When ingestion of a therapeutic dose loratadin rapidly absorbed and almost completely metabolized in the body. Loratadina defined concentration in plasma has been set up within 15 min after administration of the drug inside. In clinical trials conducted by improvement in the majority of patients began during the first 30 min after administration Klaritina. Loratadina plasma Cmax achieved through 1-1.3 hr, and Cmax principal active metabolite, dezkarboetoksiloratadina, approximately 2.5 hours

Css loratadina dezkarboetoksiloratadina achieved and the majority of patients by about 5 day admission.

In studies conducted simultaneous eating and loratadina increased systemic bioavailability and loratadina dezkarboetoksiloratadina about 40% and 15%, respectively. Time achieve Cmax loratadina dezkarboetoksiloratadina and increased slightly (about 1 hour), C max values of these substances in plasma remained unchanged and no clinical manifestations loratadina interaction with the food have been noted.

Loratadin and its metabolites do not penetrate through the GEB.

Metabolism

There was considerable variability pharmacokinetic data in all studies Klaritina (tablets and syrup), which is probably due to the wide differences primary metabolism.
The studies showed that dezkarboetoksiloratadina profiles in plasma concentrations of both dosage forms are comparable. Pharmacokinetics loratadina dezkarboetoksiloratadina and is not dependent on the dose (dose in the range of 10 mg to 40 mg) and duration of treatment.
In almost all cases, metabolites were more active than loratadin unchanged.
In the in vitro study on liver mikrosomah Rights found that loratadin becoming a dezkarboetoksiloratadin mainly influenced tsitohroma P4503 A4 (CYP3A4) and to a lesser extent, tsitohroma R450 2D6 (CYP2D6). In the presence ketokonazola, CYP3A4 inhibitor, loratadin becoming a dezkarboetoksiloratadin mainly under the influence of CYP2D6.
Derivation

The average T1 / 2 loratadina was 8.4 h (3-20 h), dezkarboetoksiloratadina-28 h (8.8-92 h)