Ziprasidone intermediate | Ziprasidone intermediate: 5-(2-chloroethyl) -6-chloro-1, 3-dihydro-indole-2-(2H)-one, 5-chloroacetyl-6-chloro-1, 3-dihydro-2H-indole-2-one, 3-(1-piperazinyl)-1, 2-benzisothiazole hydrochloride zipiperidone is an atypical antipsychotic, belonging to benzothiazole piperazine compounds, in vitro, This product has a strong affinity for dopamine D2, D3, 5-HT2A, 5-HT2C, 5-HT1A, 5-HT1D and α1 receptor adrenaline; the affinity for histamine H1 receptor is medium. It has antagonistic effects on dopamine D1, D2, 5-HT2A, 5-HT1D, and agonistic effects on 5-HT1A receptors. This product inhibits the reuptake of 5-HT and norepinephrine by presynaptic membrane. The mechanism of action is still unclear. It may produce anti-schizophrenia effects through the combined antagonism of dopamine D2 and 5-HT2. Its blocking intensity is similar to risperidone and haloperidol, and is better than olanzapine and quetiapine. It is strong and is mainly used for acute or chronic, initial or recurrent schizophrenia. It is effective for negative and positive symptoms of schizophrenia. Especially negative symptoms are better. It can reduce hallucinations, delusions, thinking and behavior abnormalities and other positive symptoms; also improve mood monotony, volitional behavior reduction and other negative symptoms. Atypical antipsychotics, also known as a new generation of antipsychotics, refer to antipsychotic drugs that block dopamine D2 receptors less than 5-HT2A receptors, such as clozapine, ritone, olanzapine, quetiapine, ziprasidone and other drugs currently used clinically belong to this category. In addition to the early clinical application of clozapine in atypical antipsychotics (70 s). Atypical antipsychotics not only block dopamine D2 receptor, but also have a stronger blocking effect of 5-HT2A receptor. When blocking the midbrain-limbic pathway dopamine D2 receptor, it can improve the patient's positive symptoms; when blocking the 5-HT2A receptor on the presynaptic membrane of the midbrain-cortical pathway, it can cause dopamine deinhibitory release, excite the dopamine D1 receptor in the dorsolateral prefrontal cortex, improve negative and cognitive symptoms, excite the dopamine D1 receptor in the medial dorsal part of the prefrontal cortex and the orbit, and improve depression symptoms; when the 5-HT2A receptor on the presynaptic membrane of the substantia nigra-striatum pathway is blocked, it causes the deinhibitory release of dopamine, which can partially offset the blockade of the dopamine D2 receptor by the drug, so the extrapyramidal system responds Slight (long-term use is not easy to cause tardive dyskinesia); when the 5-HT2A receptor on the presynaptic membrane of the hypothalamus-funnel is blocked, it causes the deinhibitory release of dopamine, which partially offsets the blockade of dopamine D2 receptors by the drug, therefore, hyperprolactinemia is not obvious. |