Ganaton, 50 mg 40 pcs

Pharmacodynamics

The mechanism of action. Itopride hydrochloride increases gastric motility due to antagonism of D2-dopamine receptors and inhibition of acetylcholinesterase. Itopride activates the release of acetylcholine and inhibits its degradation.

Itopride hydrochloride also gives antiemetic effect due to interaction with D2-receptors located in the trigger zone. Itopride causes dose-dependent suppression of apomorphine-induced vomiting.

Itopride hydrochloride activates gastric propulsive motility through antagonism of D2 receptors and dose-dependent inhibition of acetylcholinesterase activity.

Itopride hydrochloride has a specific effect on the upper gastrointestinal tract, accelerates transit through the stomach and improves gastric emptying. Itopride hydrochloride has no effect on serum levels of gastrin.

Pharmacokinetics

Intake. Itopride hydrochloride is rapidly and almost completely absorbed from the gastrointestinal tract. Its relative bioavailability is 60%, which is due to metabolism during the first passage through the liver. Food has no effect on bioavailability.

After oral administration of 50 mg of itopride hydrochloride Cmax is reached after 0.5-0.75 hours and is 0.28 µg/ml. When the drug was repeatedly administered at a dose of 50-200 mg 3 times/day for 7 days, the pharmacokinetics of the drug and its metabolites were linear and cumulation was minimal.

Distribution. Binds to plasma proteins (mainly to albumin) by 96%. Binding to α1-acid glycoprotein is less than 15% of total binding.

Actively distributed in tissues (Vd is 6.1 L/kg) and found in high concentrations in the kidneys, small intestine, liver, adrenal glands and stomach. Penetrates into the brain and spinal cord in minimal amounts. Penetrates into breast milk.

Metabolism. Itopride undergoes active biotransformation in the liver. Three metabolites have been identified, only one of which has little activity that has no pharmacological significance (about 2-3% of that of itopride). The primary metabolite is N-oxide, which is formed by oxidation of the quaternary amino-N-dimethyl group.

Itopride is metabolized by flavin-dependent monooxygenase (FMO3). The number and efficiency of FMO3 isoenzymes in humans can vary depending on the genetic polymorphism, which in rare cases leads to the development of an autosomal recessive condition known as trimethylaminuria (the “smell of fish” syndrome). In patients with trimethylaminuria, the T1/2 of ithopride is prolonged.

According to in vivo pharmacokinetic studies, itoprid has no inhibitory or inducing effect on CYP2C19 and CYP2E1. Therapy with itopride has no effect on CYP or uridine diphosphate glucuronidyltransferase activity.

Excretion. Itopride hydrochloride and its metabolites are excreted mainly in the urine. Renal excretion of ithopride and its N-oxide after a single oral administration of the drug in therapeutic doses in healthy subjects was 3.7% and 75.4%, respectively.

The terminal T1/2 of etopride hydrochloride is about 6 h.

Indications

Gastritis, Vomiting, Bloating, Pelvic pain, Nausea, Heartburn, GI motility disorders, Appetite disorders, Meteorism

• Stomach bloating.
• Sense of rapid satiety.
• Pains or discomfort in the upper abdomen.
• Anorexia.
• Burn.
• Nausea.
• Vomiting.

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Active ingredient

Itoprid

Composition

1 tablet contains:

Active ingredient:

itopride hydrochloride – 50 mg;

Associates:

Lactose – 34.975 mg (including excess due to loss in weight during manufacturing – 2.93%),

Corn starch – 15 mg,

Carmellose – 20 mg,

Anhydrous silicic acid – 4 mg,

magnesium stearate – 1 mg,

hypromellose – 4.4 mg,

macrogol 6000 – 0.4 mg,

titanium dioxide – 0.2 mg,

carnauba wax – 0.025 mg.