Domrid (domperidone maleatee) oral suspension 1 mg/ml. 60 ml. vial with spoon


Manufacturer: Ukraine

Prevention of vomiting and nausea caused by organic, functional diseases or intoxication due to medication, radiation therapy or chemotherapy.



Domrid SR 60 ml Composition:

active substance: domperidone 1 ml of suspension contains 1 mg domperidone
Domrid SR 60 ml excipients: sucrose, polysorbate 80, anhydrous colloidal silicon dioxide, sodium carboxymethyl cellulose, sodium chloride, propylene glycol, glycerin, methyl parahydroxybenzoate (E 218), propyl parahydroxybenzoate (E 216), Ponso 4R (E 124), strawberry water flavoring additive.

Domrid SR 60 ml Dosage form.

Oral suspension.

Basic physical and chemical properties.

Suspension of pink color with a characteristic odor. Pharmacotherapeutic group. Peristalsis stimulants. ATX code A03F A03.

Pharmacological properties.


Domperidone is a dopamine antagonist with antiemetic properties. Domperidone slightly crosses the blood-brain barrier. The use of domperidone is very rarely accompanied by extrapyramidal side effects, especially in adults, but domperidone stimulates the release of prolactin from the pituitary gland. Its antiemetic effect is possibly due to a combination of peripheral (gastrokinetic) action and antagonism to dopamine receptors in the chemoreceptor trigger zone, which is located behind the blood-brain barrier in the posterior area (area postrema). Animal studies, as well as the low concentrations found in the brain, indicate a predominantly peripheral effect of domperidone on dopamine receptors.

Human studies have shown that when taken orally, domperidone increases pressure in the lower esophagus, improves antroduodenal motility, and accelerates gastric emptying. Domperidone does not affect gastric secretion.


Domperidone is rapidly absorbed when taken orally on an empty stomach, the maximum plasma concentration is reached after about 60 minutes. The low absolute bioavailability of oral domperidone (approximately 15%) is due to extensive first-pass metabolism in the intestinal wall and in the liver. Although in healthy people the bioavailability of domperidone increases when taken after meals, patients with gastrointestinal complaints should take domperidone 15-30 minutes before meals. Reduced gastric acidity reduces the absorption of domperidone. When the drug is taken orally after a meal, the maximum absorption slows down slightly, and the area under the curve (AUC) slightly increases.

When taken orally, domperidone does not accumulate and does not induce its own metabolism.The maximum level in blood plasma after 90 minutes (21 ng / ml) after two weeks of oral administration of 30 mg per day was almost the same as after taking the first dose (18 ng / ml ), domperidone is 91-93% bound to blood plasma proteins. Studies of the distribution of domperidone, which were carried out in animals using a drug labeled with a radioactive isotope, showed its significant distribution in tissues, but a low concentration in the brain. In animals, small amounts of the drug penetrate the placenta. Metabolism.

Domperidone is rapidly and extensively metabolized in the liver by hydroxylation and N-dealkylation.

Excretion in urine and feces is 31% and 66% of the oral dose, respectively. Excretion of the drug unchanged is a small percentage (10% in feces and approximately 1% in urine). The plasma half-life after taking a single dose is 7-9 hours in healthy volunteers, but is longer in patients with severe renal failure.

Clinical characteristics.


For the relief of symptoms of nausea and vomiting.


Domrid is contraindicated:

Interaction with other medicinal products and other types of interactions.

Anticholinergic drugs can neutralize the antidispeptic effect of domperidone. In connection with pharmacodynamic and / or pharmacokinetic interactions, the risk of prolongation of the QT interval increases.

The concomitant use of the following medicines with domperidone is contraindicated.

All medicines that prolong the QT interval:

With the simultaneous oral administration of ketoconazole or erythromycin in vivo, it was confirmed that these drugs significantly suppress the first pass metabolism of domperidone, mediated by CYP3A4. With the concomitant use of 10 mg of domperidone orally 4 times a day and 200 mg of ketoconazole orally 2 times a day during the observation period, there was an increase in the QTc interval by an average of 9.8 ms, some values ​​ranged from 1.2 to 17.5 ms. With the simultaneous use of 10 mg of domperidone 4 times a day and 500 mg of erythromycin orally 3 times a day, the QTc interval during the observation period was extended, on average, by 9.9 msec, the interval of individual values ​​ranged from 1.6 to 14.3 msec.