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Stimulation of ATP Production in Heart Muscle: In rabbits, heart muscle pretreated with ubidecarenone intraperitoneally, the decrease in ATP production in heart muscle seen after post-ischemic reperfusion was inhibited, so that post-ischemic reperfusion-induced myocardial cell injury was only slight.
Improvement of Diminished Cardiac Function: When ubidecarenone was administered orally from the stage of myocardial injury to the stage of cardiac hypertrophy in models of cardiomyopathy (hamsters with cardiomyopathy), diminished myocardial contractility and expansibility were a lesser extent in the treated animals than in the untreated group or digoxin-treated group.
In the rat models of myocardial infarction, ubidecarenone slightly inhibited a post-infarction decrease in cardiac function. When the effect of ubidecarenone on the post-infarction prognosis was determined in rat models of myocardial infarction, the long-term survival rate was higher for the treated group than for the untreated group.
Anti-aldosterone Effect: Ubidecarenone inhibited the secretion of aldosterone and antagonized Na+ retention brought about by the aldosterone in rats, resulting in the acceleration of Na+ diuresis. However, ubidecarenone has no effect on K+ excretion.
Clinical Studies: Clinical Efficacy: In double-blind clinical trials and open-labeled clinical trials, Decaquinon has been demonstrated to be useful for treating objective and subjective symptoms (edema, pulmonary congestion, hepatic enlargement, anginal symptoms and others) associated with congestive heart failure due to ischemic heart disease, hypertension or rheumatic heart disease and others.
Pharmacokinetics: Blood Concentration of Decaquinon Uncoated Tablets 10 mg and Decaquinon Sugar-Coated Tablets 10 mg: Ten (10) tablets of Decaquinon uncoated tablets 10 mg or of Decaquinon sugar-coated tablets 10 mg were administered orally to healthy adult male volunteers at a single dose (ubidecarenone 100 mg) in a crossover design, and changes in the plasma concentration were compared. For both dosage forms, the time to reach peak plasma concentration (about 0.5 mcg/mL of exogenous CoQ10) was 6 hrs after administration and thereafter, the plasma concentration gradually declined. There was no statistically significant difference between the 2 different dosage forms. (See figure and table.)
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