In the Chinese market, atypical antipsychotics are clozapine, risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole, paliperidone, aminosulfuronyl chloride, and sulpiride, the variety of choices on the large, but do not know the similarities and differences, the choice will be blind, which is not a psychiatrists should have the qualities of the paper will be atypical antipsychotic according to the similarity of the drugs are divided into six groups, to compare their similarities and differences. Clozapine than olanzapine (a) similarities 1, efficacy: Clozapine and olanzapine have anti-dopamine D2 receptor, anti-α1 receptor, N-methyl-D-aspartate (NMDA) receptor, gamma-aminobutyric acid (GABA) can be proposed, through the “two resistance to the two proposed” and anti-psychotic symptoms (positive symptoms) and the best two drugs to resist positive symptoms. Clozapine and olanzapine are the best two drugs against positive symptoms. Clozapine and olanzapine have NMDA-like properties, worsening compulsion, with clozapine being the most serious. Adverse effects: Clozapine and olanzapine anti-histamine H1 receptor effect is very strong, so eat more, sleep more, the effect of weight gain is very prominent, and through eating more caused by hyperglycemia and hyperlipidemia, are metabolized by the liver 1A2 enzyme, damage to liver function are more serious. (B) Differences 1, efficacy: Clozapine partially agonist muscarinic M4 receptor, anti-positive symptoms, olanzapine lacks this mechanism, so it is worse than clozapine anti-positive symptoms, olanzapine’s anti-D2 receptor is stronger than that of clozapine, so the therapeutic amount is lower than that of clozapine (10-20mg/d: 300-400mg/d). Adverse reactions: Clozapine’s anti-D2 receptor is weaker than that of olanzapine, so the extrapyramidal reaction and hyperprolactinemia are lighter than that of olanzapine; Clozapine’s anticholinergic effect is stronger than that of olanzapine, so the rate of constipation is higher than that of olanzapine; Clozapine agitates the M4 receptor, which causes salivation and incontinence, and olanzapine does not have these effects; Clozapine’s anti-alpha1 receptor has a stronger total effect than that of olanzapine, so the effect of upright hypotension is more serious than that of olanzapine. Clozapine’s K+ channel blocking performance is stronger than olanzapine, so prolonging the QTc interval effect is heavy, arrhythmia rate is high; Clozapine’s myelotoxicity is stronger than that of olanzapine, so it causes a high rate of granulocyte deficiencies; Clozapine’s half-life is only half of that of olanzapine (16 hours:30 hours); Because of the low price of clozapine and the risk of high, fluvoxamine blocks 1A2 enzyme and increases the blood concentration of clozapine by 1-fold on average, and by as much as 5-10 times, the risk of combination is high. 10 times, the combination of risk, should be avoided, olanzapine expensive and low risk, fluvoxamine block 1A2 enzyme, increase olanzapine blood concentration 1/3, the combination of risk is small, save money, should be advocated. Second, risperidone than paliperidone (a) similarities 1, efficacy: paliperidone is the active metabolite of risperidone 9-hydroxy risperidone, and risperidone are potent blockade of the D2 receptor, the treatment of positive symptoms, and risperidone blockade of the 5-HT2A receptor, the treatment of schizophrenia, the negative symptoms, cognitive symptoms and depressive symptoms. 2, adverse reactions: risperidone and paliperidone both potently block D2 receptors, so extrapyramidal reactions and hyperprolactinemia are prominent. (B) differences 1, efficacy: paliperidone blocking D2 receptor effect is stronger than risperidone, so the anti-positive symptoms effect is better than risperidone; paliperidone blocking 5-HT2A receptor effect is weaker than risperidone, so the anti-negative symptoms effect is worse than risperidone. 