75 mg, 150 mg and 300 mg capsules
100 mg/mL intramuscular injection in 2 mL ampoules
The dopamine hypothesis of the pathophysiology of schizophrenia proposes that dopamine over activity leads to schizophrenic symptoms. Antipsychotic drugs antagonise the actions of dopamine in sub-cortical pathways, but there are often extra pyramidal adverse effects. As remoxipride is a selective antagonist of central D 2 dopamine receptors, it has fewer extra pyramidal adverse effects.
Remoxipride is absorbed rapidly from the gut and is 70-80% bound to plasma proteins. The drug is metabolised by the liver and excreted by the kidney. In severe renal or hepatic disease, the plasma half-life of 4-7 hours may be doubled, so lower doses are required.
The drug is as effective as other antipsychotics such as haloperidol in the treatment of schizophrenia and schizophrenia-like psychoses. However, remoxipride binds specifically to the D 2 receptor and has little affinity for other central receptors e.g. adrenergic, muscarinic and 5-HT receptors. Therefore, the incidence of adverse effects is less than with other antipsychotics, but the range of adverse effects is similar.
In clinical trials, the common extra pyramidal effects have been tremor, akathisia and rigidity. Although the incidence of these adverse effects is 10-20%, this is significantly less than one would expect with haloperidol. However, there have been recent overseas reports of patients developing a plastic anaemia. The company now advises that all patients should have a normal blood count before starting treatment and it should be monitored during treatment. Patients need to be advised to report promptly any bruising, bleeding, fever or other signs of infection.