Nurocol Mechanism of Action

Pharmacological Category: Nootropic preparation.
Pharmacology: Pharmacodynamics: FC Tablet: It is a nootropic preparation. Citicoline as a predecessor of key ultrastructural component of cell membrane (mainly phospholipids) has a wide spectrum of action: it promotes a restoration of damaged cell membranes, inhibits an action of phospholipase, preventing a formation of free radicals and prevents cell death by acting on mechanisms of apoptosis. It is a source of choline; it increases a synthesis of acetylcholine and stimulates biosynthesis of structural (foot) phospholipids in neuron membrane. It improves the transmission of nerve impulses in cholinergic neurons; it has a positive effect on plasticity of neuronal membranes and receptor function. It improves cerebral blood flow, enhances cerebral metabolic processes and activates the structure of cerebral reticular formation. In acute phase of a stroke it reduces the volume of damaged tissue and improves cholinergic transmission.
Citicoline alleviates symptoms, which occur during hypoxia and cerebral ischemia, including memory impairment, emotional liability, lack of initiative, difficulty during daily activities and self-service. In craniocerebral injury it reduces the duration of post-traumatic coma and the severity of neurological symptoms. Citicoline has anti-edema properties and reduces cerebral edema due to its stabilizing effect on neuronal membrane. It accelerates the recovery and reduces the duration and intensity of post-traumatic syndrome. Citicoline is effective in the treatment of cognitive, sensory and motor neurological disorders of degenerative and vascular etiology.
Injection: Citicoline is a complex organic molecule that functions as an intermediate in the biosynthesis of cell membrane phospholipids. Citicoline is also known as CDP-choline or cytidine diphosphate choline (cytidine 5'-diphosphocholine). CDP-choline belongs to the group of biomolecules in living systems known as nucleotides that play important roles in cellular metabolism. The pharmacologic action of Citicoline appears to involve mechanisms that extend beyond phospholipid metabolism. Citicoline metabolites-choline, methionine, betaine, and cytidine derived nucleotides - enter a number of metabolic pathways. Biochemical markers of cholinergic nerve transmission are known to be deficient in conditions characterized by degeneration of cholinergic neurons, such as Alzheimer's disease (AD). Citicoline modestly improves cognitive function in AD by serving as an acetylcholine precursor. The brain uses choline preferentially for acetylcholine synthesis, which can limit the amount of choline available for phosphatidylcholine production.
Citicoline has also been investigated as a therapy for stroke patients. Three mechanisms are postulated: repair of the neuronal membrane via increased synthesis of phosphatidylcholine; repair of damaged cholinergic neurons via potentiation of acetylcholine production; and reduction of free fatty acid build-up at the site of stroke-induced nerve damage. Citicoline protects cholinergic neurons from auto cannibalism, a process in which membrane phospholipids are catabolized to provide choline for synthesis of acetylcholine. This occurs when choline supplies are depleted, necessitating sacrifice of membrane phospholipids to maintain neurotransmission. As an exogenous source of choline for acetylcholine production, Citicoline thus spares membrane phospholipids (in particular, phosphatidylcholine) and prevents neuronal cell death.
Pharmacokinetics: FC Tablet: Citicoline is well absorbed in oral, intramuscular and intravenous introduction. After the preparation introduction it is observed a significant increase of choline in plasma. The preparation is almost completely absorbed in oral administration. Studies have shown that the bioavailability in per oral and parenteral routes of introduction was similar.
The preparation is metabolized in intestine and liver with the formation of choline and cytidine. After Citicoline introduction it is assimilated by cerebral tissues, while cholines act on phospholipids, cytidine on cytidine nucleoids and nucleic acids. Citicoline quickly reaches cerebral tissues and actively integrates into cell membrane, cytoplasm and mitochondria, activating an activity of phospholipids.
Only a minor part of introduced dose is excreted with urine and feces (less than 3%). Approximately 12% of introduced dose are excreted via respiratory tract. The preparation excretion via urine and respiratory tract has two phases: first phase rapid excretion (with urine within the first 36 hours, via airways within the first 15 hours), the second phase slow excretion. Major part of the dose is included into the process of metabolism.
Injection: Absorption: Citicoline is well absorbed following intramuscular administration. After intramuscular doses of Citicoline 1,000 mg, peak increases in plasma choline levels were seen in 0.4 hours, with levels increasing from 11 micromol/L (baseline) to 25 micromol/L.
Distribution: Choline derived from Citicoline crosses the blood-brain barrier, presumably serving as a source of acetylcholine and phosphatidylcholine (lecithin) synthesis. The major portion of a dose of Citicoline appears to be incorporated into tissues and/or used in biosynthetic/biodegradation pathways, including lecithin/lipid membrane synthesis.
Metabolism: Citicoline is metabolized in the liver to free choline. The liver is capable of synthesizing lecithin from choline. The half-life of free choline is of 2 hours after intramuscular administration.
Excretion: Only small amounts of dose are recovered in the urine and faeces (less than 3% each). Approximately 12% of a dose is eliminated through the lungs as carbon dioxide.