2, adverse reactions: risperidone blocking α1 receptor effect is strong, susceptible to upright hypotension, need to be from 1mg/d gradual increment; paliperidone blocking α1 receptor effect is less than risperidone’s 1/3, the risk of upright hypotension is less, so from 6mg/d gradual increment. Paliperidone 40% of the hepatic 2D6 and 3A4 enzyme metabolism, and risperidone 100% of the hepatic 2D6 and 3A4 enzyme metabolism, so paliperidone caused by hepatic damage than risperidone for the light, and its blood concentration than risperidone is less affected by other drugs (eg, paroxetine inhibition of 2D6 and 3A4 enzymes). Third, Sulpiride than amisulpride (a) similarities 1, efficacy: amisulpride and sulpiride are benzamides, are selective D2 and D3 receptor blockers, the therapeutic range are 50 ~ 1200mg / d. Low dose (50 ~ 300mg / d) are selective blockade of high affinity D2 receptor on the presynaptic membrane, causing DA de-inhibitory release, agonizing the prefrontal cortex postsynaptic membrane D1 receptor, improve the effect of the prefrontal cortical D1 receptor on the presynaptic membrane, and improve the effect of the prefrontal cortex. D1 receptors on the prefrontal cortex postsynaptic membrane, improving negative symptoms, cognitive impairment, and depressive symptoms. Higher doses (400 mg/d or more) block low-affinity D2 receptors on the postsynaptic membrane and treat positive symptoms. Both do not block 5-HT2A receptors, but both exert atypical antipsychotic effects. 2, adverse reactions: amisulpride and sulpiride have poor ability to enter the blood-brain barrier, and their blood concentrations are high outside the blood-brain barrier (such as the pituitary) and low inside (such as the striatum), so hyperprolactinemia is severe and extrapyramidal reactions are mild, and they require a high dosage to be antipsychotic. Amisulpride and sulpiride at low doses increase DA energy and alertness, so it is advisable to take it in the morning and in the middle of the day, not in the middle of the day and in the evening, so as not to cause insomnia and bedtime neurogenic dysuria. (ii) Differences The potency of amisulpride in blocking D2/D3 receptors is 5-10 times that of sulpiride, which is theoretically more effective in treating positive symptoms; amisulpride potently blocks 5-HT7A receptors and is antidepressant, whereas sulpiride does not block 5-HT7A receptors, so the antidepressant effect of amisulpride is better than that of sulpiride; amisulpride’s quantity-performance relationship is clear, and sulpiride’s is ambiguous. Fourth, aripiprazole than Cariprazine (a) similarities Aripiprazole partially agonist D2 receptors, improve the negative symptoms, reduce severe extrapyramidal reactions or secondary negative symptoms; partially agonist D3 receptors, improve cognitive symptoms; aripiprazole partially agonist 5-HT1A and antagonist 5-HT2A receptors, increase DA energy, improve the negative symptoms and depressive symptoms. Cariprazine (Cariprazine) is similar to aripiprazole in that it partially agonizes D2/D3 receptors, moderately agonizes 5-HT1A receptors and mildly antagonizes 5-HT2A receptors, exerting effects similar to those of aripiprazole. (ii) Differences Aripiprazole has no anti-H1 receptor effect and therefore has no polyphagia, hypersomnia, or weight gain effect, whereas cariprazine has a low-to-moderate anti-H1 receptor effect, and its polyphagia, hypersomnia, and weight gain effects should be heavier than those of aripiprazole. The clearance half-life of aripiprazole is 3 days, the clearance half-life of cariprazine is 48 to 144 hours (2 to 6 days, recorded as 4 days), and the clearance half-life of its main active metabolites, desmethylcariprazine and 2-desmethylcariprazine, is as long as 2 to 3 weeks. After repeated treatment, the blood concentration of 2-desmethylcariprazine is 3 to 6 times higher than that of cariprazine, so that the duration of cariprazine’s action is much longer than that of aripiprazole. Suddenly stopping the drug adverse effects subside more slowly, withdrawal reaction is lighter. Aripiprazole than quetiapine (a) similar 1, efficacy: aripiprazole on the D2 receptor affinity is very strong, and even stronger than haloperidol, but it is only D2 receptor partial blocker, so the anti-positive symptoms effect is poor, quetiapine, although it is a D2 receptor complete blocker, but it is low affinity for D2 receptors, easy to fall off from the D2 receptor, quetiapine, there is also an anti-α1-receptor effect, but it is also weak, so the anti-positive symptoms effect is also poor. The effect of positive symptoms is also poor, these two drugs have become the two drugs with the worst effect of anti-positive symptoms among the existing atypical antipsychotics in China. 