CHOLINERV Citicoline 100mg / mL Oral Drops 15mL
RXDRUG-DR-XY33558
Discreet Packaging
We recognize that purchasing medications can be a deeply personal matter. To respect your privacy, we ensure that all orders are packaged discreetly, with no indication of the contents on the packaging. This means that even our couriers remain unaware of the package contents.
Furthermore, we uphold strict confidentiality standards. We guarantee that your order information will never be disclosed to any third party. Your trust is paramount to us, and we are committed to safeguarding your privacy at every step of the process. Our dedication to discretion and confidentiality is part of our unwavering commitment to you, our valued customer.
FDA-registered Products
FDA-licensed Pharmacies
Features
Brand
Cholinerv
Full Details
Dosage Strength
100mg /ml
Drug Ingredients
- Citicoline
Drug Packaging
Oral Drops 15ml
Generic Name
Citicoline
Dosage Form
Oral Drops
Registration Number
DR-XY33558
Drug Classification
Prescription Drug (RX)
Description
Indications/Uses
Acute and recovery phase of cerebral infarction (e.g., ischemia due to stroke); Cognitive dysfunction due to degenerative (i.e., Alzheimer's disease) and cerebrovascular disease; Cerebral insufficiency (e.g., dizziness, memory loss, poor concentration, disorientation) due to head trauma or brain injury; Parkinson's disease.
Dosage/Direction for Use
Tab 500 mg once or bid. Drops Adult 100-200 mg bid or tid.
Dosing must be individualized and adjusted according to disease severity. (See table.)
Overdosage
Citicoline exhibits very low toxicity profile in humans. In clinical use it has been observed to be safe at doses up to 2 g/day.
The LD50 of a single IV dose of citicoline was 4.6 and 4.15 g/kg in mice and rats, respectively. An oral LD50 could not be determined as no deaths occurred at the maximum possible oral dose.
In an unpublished acute toxicity study, free-base citicoline was administered to male and female rats at a dose of 2 g/kg body weight for 14 days. No changes in body weight, deaths, clinical symptoms, or gross pathological changes were observed.
The LD50 of a single IV dose of citicoline was 4.6 and 4.15 g/kg in mice and rats, respectively. An oral LD50 could not be determined as no deaths occurred at the maximum possible oral dose.
In an unpublished acute toxicity study, free-base citicoline was administered to male and female rats at a dose of 2 g/kg body weight for 14 days. No changes in body weight, deaths, clinical symptoms, or gross pathological changes were observed.
Administration
May be taken with or without food: Take w/ or between meals.
Contraindications
Hypersensitivity to any component of the product.
Patients with hypertonia of the parasympathetic nervous system.
Patients with hypertonia of the parasympathetic nervous system.
Special Precautions
May aggravate increase in cerebral blood flow in persistent intracranial hemorrhage. Pregnancy & lactation.
Large doses of citicoline could aggravate increase in cerebral blood flow in episodes of persistent intracranial hemorrhage.
Use in Children: No data on use in children.
Use in Children: No data on use in children.
Use In Pregnancy & Lactation
There is not enough evidence on citicoline's safety in pregnant and breastfeeding women. Citicoline should be used in pregnancy and breastfeeding only when benefits justify the potential risks.
Adverse Reactions
Cardiovascular: Bradycardia, tachycardia, hypotension.
Gastrointestinal: Diarrhea, epigastric distress, stomach pain.
Nervous: Dizziness, headache, fatigue.
Skin: Rash.
Gastrointestinal: Diarrhea, epigastric distress, stomach pain.
Nervous: Dizziness, headache, fatigue.
Skin: Rash.
Drug Interactions
Citicoline must not be administered with products containing meclofenoxate.
Citicoline potentiates the effects of L-dopa.
Citicoline potentiates the effects of L-dopa.
Storage
Store at temperatures not exceeding 30°C.
Action
Pharmacology: Pharmacodynamics: 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, i.e. 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. Citicoline modestly improves cognitive function in Alzheimer's disease 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 been investigated as a therapy for stroke patients. Three mechanisms are postulated: (1) repair of the neuronal membrane via increased synthesis of phosphatidylcholine; (2) repair of damaged cholinergic neurons via potentiation of acetylcholine production; and (3) reduction of free fatty acid build-up at the site of stroke-induced nerve damage.
Citicoline protects cholinergic neurons from autocannibalism, a process in which membrane phospholipids are catabolized to provide choline for the 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: Citicoline is a water-soluble compound with greater than 90% bioavailability. Pharmacokinetic studies in healthy adults have shown oral doses of citicoline to be rapidly absorbed, with less than 1% excreted in the feces. Plasma levels peak in a biphasic manner, at 1 hour after ingestion followed by a second larger peak at 24 hours post-dosing.
Citicoline is metabolized in the gut wall and liver. The byproducts of exogenous citicoline formed by hydrolysis in the intestinal wall are choline and cytidine. After absorption, choline and cytidine are dispersed throughout the body, enter systemic circulation for utilization in various biosynthetic pathways and cross the blood-brain barrier for re-synthesis into citicoline in the brain.
Pharmacokinetic studies using 14C citicoline show citicoline elimination occurs mainly via respiratory CO2 and urinary excretion, in two phases, mirroring the biphasic plasma peaks. The initial peak in plasma concentration is followed by a sharp decline, which then slows over the next 4 to 10 hours. In the second phase, an initially rapid decline after the 24-hour plasma peak is similarly followed by a slower elimination rate. The elimination half-life is 56 hours for CO2 and 71 hours for urinary excretion.
The pharmacologic action of citicoline appears to involve mechanisms that extend beyond phospholipid metabolism. Citicoline metabolites, i.e. 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. Citicoline modestly improves cognitive function in Alzheimer's disease 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 been investigated as a therapy for stroke patients. Three mechanisms are postulated: (1) repair of the neuronal membrane via increased synthesis of phosphatidylcholine; (2) repair of damaged cholinergic neurons via potentiation of acetylcholine production; and (3) reduction of free fatty acid build-up at the site of stroke-induced nerve damage.
Citicoline protects cholinergic neurons from autocannibalism, a process in which membrane phospholipids are catabolized to provide choline for the 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: Citicoline is a water-soluble compound with greater than 90% bioavailability. Pharmacokinetic studies in healthy adults have shown oral doses of citicoline to be rapidly absorbed, with less than 1% excreted in the feces. Plasma levels peak in a biphasic manner, at 1 hour after ingestion followed by a second larger peak at 24 hours post-dosing.
Citicoline is metabolized in the gut wall and liver. The byproducts of exogenous citicoline formed by hydrolysis in the intestinal wall are choline and cytidine. After absorption, choline and cytidine are dispersed throughout the body, enter systemic circulation for utilization in various biosynthetic pathways and cross the blood-brain barrier for re-synthesis into citicoline in the brain.
Pharmacokinetic studies using 14C citicoline show citicoline elimination occurs mainly via respiratory CO2 and urinary excretion, in two phases, mirroring the biphasic plasma peaks. The initial peak in plasma concentration is followed by a sharp decline, which then slows over the next 4 to 10 hours. In the second phase, an initially rapid decline after the 24-hour plasma peak is similarly followed by a slower elimination rate. The elimination half-life is 56 hours for CO2 and 71 hours for urinary excretion.
MedsGo Class
Other CNS Drugs & Agents for ADHD
Please sign in so that we can notify you about a reply