Pharmacology and mechanism of action
Alizapride is an antiemetic and belongs to the group of prokinetics. It is similar in structure and action to the commonly used prokinetic metoclopramide. Alizapride can cross the blood-brain barrier, which makes its action possible.
The antiemetic effect of alizapride is due to its antagonistic action at D2 receptors in the central nervous system (CNS). This prevents nausea and vomiting induced by most stimuli.
Pharmacokinetics
Excretion of alizapride occurs through the kidney. The half-life is approximately 3 hours.
Drug Interactions
The following drugs may potentiate the effects of alizapride:
- Analgesics and cough suppressants from the opioid group.
- sedatives and tranquilizers (e.g., barbiturates, hypnotics)
- Benzodiazepines
- H1 antihistamines
- Certain antidepressants (mirtazapine, doxepin, mianserin, amitriptyline)
- Clonidine and other centrally acting anithypertensives.
The effects of the following medicines may be increased by taking alizapride:
- Neuroleptics such as phenothiazines and chlorpromazine are potentiated and also increase the effect of alizapride
- Antihypertensives may increase the risk of excessive blood pressure lowering
The following drugs cause the effect of alizapride to be attenuated or reversed:
- Dopamine agonists such as levodopa, ropinirole, or cabergoline have an opposite effect at the dopamine receptor and may reverse the effect of alizapride
- Anticholinergics such as atropine weaken the effect
Other interactions:
Concomitant use with cortisone preparations may increase the risk of muscle spasms and involuntary movements.
Alcohol may increase the sedative effect of alizapride and should therefore not be consumed while taking it.
