Mexiprim^® (Tablets, Solution) Instructions for Use

ATC Code

N07XX (Other drugs for the treatment of nervous system diseases)

Active Substance

Ethylmethylhydroxypyridine succinate (Grouping Name)

Clinical-Pharmacological Group

Antioxidant drug

Pharmacotherapeutic Group

Other agents for the treatment of nervous system diseases

Pharmacological Action

Mexiprim^® is a derivative of 3-hydroxypyridine; it exerts antioxidant, antihypoxic, anti-ischemic, membrane-protective, nootropic, stress-protective, anticonvulsant, anxiolytic, and hypolipidemic effects.

The mechanism of action of the drug is due to its antioxidant, antihypoxic, and membrane-protective effects. Mexiprim^® reduces the manifestations of oxidative stress, inhibits lipid peroxidation, increases the activity of superoxide dismutase, increases the lipid-protein ratio, and improves the structure and function of cell membranes. The drug modulates the activity of membrane-bound enzymes (calcium-independent phosphodiesterase, adenylate cyclase, acetylcholinesterase), receptor complexes (benzodiazepine, GABA, acetylcholine), which enhances their ligand-binding ability, contributes to the preservation of the structural and functional organization of biomembranes, neurotransmitter transport, and improvement of synaptic transmission.

Mexiprim^® increases the dopamine content in the brain. It causes an enhancement of compensatory activation of aerobic glycolysis and a reduction in the inhibition of oxidative processes in the Krebs cycle under hypoxic conditions, with an increase in ATP and creatine phosphate content, activation of the energy-synthesizing functions of mitochondria, and stabilization of cell membranes.

The drug has a wide spectrum of pharmacological activity; it increases the body’s resistance to stress and the effects of various damaging factors in pathological conditions (hypoxia and ischemia, impaired cerebral circulation, intoxication with ethanol and antipsychotic drugs).

Under conditions of a critical decrease in coronary blood flow, it helps preserve the structural and functional organization of cardiomyocyte membranes and stimulates the activity of membrane enzymes (phosphodiesterase, adenylate cyclase, acetylcholinesterase). It supports the activation of aerobic glycolysis developing during acute ischemia and promotes the restoration of mitochondrial oxidative-reduction processes under hypoxic conditions, increasing the synthesis of ATP and creatine phosphate. It ensures the integrity of the morphological structures and physiological functions of the ischemic myocardium. It improves the clinical course of myocardial infarction, increases the effectiveness of the therapy, reduces the frequency of arrhythmias and intracardiac conduction disturbances. It normalizes metabolic processes in the ischemic myocardium, increases the antianginal activity of nitrates, improves the rheological properties of blood, and reduces the consequences of reperfusion syndrome in acute coronary insufficiency.

It improves the functional state of the ischemic myocardium. Under conditions of coronary insufficiency, it increases the collateral blood supply to the ischemic myocardium, helps preserve the integrity of cardiomyocytes and maintain their functional activity. It effectively restores myocardial contractility in reversible cardiac dysfunction.

It improves brain tissue metabolism and blood supply, improves microcirculation and the rheological properties of blood, and reduces platelet aggregation. It stabilizes the membrane structures of blood cells (erythrocytes and platelets). It has a hypolipidemic effect, reducing the content of total cholesterol and LDL.

It exhibits an anxiolytic effect not accompanied by a muscle relaxant effect; it has nootropic properties, preventing and reducing learning and memory impairments occurring with aging and under the influence of various pathogenic factors; it has an anticonvulsant effect; it increases concentration and performance.

The anti-stress effect is manifested in the normalization of post-stress behavior, somatovegetative disorders, restoration of sleep-wake cycles, impaired learning and memory processes, and reduction of dystrophic and morphological changes in various brain structures.

It reduces enzymatic toxemia and endogenous intoxication in acute pancreatitis.

It has a pronounced antitoxic effect in withdrawal syndrome. It eliminates neurological and neurotoxic manifestations of acute alcohol intoxication, restores behavioral disorders, autonomic functions, and helps reduce the severity of cognitive impairments caused by long-term ethanol use. Under the influence of the drug, the action of tranquilizing, neuroleptic, antidepressant, hypnotic, and anticonvulsant drugs is enhanced, which allows reducing their doses and side effects.

Pharmacokinetics

Absorption and Distribution

It is rapidly absorbed when taken orally. C_max when used in doses of 400-500 mg is 3.5-4.0 µg/ml. It is rapidly distributed in organs and tissues. The mean residence time (MRT) of the drug in the body when taken orally is 4.9-5.2 hours.

Metabolism

It is metabolized in the liver by glucuronoconjugation. Five metabolites have been identified: 3-hydroxypyridine phosphate – formed in the liver, breaks down into phosphoric acid and 3-hydroxypyridine under the action of alkaline phosphatase; the 2nd metabolite is pharmacologically active, formed in large quantities and detected in urine on days 1-2 after administration; the 3rd is excreted in large quantities in the urine; the 4th and 5th are glucuronoconjugates.

