml/min/1.73 m2), the AUC for rizatriptan was approximately 44% greater than that in patients with normal renal function. The maximal plasma concentration of rizatriptan in patients with all degrees of renal impairment was similar to that in healthy subjects.

5.3 Preclinical safety data

Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity, carcinogenic potential, toxicity to reproduction and development

6 PHARMACEUTICAL PARTICULARS

List of excipients

6.1


Calcium silicate Crospovidone type A Silica, Colloidal anhydrous Silicified microcrystalline cellulose Mannitol (E421)

Aspartame (E951)

Magnesium Stearate

Sweet Orange Flavour (Arabic gum E414, Ascorbic acid E300, Ethyl butyrate, Maltodextrin, Orange oil)

6.2    Incompatibilities

Not applicable.

6.3    Shelf life

3 years

6.4    Special    precautions for storage

Store in    the original package.

6.5    Nature    and contents of container

Al//Al blisters: 2, 3, 6, 18 orodispersible tablets Not all pack sizes may be marketed.

6.6    Special    precautions for disposal

No special requirements.

7    MARKETING AUTHORISATION HOLDER

Sandoz Limited Frimley Business Park,

Frimley,

Camberley,

Surrey,

GU16 7SR.

United Kingdom

8    MARKETING AUTHORISATION NUMBER(S)

PL 04416/0935

9 DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION

06/08/2009

10 DATE OF REVISION OF THE TEXT

12/08/2013