What does norquetiapine do?

The available data are sufficient to arrive at the conclusion that antidepressant activity of quetiapine is mediated, at least in part, by the active metabolite norquetiapine, which selectively inhibits noradrenaline reuptake, is a partial 5-HT1A receptor agonist, and acts as an antagonist at presynaptic α2, 5-HT2C.

Is norquetiapine active?

Norquetiapine is a major active metabolite in humans with a pharmacological profile that differs distinctly from that of quetiapine.

How does quetiapine work?

The main effect that quetiapine has is to block the effects of dopamine in the brain, resulting in a reduction of symptoms. Quetiapine also has effects on other neurotransmitters in the brain such as serotonin, and its beneficial effects may be related to this as well.

What are the side effects of norquetiapine and quetiapine?

Both quetiapine and norquetiapine strongly antagonize this receptor, thereby easing dopamine release in the said pathways and resulting in low incidence of extrapyramidal side effects and hyperprolactinemia.16)

What kind of receptors does quetiapine bind to?

In addition, quetiapine also binds to other alpha-1, alpha-2 adrenergic and histamine H1 receptors. Quetiapine is an atypical antipsychotic used in the treatment of schizophrenia and bipolar disorder. Use of quetiapine has been associated with serum aminotransferase elevations and in rare instances with clinically apparent acute liver injury.

How is norquetiapine produced in the cytochrome P450 system?

N -desalkyl quetiapine or norquetiapine is quetiapine’s key metabolite and is produced by the action of isoenzymes CYP 3A4 in the cytochrome P450 system. 13) Minor metabolism occurs via CYP2D6 into 7-hydroxy quetiapine which is thought not to possess any active properties.

How does quetiapine fumarate work in the brain?

Quetiapine fumarate antagonizes serotonin activity mediated by 5-HT 1A and 5-HT2 receptors. With a lower affinity, this agent also reversibly binds to dopamine D1 and D2 receptors in the mesolimbic and mesocortical areas of the brain leading to decreased psychotic effects, such as hallucinations and delusions.