Ipaton coated tablets 250 mg. №20

$38.00

Manufacturer: Hungary

Prevention of cerebrovascular and cardiovascular acute ischemic complications in patients with disorders of cerebral and peripheral arterial circulation. Prevention and correction of platelet dysfunction caused by artificial blood circulation during surgery and long-term hemodialysis. Prevention of subacute occlusion of the coronary stent after its implantation. The use of the drug for the above indications is recommended primarily for patients with hypersensitivity to acetylsalicylic acid or in case of ineffective treatment with it.

Category:

Description

Ipaton Composition
active substance: 1 tablet contains 250 mg of ticlopidine hydrochloride;

excipients: microcrystalline cellulose, potato starch, citric acid monohydrate, stearic acid, colloidal silicon dioxide, magnesium stearate, polyethylene glycol 6000, titanium dioxide (E 171), hypromellose.

Ipaton Dosage form
Film-coated tablets.

Basic physical and chemical properties: round, biconvex coated tablets, engraved with the stylized letter “E” and the number “421” on one side, odorless white or almost white.

Ipaton Pharmacotherapeutic group
Antithrombotic agents. ATX code B01A C05.

Pharmacodynamics
Ticlopidine is a platelet aggregation inhibitor. It blocks adenosine phosphate (ADP) -induced platelet aggregation by inhibiting the P2Y12 receptor, resulting in increased bleeding time. The action of ticlopidine is dose-dependent. Does not show activity in vitro. Ticlopidine demonstrates only in vivo effects, the presence of its active metabolite circulating in the blood has been confirmed. COX is not inhibited.

Ticlopidine is a potent inhibitor of the cytochrome P450 system (CYP2B6 enzyme), moreover, to a lesser extent, but it also inhibits the CYP2C19 and CYP2D6 enzyme systems.

The bleeding time according to Ivy’s test is doubled. The lengthening of bleeding time without compression does not occur to the same extent.

In most patients, bleeding time and other platelet functions return to normal within one week after stopping treatment.

When using ticlopidine at a dose of 250 mg 2 times a day, suppression of platelet aggregation is observed after 2 days, and the maximum effect is achieved on the 5-8th day. At a therapeutic dose, ticlopidine inhibits ADP-induced (2.5 μmol / L) platelet aggregation by 50-70%. Lower doses cause less pronounced inhibition of platelet aggregation.

The reduction in the risk of cardiovascular complications caused by ticlopidine has been studied in various blinded controlled clinical trials.

Pharmacokinetics
After oral administration of a single dose, ticlopidine is rapidly and almost completely absorbed. The maximum concentration in blood plasma is reached after 2 hours.

When using the drug after a meal, the bioavailability of the drug increases by 20%. Stable plasma concentration is achieved after 7-10 days of taking the drug at a dose of 250 mg 2 times a day.

The half-life is approximately 30-50 hours.

Antiplatelet activity is not directly related to the level of the substance in the blood plasma. Ticlopidine is metabolized in the liver, about 50-60% of the administered dose is excreted in the urine, 20-30% in the feces.

Indications
Prevention of cerebrovascular and cardiovascular acute ischemic complications in patients with impaired cerebral and peripheral arterial circulation.

Prevention and correction of platelet dysfunction caused by extracorporeal circulation during surgery and prolonged hemodialysis.

Prevention of subacute occlusion of a coronary stent after implantation.

The use of the drug for the above indications is recommended primarily for patients with hypersensitivity to acetylsalicylic acid or in case of ineffectiveness of its treatment. (See the section “Peculiarities of application”).

Contraindications
hypersensitivity to ticlopidine or to other components of the medicinal product listed in the “Composition” section;
hemorrhagic diathesis;
organ damage associated with a tendency to bleeding, for example, exacerbation of gastric ulcer and duodenal ulcer, acute phase of hemorrhagic stroke;
diseases of the hematopoietic system, accompanied by an increase in bleeding time;
severe liver failure;
leukopenia, thrombocytopenia, history of agranulocytosis;
neutropenia (neutrophil count <1500 / mm 3) or thrombocytopenia (platelet count <100,000 / mm 3).
Under no circumstances should the drug be used for the primary prevention of thromboembolism in healthy individuals.