2, adverse reactions: aripiprazole is also a D2 receptor partial agonist, so it slightly reduces the prolactin blood concentration, quetiapine and clozapine block D2 receptor effect is very weak, almost no effect of elevating the prolactin blood concentration, these three drugs have become the most atypical antipsychotics in the country’s existing atypical antipsychotics without hyperprolactinemia of the three drugs. (ii) Differences 1, anti-negative symptoms and cognitive impairment: aripiprazole blocks 5-HT2A receptors, activates 5-HT1A receptors, and increases DA release, aripiprazole partially agonizes D2 and D3 receptors, and is anti-negative symptoms and cognitive impairment from 4 aspects, quetiapine blocks 5-HT2A receptors to increase DA release, blocks α2 receptors to cause norepinephrine (NE) release, and mildly blocks NE recycling while increasing NE conduction, and anti-negative symptoms and cognitive impairment in 3 ways. Aripiprazole has no anti-α1 and anti-H1 receptor effects, so it will not offset its anti-negative symptoms and cognitive impairment, while quetiapine has anti-α1 and anti-H1 receptor effects, which will offset its anti-negative symptoms and cognitive impairment, so the anti-negative symptoms and cognitive impairment effects of aripiprazole are stronger than quetiapine. 2.Antidepressant: Aripiprazole blocks 5-HT2A receptor and activates 5-HT1A receptor, anti-blocking depression, but aripiprazole has no anti-α1 receptor and anti-H1 receptor effect, it is not sedative, not applicable to anxiety depression, and only applicable to blocking depression. On the contrary, quetiapine is antidepressant by blocking 5-HT2A receptor, blocking α2 receptor and mildly blocking NE recycling. However, quetiapine has anti-α1 receptor and anti-H1 receptor effects and is sedative, so it is suitable for anxiety depression but not for blocked depression. 3, blocking the D2 receptor: aripiprazole partially blocking the D2 receptor, initially thought that no extrapyramidal reaction, and later practice has proved that aripiprazole cause sedation can not be about the same frequency as haloperidol, but caused by akinetic eye crisis rare, caused by the Parkinson’s disease is rare, so the aripiprazole starting amount of 5mg/early will be combined with Benzhexol 2mg/early, so as not to cause the inability to sit still. On the contrary, quetiapine and clozapine basically no extrapyramidal reaction, if it appears, it is an exception, so quetiapine that is used to 800mg/d, do not need to prophylactic use of Benzhexol. 4, three anti-effects: (1) anti-α1 receptor: quetiapine blocking α1 receptor is very weak, generally do not worry about causing upright hypotension, unless the patient is susceptible, and aripiprazole does not block the α1 receptor effect, do not worry about hypotensive effect. (2) anticholinergic receptors: quetiapine’s anticholinergic effect is not strong, but for those who have contraindications to anticholinergic drugs (such as angle-closure glaucoma, paralytic intestinal obstruction, or urinary retention) or to avoid the use of aripiprazole, and aripiprazole has no anticholinergic energy, the face of the contraindications to anticholinergic drugs, the choice of aripiprazole than quetiapine seems to be more appropriate, but then the problem is that aripiprazole easy to cause sitting still can’t be, and need to be coadministered with benedryl, which is an anti-choline agent. Benzhexol is an anticholinergic, again violating the contraindication. (3) anti-H1 receptor: aripiprazole does not block the H1 receptor, so there is no eat more, sleep more, weight gain effect, while quetiapine blocks the H1 receptor, eat more, sleep more, weight gain effect, the fear of fat patients, the choice of aripiprazole is more suitable, aripiprazole increases the DA energy, improves vigilance, tends to cause insomnia, it is appropriate to take early, in the middle of the day, quetiapine blocks the H1 receptor, reduces vigilance, tends to drowsiness, it is appropriate to take in the middle and evening. Quetiapine blocks H1 receptors, decreases alertness and tends to cause drowsiness. Dosage and duration of action: Aripiprazole has high affinity for D2 receptor, so the dosage is low (15-30mg/d), quetiapine