Quetiapine is an atypical antipsychotic, which exhibits higher affinity for serotonin than to dopamine receptors of the brain. Quetiapine also has a high affinity for histamine adrenoretseptoram and smaller relative to adrenoretseptoram. There were no appreciable affinity for cholinergic muscarinic to quetiapine and benzodiazepine receptors. The standard tests shows quetiapine antipsychotic activity.
Results of the study of extrapyramidal symptoms deca durabolin cycle in animals revealed that quetiapine causes weak catalepsy at a dose that effectively blocking dopamine D 2 receptors. Quetiapine is a selective decrease in the activity of mesolimbic A10 dopaminergic neurones versus the A9 nigrostriatal neurones involved in motor function.
In clinical trials (with the use of quetiapine in a dose of 75-750 mg / day), there were no differences between the use of quetiapine and placebo in the incidence of cases of extrapyramidal symptoms and concomitant use of anticholinergic drugs.
Seroquel does not cause long-term increase prolactin concentration in blood plasma. Numerous studies fixed dose there were no differences in the level of prolactin using quetiapine or placebo.
In clinical studies showed quetiapine and efficacy in the treatment of positive and negative symptoms of schizophrenia. Effects of quetiapine on the receptors of the deca durabolin cycle can be extended to 12 hours after ingestion.
When quetiapine orally is well absorbed from the gastrointestinal tract and is extensively metabolised by the liver. The major metabolites found in the plasma does not possess a pronounced pharmacological activity.
Food intake did not significantly affect the bioavailability of quetiapine. The half-life of about 7 hours. Approximately 83% of quetiapine binds to plasma proteins.
The pharmacokinetics of quetiapine linear, differences in pharmacokinetic parameters in men and women is not observed.
The average clearance of quetiapine in elderly patients is 30-50% less than in patients aged 18 to 65 years.
The average plasma clearance of quetiapine is less than approximately 25% in patients with severe renal impairment (creatinine clearance less than 30 ml / min / 1.73m 2 ) and in patients with liver disease (stable alcoholic cirrhosis), but the individual clearance figures are within the corresponding healthy people.
Approximately 73% of quetiapine is excreted in urine and 21% in faeces. Less than 5% of quetiapine is not metabolized and excreted unchanged by the kidneys or in the faeces
It is found that metabolism is a key enzyme quetiapine mediated by cytochrome P450.
The pharmacokinetic study of quetiapine in varying doses to the appointment quetiapine receiving ketoconazole or concurrently with ketoconazole, resulted in an increase in average maximum concentration deca durabolin cycl and area under “concentration-time” curve of quetiapine at 235% and 522% , respectively, and also led to a decrease in clearance of quetiapine, an average of 84%. The half-life of quetiapine increased, but the average time to maximum concentration did not change.
Quetiapine and its metabolites have some weak inhibitory activity towards cytochrome , but only at concentrations 10-50 times greater than the concentration observed in a commonly used effective dosage of 300-450 mg / d.
Based on the results in vitro, not to be expected that co-administration of quetiapine with other drugs will result in clinically significant inhibition of cytochrome deca durabolin cycle mediated metabolism of other drugs.