Description of the drug HIDRASEK®

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Description of the drug HIDRASEK®

After oral administration, racecadotril is rapidly absorbed. The time until plasma enkephalinase inhibition begins is 30 minutes. Cmax is achieved 2.5 hours after application. Eating does not affect the bioavailability of racecadotril, but after ingestion the activity of the drug appears with a delay of approximately 1.5 hours.

In the blood plasma after the use of racecadotril, labeled with the radioactive isotope 14C, the radiocarbon content was many times higher than in blood cells and 3 times higher than in whole blood. Thus, the drug slightly binds to blood cells. Radiocarbon is moderately distributed in other tissues of the body, as evidenced by the apparent plasma Vd of 66.4 kg. 90% of the active metabolite of racecadotril (thiorphan) ((RS)-N(1-oxo-2-(mercaptomethyl)-3-phenylpropyl) glycine) is bound to plasma proteins, mainly albumin.

When taking racecadotril at a dose of 100 mg, the time of peak inhibition of plasma enkephalinase is approximately 2 hours and corresponds to 75% inhibition. The duration and effectiveness of racecadotril depends on the dose. In adults, the time to peak inhibition of plasma enkephalinase is approximately 2 hours and corresponds to 75% inhibition at a dose of 100 mg. Plasma enkephalinase inhibition time is approximately 8 hours.

Racecadotril is rapidly hydrolyzed to thiorphan, an active metabolite, which in turn is transformed into inactive metabolites. Taking repeated doses of racecadotril does not lead to its accumulation in the body. Data obtained from in vitro studies indicate that racecadotril/thiorphan and the four major inactive metabolites do not inhibit the CYP enzyme isoforms (3A4, 2D6, 2C9, 1F2, and 2C19) to an extent that may be clinically significant. Data obtained from in vitro studies indicate that racecadotril/thiorphan and the four major inactive metabolites do not induce CYP enzyme isoforms (3A, 2A6, 2B6 2C9/2C19, 1A, 2E1) and conjugated uridine glucuronyl transferase enzymes (UGTs) to an extent that may be clinically significant.

The biological T1/2 of racecadotril, measured as the inhibition time of plasma enkephalinase, is approximately 3 hours. Racecadotril is excreted from the body in the form of active and inactive metabolites, primarily by the kidneys, and to a much lesser extent in the feces. Excretion through the lungs is negligible.

In patients with hepatic impairment (Child-Pugh class B), the kinetic profile of the active metabolite racecadotril demonstrated similar Tmax and T1/2 and lower Cmax (-65%) and AUC (-29%) compared with those in healthy people.

In patients with severe renal impairment (creatinine clearance 11–39 ml/min), the kinetic profile of the active metabolite racecadotril demonstrated a lower Cmax (-49%) and higher AUC (+16%) and T1/2 compared to healthy volunteers ( CC >70 ml/min).

Gidrasec Instructions for use

Pharmacodynamics

Racecadotril is a prodrug that is hydrolyzed to its active metabolite, thiorphan, which is an inhibitor of enkephalinase, a surface peptidase (located on the cell membrane) localized in various tissues, especially the epithelium of the small intestine. This enzyme is responsible for both the hydrolysis of exogenous peptides and the breakdown of endogenous peptides such as enkephalins. As a result, racecadotril protects endogenous enkephalins, which exhibit physiological activity at the level of the digestive tract, prolonging their antisecretory effect.

Racecadotril is an intestinal antisecretory substance. It reduces intestinal hypersecretion of water and electrolytes caused by cholera enterotoxin or inflammation and does not affect basal intestinal secretion.

Racecadotril has a rapid antidiarrheal effect without altering the transit time of intestinal contents through the intestines.

Racecadotril has a rapid antidiarrheal effect without altering the transit time of intestinal contents through the intestines.

Racecadotril does not cause bloating.

In clinical studies, the incidence of secondary constipation with racecadotril was comparable to placebo.

Pharmacokinetics

Suction

After oral administration, racecadotril is rapidly absorbed. The time until plasma enkephalinase inhibition begins is 30 minutes.

Eating does not affect the bioavailability of racecadotril, but after eating, the drug's activity appears with a delay of approximately one and a half hours.

Distribution

In the blood plasma, after the use of racecadotril, labeled with the radioactive isotope 14C, the radiocarbon content was many times higher than in blood cells, and 3 times higher than in whole blood. Thus, the drug slightly binds to blood cells. Radiocarbon is moderately distributed in other tissues of the body, as evidenced by its apparent volume of distribution in plasma of 66.4 kg. 90% of the active metabolite of racecadotril, (thiorphan) ((RS)-N-(1-oxo-2-(mercaptomethyl)-3-phenylpropyl) glycine), is bound to plasma proteins, predominantly albumin. The pharmacokinetic properties of racecadotril do not change as a result of repeated doses, or when administered to elderly patients.

