Riluzole is a drug used to treat amyotrophic lateral sclerosis.
The etiology and pathogenesis of amyotrophic lateral sclerosis (ALS) are not known, although a number of hypotheses have been advanced. One hypothesis is that motor neurons, made vulnerable through either genetic genetic predisposition or environmental factors, are injured by glutamate. In some cases of familial ALS the enzyme superoxide dismutase has been found to be defective.
The mode of action of Riluzole is unknown. Its pharmacological properties include the following, some of which may be related to its effect:
an inhibitory effect on glutamate release,
inactivation of voltage-dependent sodium channels, and
ability to interfere with intracellular events that follow transmitter binding at excitatory amino acid receptors.
Riluzole has also been shown, in a single study, to delay median time to death in a transgenic mouse model of ALS. These mice express human superoxide dismutase bearing one of the mutations found in one of the familial forms of human ALS.
It is also neuroprotective in various in vivo experimental models of neuronal injury involving excitotoxic mechanisms. In in vitro tests, riluzole protected cultured rat motor neurons from the excitotoxic effects of glutamic acid and prevented the death of cortical neurons induced by anoxia.
Due to its blockade of glutamatergic neurotransmission, riluzole also exhibits myorelaxant and sedative properties in animal models at doses of 30 mg/kg (about 20 times the recommended human daily dose) and anticonvulsant properties at a dose of 2.5 mg/kg (about 2 times the recommended human daily dose).
To extend life in patients with amyotrophic lateral sclerosis, initiated by specialist experienced in the management of motor neurone disease BY MOUTH Adult: 50 mg twice daily
There have been no clinical studies to evaluate the interactions of riluzole with other medicinal products. In vitro studies using human liver microsomal preparations suggest that CYP 1A2 is the principal isozyme involved in the initial oxidative metabolism of riluzole. Inhibitors of CYP 1A2 (eg, caffeine, diclofenac, diazepam, nicergoline, domipramine, imipramine, fluvoxamine, phenacetin, theophylline, amitriptyline and quinolones) could potentially decrease the rate of riluzole elimination, while inducers of CYP 1A2 (eg, cigarette smoke, charcoal-broiled food, rifampicin and omeprazole) could increase the rate of riluzole elimination.
Acute porphyria. CAUTIONS History of abnormal hepatic function (consult product literature for details) . interstitial lung disease
Common or very common Abdominal pain . asthenia . diarrhoea . dizziness . drowsiness . headache . nausea . oral paraesthesia . tachycardia . vomiting Uncommon Anaemia . angioedema . interstitial lung disease . pancreatitis Rare Neutropenia Very rare Hepatitis
PREGNANCY Avoid?no information available. BREAST FEEDING Avoid?no information available.
Store in a cool and dry place, protected from light, do not store above 30°C.
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