Rispaxol, 2 mg 20 pcs.

Rispaxol is an antipsychotic (neuroleptic), a benzisoxazole derivative; it also has sedative, antiemetic and hypothermic effects.

Risperidone is a selective monoaminergic antagonist with strong affinity for serotonergic 5-HT2 and dopaminergic D2 receptors, also binds to alpha1-adrenoceptors and, with some less affinity, to Hl-histaminergic and alpha2-adrenergic receptors. It has no tropinity to cholinoreceptors

Antipsychotic action is caused by blockade of dopamine D2-receptors of mesolimbic and mesocortical system.
Sedative action is caused by the blockade of adrenoreceptors of reticular formation of brain stem; antiemetic action – by the blockade of dopamine D2-receptors of trigger zone of vomiting center; hypothermic action – by the blockade of dopamine receptors of hypothalamus.

Reduces productive symptomatology (delirium, hallucinations, aggression), automatism. Causes less suppression of motor activity and is less likely to induce catalepsy than classical antipsychotics (neuroleptics).

The balanced central antagonism to serotonin and dopamine may reduce the risk of extrapyramidal symptomatology.
Risperidone may cause a dose-dependent increase in plasma prolactin concentrations.

Pharmacokinetics

In oral administration, risperidone is completely absorbed (regardless of food intake) and maximum plasma concentrations are observed after 1-2 hours.

Risperidone is metabolized with participation of P-450 IID6 cytochrome to form 9-hydroxyrisperidone, which has similar pharmacological effects. Risperidone and 9-hydroxyrisperidone constitute an effective antipsychotic fraction.
When administered orally, risperidone is excreted with a half-life of about 3 hours. The half-life of 9-hydroxysperidone and the active antipsychotic fraction has been found to be 24 hours.

In most patients the equilibrium concentration of risperidone is observed one day after initiation of treatment. The equilibrium state of 9-hydroxysperidone in most cases is reached 3-4 days after the start of treatment. The concentration of risperidone in plasma is proportional to the dose of the drug (within the therapeutic doses).

Risperidone is rapidly distributed in the body. The volume of distribution is 1 -2 l/kg. In plasma, risperidone binds to albumin and a-1-glycoprotein. The binding of risperidone to plasma proteins is 88%, 9-hydroxirisperidone -77%.

Extracted by the kidneys – 70% (of which 35 – 45% in the form of pharmacologically active fraction) and 14% – in the bile. The remaining amount falls on inactive metabolites.

In elderly patients after a single oral administration of the drug increased concentrations of the active fraction in plasma up to 30% and in patients with renal insufficiency up to 60% were observed, as well as decreased clearance of antipsychotic fraction.

The presence of hepatic insufficiency did not affect the plasma concentrations of risperidone, but in such patients the mean plasma free fraction was 35% higher.

Indications

Schizophrenia (acute and chronic) and other psychotic conditions with a predominance of productive (delusions, hallucinations, aggressiveness), negative (blunted affect, emotional and social detachment, poverty of speech) or affective (anxious depression) symptoms;
behavioral disorders due to dementia (with the appearance of symptoms of aggressiveness, impairment of activity or psychotic symptoms) or mental retardation or reduced level of intelligence (with dominance of destructive behavior);
mania in bipolar disorders (auxiliary therapy).

Pharmacological effect

Rispaxol is an antipsychotic drug (neuroleptic), a derivative of benzisoxazole; It also has a sedative, antiemetic and hypothermic effect.

Risperidone is a selective monoaminergic antagonist with pronounced affinity for serotonergic 5-HT2 and dopaminergic D2 receptors; it also binds to alpha1-adrenergic receptors and, with slightly lower affinity, to Hl-histaminergic and alpha2-adrenergic receptors. Does not have tropism for cholinergic receptors

The antipsychotic effect is due to the blockade of dopamine D2 receptors of the mesolimbic and mesocortical systems.
The sedative effect is due to the blockade of adrenergic receptors in the reticular formation of the brain stem; antiemetic effect – blockade of dopamine D2 receptors in the trigger zone of the vomiting center; hypothermic effect – blockade of dopamine receptors of the hypothalamus.

Reduces productive symptoms (delusions, hallucinations, aggressiveness), automatism. Causes less suppression of motor activity and induces catalepsy to a lesser extent than classical antipsychotics (neuroleptics).

Balanced central antagonism of serotonin and dopamine may reduce the risk of extrapyramidal symptoms.
Risperidone may cause a dose-dependent increase in plasma prolactin concentrations.

Pharmacokinetics

When taken orally, risperidone is completely absorbed (regardless of food intake) and maximum plasma concentration levels are observed after 1-2 hours.