Excretion

T_1/2 when taken orally is 2.0-2.6 hours. It is rapidly excreted in the urine mainly as metabolites and in small amounts unchanged. It is most intensively excreted within the first 4 hours after taking the drug. The excretion parameters of the unchanged drug and metabolites in urine have individual variability.

Indications

• Consequences of acute cerebrovascular accidents, including after transient ischemic attacks, in the subcompensation phase as preventive courses;
• Mild traumatic brain injury, consequences of traumatic brain injuries;
• Encephalopathies of various origins (dyscirculatory, dysmetabolic, post-traumatic, mixed);
• Autonomic dystonia syndrome;
• Mild cognitive disorders of atherosclerotic origin;
• Anxiety disorders in neurotic and neurosis-like states;
• Ischemic heart disease as part of complex therapy;
• Relief of withdrawal syndrome in alcoholism with a predominance of neurosis-like and autonomic-vascular disorders, post-withdrawal disorders;
• Conditions after acute intoxication with antipsychotic drugs;
• Asthenic conditions, as well as for the prevention of the development of somatic diseases under the influence of extreme factors and loads;
• Exposure to extreme (stress) factors.

ICD codes

Dosage Regimen

Tablets

The drug is taken orally at 125-250 mg (1-2 tablets) 3 times/day.

The initial dose is 125-250 mg (1-2 tablets) 1-2 times/day with a gradual increase until a therapeutic effect is achieved. The maximum daily dose is 750 mg (6 tablets).

The duration of treatment is 2-6 weeks; for the relief of alcohol withdrawal – 5-7 days. The duration of the therapy course in patients with IHD is at least 1.5-2 months. Treatment is discontinued gradually, reducing the dose over 2-3 days.

Repeated courses (as recommended by a doctor) are advisable in the spring and autumn periods.

Solution

Mexiprim^® is administered intramuscularly or intravenously (bolus or drip). To prepare the infusion solution, the drug should be diluted with isotonic sodium chloride solution.

Doses are selected individually depending on the pathology and severity of the patient’s condition. The initial dose is 50-100 mg 1-3 times/day. Subsequently, it is possible to increase the dose until a therapeutic effect is achieved. The maximum daily dose is 800 mg.

Bolus Mexiprim^® is administered slowly, over 5-7 minutes, drip – at a rate of 40-60 drops/minute.

In the treatment of acute cerebrovascular accidents, Mexiprim^® is used in complex therapy in the first 2-4 days intravenously drip at a dose of 200-300 mg once/day, then intramuscularly at 100 mg 3 times/day. The duration of treatment is 10-14 days.

In dyscirculatory encephalopathy in the decompensation phase, Mexiprim^® should be prescribed intravenously bolus or drip at a dose of 100 mg 2-3 times/day for 14 days. Then the drug is administered intramuscularly at 100 mg/day for the next 2 weeks. For course prevention of dyscirculatory encephalopathy, the drug is administered intramuscularly at a dose of 100 mg 2 times/day for 10-14 days.

In mild cognitive impairments in elderly patients and in anxiety disorders, the drug is used intramuscularly at a daily dose of 100-300 mg for 14-30 days.

In alcohol withdrawal syndrome, Mexiprim^® is administered at a dose of 100-200 mg intramuscularly 2-3 times/day or intravenously drip 1-2 times/day for 5-7 days.

In acute intoxication with antipsychotic drugs, the drug is administered intravenously at a dose of 50-300 mg/day for 7-14 days.

Adverse Reactions

From the digestive system rarely – nausea, dry mouth.

Other rarely – drowsiness, allergic reactions.

Contraindications

• Acute impairment of liver and kidney function;
• Pregnancy;
• Breastfeeding period;
• Childhood;
• Hypersensitivity to the active substance and other components of the drug.

Use in Pregnancy and Lactation

The use of the drug is contraindicated during pregnancy and lactation.

Use in Hepatic Impairment

The drug is contraindicated in acute impairment of liver function.

Use in Renal Impairment

The drug is contraindicated in acute impairment of kidney function.

Pediatric Use

The use of the drug in children is contraindicated.

Special Precautions

Effect on the ability to drive vehicles and operate machinery

During the treatment period, caution should be exercised when driving vehicles and engaging in other potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Overdose

Symptoms: sleep disturbances (insomnia, in some cases drowsiness).

Treatment: symptomatic therapy.

Drug Interactions

Mexiprim^® is compatible with all drugs used to treat somatic diseases.

It enhances the action of benzodiazepine drugs, antidepressants, anxiolytics, antiepileptic drugs (carbamazepine), antiparkinsonian drugs (levodopa), and nitrates.

It reduces the toxic effect of ethanol.

Storage Conditions

The drug should be stored in the consumer packaging (cardboard pack) in a place inaccessible to children at a temperature not exceeding 30°C (86°F).

Shelf Life

The shelf life is 5 years. Do not use after the expiration date printed on the package.

Dispensing Status

The drug is dispensed by prescription.

Important Safety Information

This information is for educational purposes only and does not replace professional medical advice. Always consult your doctor before use. Dosage and side effects may vary. Use only as prescribed.