Tazicon Mechanism of Action

Pharmacology: Trimetazidine HCl (Tazicon) has been proven to exert anti-anginal properties due to its specific metabolic mechanism of action. Indeed, Trimetazidine Hydrochloride reduces the metabolic damage caused during ischemia, by acting on a critical step in cardiac metabolism: fatty acid B-oxidation. This is made possible by selective inhibition of an enzyme of fatty acid B-oxidation: the long-chain 3-ketoacyl CoA thiolase (3-KAT). This inhibition results in reduction in fatty acid oxidation & stimulation of glucose oxidation. Thus, the coupling of glycolysis with glucose oxidation is improved, and ATP production is further increased, while the deleterious consequences of acidosis and of Ca²⁺ overload are limited.
Pharmacodynamics: In patients with ischaemic heart disease, trimetazidine acts as a metabolic agent, preserving the myocardial high-energy phosphate intracellular levels. Anti-ischemic effects are achieved without concomitant haemodynamic effects.
Pharmacokinetics: Absorption: Trimetazidine after oral administration and absorption from the digestive tract reaches the maximum concentration in the serum after about 5 hours from administration of the drug. The steady concentration of the drug in the serum is reached after 60 hours and is stable throughout the period of treatment. No interactions with food stuffs have been found.
Distribution: The drug binds to plasma proteins at about 16%. The volume of distribution is 4.8 l/kg, which means good penetration of the drug into the tissues.
Elimination: Trimetazidine is eliminated mainly in the urine, in unchanged form. The average half-life is 7 hours, in patients over age 65 years it increases to 12 hours.
Pharmacokinetics in special populations: No pharmacokinetic data are available for the use of trimetazidine in hepatically impaired patients.