Depressions that are accompanied by anxiety, asthenia, and loss of initiative. Chronic neurotic disorders accompanied by anxiety, depression, and inactivity. Psychosomatic disorders with asthenic reactions. Schizophrenia and other psychoses, especially with symptoms such as hallucinations, delusions, and thinking disorders complicated by apathy, anergia, depressed mood, and seclusion.
Fluanxol Depo Storage
active substance: flupentixol;
1 ml of solution for injection contains 20 mg of cis (Z) -flupentixol decanoate;
Excipients: medium chain triglycerides.
Fluanxol Depo Dosage form
Solution for injection.
Basic physical and chemical properties: transparent, from colorless to slightly yellowish color oil solution, almost free from mechanical inclusions.
Fluanxol Depo Pharmacotherapeutic group
Psycholeptics. Antipsychotics. Thioxanthene derivatives. Flupentixol.
ATX code N05A F01.
Flupentixol is a thioxanthene neuroleptic.
The antipsychotic effect of neuroleptics has been associated with dopamine receptor blockade and possible 5HT receptor blockade. In vitro and in vivo, flupentixol has a high affinity for both dopamine D1 and D2 receptors. The atypical antipsychotic clozapine has a flupentixol-like affinity for D1 and D2 receptors in vitro and in vivo.
Flupentixol has a high affinity for α1-adrenoceptors and 5HT2-receptors, although slightly lower than chlorprothixene, high-dose phenothiazines and clozapine, but has no affinity for cholinergic muscarinic receptors. It has weak antihistaminergic properties and has no blocking effect on α2-adrenoceptors.
Flupentixol is a potent neuroleptic, as evidenced by all behavioral studies of neuroleptic activity (the ability to block dopamine receptors). At average daily dosage and oral use for antipsychotic treatment, affinity for dopamine D2-receptor blocking sites has been observed in in vitro and in vivo models.
Perioral movements of rats depend on stimulation of D1-receptors or blockade of D2-receptors. Movements can be prevented with flupentixol. Similarly, studies in monkeys indicate that oral hyperkinesia is more associated with D1 receptor stimulation and less associated with D2 receptor hypersensitivity. This allows us to conclude that the activation of D1 is responsible for the development of a similar effect in humans, ie the development of dyskinesia. Thus, blockade of D1 receptors should be beneficial in preventing the development of dyskinesia in humans.
Supportive care for schizophrenia and other psychoses, especially with symptoms such as hallucinations, delusions, and thought disorders complicated by apathy, anergy, depression, and loneliness.
Hypersensitivity to any component of the drug.
Circulatory collapse, central nervous system depression of any origin (eg due to alcohol, barbiturate or opioid intoxication), coma.
Not recommended for use in mildly excitable patients and in patients with a state of nervous excitement.