CARNICOR L-Carnitine 330mg Tablet 1's

There have been no reports of toxicity from levocarnitine overdosage. Levocarnitine is easily removed from plasma by dialysis. Large doses of levocarnitine may cause diarrhea.

Use in pregnancy is not recommended unless clearly needed. Pregnancy category: B Discontinuation of treatment in a pregnant woman with primary systemic carnitine deficiency may carry serious consequences; the risk of stopping treatment may outweigh the theoretical risks to the fetus. Animal studies showed no evidence of impaired fertility or fetal harm, however at 600 mg/kg daily there was a statistically insignificant increase in post implantation losses. There are no controlled data in human pregnancy.
In use during breastfeeding, the risks to the infant from excess carnitine intake should be weighed against the benefits of supplementation to the mother. L-Carnitine (Carnicor) concentration in milk is increased in dairy cows after exogenous administration. There is no available data on L-carnitine excretion in human milk.

Store at temperatures not exceeding 30°C. Protect from light and moisture.
Shelf-Life: 48 months (tablet) & 36 months (oral solution).

Pharmacology: Pharmacodynamics/Pharmacokinetics: L-Carnitine (Carnicor) acts as a co-factor in fatty acid metabolism specifically it transports into the mitochondrion for β-oxidation and ultimately, for energy production.
L-Carnitine (Carnicor) indirectly regulates glucose (G) utilization thru control of acetyl CoA/CoA ratio, an important regulator of pyruvate dehydrogenase (PDH) activity and consequent acetyl CoA formation which enters the TCA cycle and releases energy.
The above continuing reactions prevent lactic acid (LA) formation and accumulation.
L-Carnitine (Carnicor) by preventing acyl CoA accumulation preserves mitochondrial adenine nucleotide translocase (ANT) activity thus allowing ATP/ADP exchange (ATP for extramitochondrial utilization, ADP for mitochondrial ATP synthesis).
Of three (3) major substrates available to it, cardiac muscle utilizes free fatty acid (FFA) as preferential substrate over glucose and lactate. In fact, it is the most important energy yielding substrate for oxidative metabolism in cardiomyocytes. 60-80% of ATP generated derives from FA oxidation, the remainder from Glucose and Lactate metabolism. Important to note is that there is no anaerobic reserve for residual energy production from FA metabolism. Lipids require more oxygen than glucose or lactate forgiven amount of energy to be released.
L-Carnitine (Carnicor) has a vital role in the mitochondrial membrane transfer of FFA and energy generation of oxidative metabolism.
L-Carnitine (Carnicor) is a key metabolite of the intermediate metabolism involved in membrane transport and without which metabolic products formed in the mitochondrion under ischemic conditions cannot be eliminated.
As L-Carnitine (Carnicor) levels increase: Acyl carnitine formed from acyl CoA is transferred out of the mitochondrion and cell.
CoA is free to react with other acyl groups to reduce cell toxicity.
FFA extraction increases.
Enzyme systems regenerate e.g., pyruvate dehydrogenase (PDH) is activated, lactate production decreases, glycolysis and TCA cycle proceed and energy supply is restored. Adenine nucleotide translocase (ANT) is activated, mitochondrial transport of ATP and ADP restores energy supply.
Mitochondrial transmembrane potential is stabilized.
Restoration of energy supply improves cardiac function.
Oxygen supply improves, ischemia is relieved.
β-oxidation and other oxidative metabolic processes improve.
Cardiac performance improves.
Clinical Signs of the Ischemic Heart Improved by L-Carnitine: Rhythm restored; Extent of ST segment depression lessened; Frequency and intensity of anginal attacks decreased and nitroglycerine consumption reduced; Improved exercise tolerance; Positive inotropic effect: decreased ventricular diastolic pressure and the pre-ejection pd/LV ejection time ratio; Reduced LVEDP.