Risperidone is metabolized by cytochrome P-450 IID6 to form 9-hydroxyrisperidone, which has similar pharmacological effects. Risperidone and 9-hydroxyrisperidone are an effective antipsychotic fraction.
When taken orally, risperidone is eliminated with a half-life of approximately 3 hours. The half-life of 9-hydroxyrisperidone and the active antipsychotic fraction has been found to be 24 hours.

In most patients, steady-state risperidone concentrations are observed one day after the start of treatment. The equilibrium state of 9-hydroxyrisperidone is in most cases achieved 3-4 days after the start of treatment. The concentration of risperidone in plasma is proportional to the dose of the drug (within therapeutic doses).

Risperidone is rapidly distributed in the body. The volume of distribution is 1 -2 l/kg. In plasma, risperidone binds to albumin and a-1-glycoprotein. The binding of risperidone to plasma proteins is 88%, 9-hydroxyrisperidone -77%.

Excreted by the kidneys – 70% (of which 35 – 45% in the form of a pharmacologically active fraction) and 14% – with bile. The rest is inactive metabolites.

In elderly patients, after a single dose of the drug orally, increased concentrations of the active fraction in plasma were observed up to 30%, and in patients with renal failure – up to 60%, as well as reduced clearance of the antipsychotic fraction.

The presence of liver failure does not affect the concentration of risperidone in plasma, but in such patients the average amount of free fraction in plasma was 35% higher.

Active ingredient

Risperidone

Composition

Active ingredient:

risperidone 2 mg;

Excipients:

lactose,

anhydrous;

corn starch,

magnesium stearate,

colloidal silicon dioxide,

anhydrous;

microcrystalline cellulose

Pregnancy

During pregnancy, it is possible if the expected benefit to the mother outweighs the potential risk to the fetus.

FDA category of effect on the fetus is C.

During treatment you should stop breastfeeding.

Contraindications

Hypersensitivity.

Side Effects

From the nervous system and sensory organs: sleep disturbance, incl. insomnia or drowsiness, increased excitability, fatigue, impaired attention, restlessness, anxiety, headache, dizziness, extrapyramidal disorders (rigidity, hypokinesia, hypersalivation, akathisia, acute dystonia), tardive dyskinesia, neuroleptic malignant syndrome, thermoregulation disorder, seizures, stroke (in predisposed elderly patients), blurredness vision.

From the cardiovascular system and blood (hematopoiesis, hemostasis): orthostatic hypotension, reflex tachycardia, arterial hypertension, neutro- and thrombopenia, thrombocytopenic purpura.

From the gastrointestinal tract: nausea, vomiting, dyspeptic symptoms, abdominal pain, constipation, increased levels of liver transaminases.

From the genitourinary system: dysmenorrhea, amenorrhea, impotence, erectile dysfunction and ejaculation, anorgasmia, decreased libido, priapism, polyuria, urinary incontinence, edema.

Allergic reactions: skin rash, angioedema.

Other: rhinitis, galactorrhea, gynecomastia, weight gain, hypervolemia (due to polydipsia or syndrome of inappropriate ADH secretion), hyperglycemia (in patients with diabetes mellitus).

Interaction

Given that Rispaxol primarily affects the central nervous system, it should be used with caution in combination with other centrally acting drugs and ethanol.

Rispaxol reduces the effectiveness of levodopa and other dopamine agonists.

Clozapine reduces the clearance of risperidone.

With simultaneous use of rispaxol and carbamazepine, a decrease in the concentration of the active antipsychotic fraction of risperidone in plasma was observed. Similar effects may be observed with other liver enzyme inducers.

When used concomitantly with rispaxol, phenothiazines, tricyclic antidepressants and some beta-blockers may increase plasma concentrations of risperidone, but this does not affect the concentration of the active antipsychotic fraction.

When used concomitantly with rispaxol, fluoxetine may increase plasma concentrations of risperidone, but to a lesser extent the concentration of the active antipsychotic fraction.

When rispaxol is used together with other drugs that are highly bound to plasma proteins, no clinically significant displacement of any drug from the plasma protein fraction is observed.

Antihypertensive drugs increase the severity of the decrease in blood pressure while taking rispaxol.

Overdose

Symptoms: drowsiness, sedation, depression of consciousness, tachycardia, arterial hypotension, extrapyramidal disorders, in rare cases, prolongation of the QT interval.

Treatment: it is necessary to ensure free passage of the airways to ensure adequate oxygenation and ventilation, gastric lavage (after intubation, if the patient is unconscious) and the administration of activated charcoal in combination with laxatives.

Symptomatic therapy aimed at maintaining vital body functions.

For timely diagnosis of possible heart rhythm disturbances, it is necessary to begin ECG monitoring as soon as possible. Careful medical observation and ECG monitoring are carried out until the symptoms of intoxication completely disappear. There is no specific antidote.

Storage conditions

In a place protected from light, at a temperature not exceeding 25 °C

Shelf life

2 years

Manufacturer

Grindeks JSC, Latvia