The duration and effectiveness of racecadotril depend on the dose of the drug. In adults, the time to peak inhibition of plasma enkephalinase is approximately 2 hours and corresponds to 75% inhibition at a dose of 100 mg.

The inhibition time of plasma enkephalinase is approximately 8 hours.

In patients with hepatic impairment (Child-Pugh class B), the kinetic profile of the active metabolite racecadotril showed similar Tmax and T½ and lower Cmax (- 65%) and AUC (area under the concentration-time curve) (-29%) compared with these indicators in healthy people.

In patients with severe renal impairment (creatinine clearance 11-39 ml/min), the kinetic profile of the active metabolite racecadotril demonstrated a lower Cmax (-49%) and higher AUC (+16%) and T½ compared with healthy volunteers (clearance creatinine >70 ml/min).

Cmax is achieved 2 hours 30 minutes after application.

No accumulation was observed when the drug was repeated every 8 hours for 7 days.

Removal

Racecadotril is excreted from the body in the form of active and inactive metabolites primarily through the kidneys, and to a much lesser extent in the feces. Excretion through the lungs is negligible.

Hidrasec

Suction

After oral administration, racecadotril is rapidly absorbed. The time until plasma enkephalinase inhibition begins is 30 minutes.

Eating does not affect the bioavailability of racecadotril, but after eating, the drug's activity appears with a delay of approximately one and a half hours.

Distribution

In the blood plasma, after the use of racecadotril, labeled with the radioactive isotope 14C, the radiocarbon content was many times higher than in blood cells, and 3 times higher than in whole blood. Thus, the drug slightly binds to blood cells. Radiocarbon is moderately distributed in other tissues of the body, as evidenced by its apparent volume of distribution in plasma of 66.4 kg. 90% of the active metabolite of racecadotril, (thiorphan) ((RS)-N-(1-oxo-2-(mercaptomethyl)-3-phenylpropyl) glycine), is bound to plasma proteins, predominantly albumin. The pharmacokinetic properties of racecadotril do not change as a result of repeated doses, or when administered to elderly patients.

The duration and effectiveness of racecadotril depend on the dose of the drug. In adults, the time to peak inhibition of plasma enkephalinase is approximately 2 hours and corresponds to 75% inhibition at a dose of 100 mg.

The inhibition time of plasma enkephalinase is approximately 8 hours.

Metabolism

The biological half-life of racecadotril, measured as plasma enkephalinase inhibition time, is approximately 3 hours.

Racecadotril is rapidly hydrolyzed to thiorphan, an active metabolite, which in turn is transformed into inactive metabolites. Taking repeated doses of racecadotril does not lead to its accumulation in the body. Data obtained from in vitro

, show that racecadotril/thiorphan and the four major inactive metabolites do not inhibit the CYP enzyme isoforms (3A4, 2D6, 2C9, 1A2 and 2C19) to an extent that may be clinically significant.

Data obtained from in vitro

show that racecadotril/thiorphan and the four major inactive metabolites do not induce CYP enzyme isoforms (ZA, 2A6, 2B6, 2C9/2C19, 1A, 2E1) and conjugated uridine glucuronosyltransferase enzymes (UGTs) to an extent that may be clinically significant.

Racecadotril does not affect the protein binding of active substances such as tolbutamide, warfarin, niflumic acid, digoxin or phenytoin.

In patients with hepatic impairment (Child-Pugh class B), the kinetic profile of the active metabolite racecadotril showed similar Tmax (time to maximum blood concentration) and T1/2 (half-life) and lower Cmax (maximum blood concentration) values. (-65%) and AUC (area under the concentration-time curve) (-29%) compared with these indicators in healthy people.

In patients with severe renal impairment (creatinine clearance 11-39 ml/min), the kinetic profile of the active metabolite racecadotril demonstrated a lower Cmax (-49%) and higher AUC (+16%) and T1/2 compared to healthy volunteers ( creatinine clearance >70 ml/min.).

Cmax is reached 2 hours 30 minutes after application.

No accumulation was observed when the drug was repeated every 8 hours for 7 days.

Removal

Racecadotril is excreted from the body in the form of active and inactive metabolites primarily through the kidneys, and to a much lesser extent in the feces. Excretion through the lungs is negligible.

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