has low affinity for D2 receptor, so the dosage is high (400-800mg/d). The half-life of aripiprazole is 3 days, so after stopping the drug need to wait for 1 week and then stop benzhexol (half-life of 12 hours), in order to prevent the residual aripiprazole again caused by sedation can not be, and quetiapine’s half-life is only 7 hours, so the sedative effect after stopping the drug is seldom more than 24 hours. Sixth, aripiprazole than ziprasidone (a) similar 1, efficacy: aripiprazole and ziprasidone treatment of positive symptoms are poor, aripiprazole because it is a D2 receptor partial blocker and poor, ziprasidone because it is a moderate blockade of NE recycling, enhancement of NE energy, agonist midbrain – limbic DA pathway, enhancement of the limbic system DA can be, partially offsetting the effect of the blockade of D2 receptors and poor. In comparison, ziprasidone has a slightly stronger anti-positive symptom effect than aripiprazole. 2, adverse reactions: aripiprazole and ziprasidone cause sedation can not effect are very strong, of which aripiprazole because of the high affinity for D2 receptors, while ziprasidone because of the blockade of D2 receptors completely. Since both aripiprazole and ziprasidone block H1 receptor effects are weak, there are no bulimia and weight gain effects, and the effects of aripiprazole and ziprasidone on hepatic damage are so small that they do not seem to be reported. (ii) Differences 1, cause alertness, some patients cause sleepiness, so aripiprazole should be taken early, in the middle of the service, ziprasidone should be taken in the morning, in the middle of the service, such as sleepiness, before changing to the middle of the service, the evening service. 2, anti-D2 receptor: aripiprazole did not see delayed dyskinesia (TD) report, because it is a D2 receptor partial blocker, while ziprasidone has been reported in several cases of TD, because it is a D2 receptor complete blocker. Aripiprazole is also a D2 receptor partial agonist and slightly decreases prolactin, and ziprasidone is a complete D2 receptor blocker and elevates prolactin. 3, anti-α1 and anticholinergic: Although the anti-α1 receptor and anticholinergic effects of aripiprazole and ziprasidone are of less concern, aripiprazole is absent, while ziprasidone is just weaker, so face to face with contraindications to anticholinergic (urinary retention, paralytic intestinal obstruction, closed-angle glaucoma) and hypotension, aripiprazole is more advantageous than ziprasidone. 4, QTc interval: ziprasidone blocks K+ efflux from cardiomyocytes, causing prolongation of the QTc interval, while aripiprazole has no such concerns. Clozapine also causes QTc interval prolongation, when clozapine need to combine with other antipsychotics, combined with ziprasidone is mutually reinforcing its QTc interval prolongation, combined with aripiprazole is no concern in this regard, so clozapine is usually used in combination with aripiprazole, but not with ziprasidone. 5, pharmacokinetics: aripiprazole half-life is 3 days, while the half-life of ziprasidone is only 6 hours, so aripiprazole discontinued, Benzhexol need to wait for another week before discontinuing, while ziprasidone discontinued, Benzhexol can be synchronized with the discontinuation. Aripiprazole is metabolized by 2D6 and 3A4 enzymes, and its blood concentration is greatly affected by paroxetine, while ziprasidone is metabolized only 1/3 by 3A4 enzymes, and its blood concentration is less affected by paroxetine. Seven, perospirone than risperidone (a) similarities 1, mechanism: perospirone and risperidone are dopamine D2 receptor and 5-HT2A receptor potent blocker. Both treat positive, negative, cognitive, and depressive symptoms of schizophrenia. 2, adverse reactions: perospirone and risperidone both block D2 receptors, both extrapyramidal reactions; both block 5-HT2A receptors, both partially elevated blood glucose; both have no anticholinergic effect, contraindications to anticholinergic (angle-closure glaucoma, paralytic bowel obstruction, urinary retention) can be used. 3, peak time: the peak time of perospirone and risperidone are 1 hour, are metabolized into hydroxylated active metabolites. (B) differences 1, positive symptoms: piperopilone blocking D2 receptor performance is stronger than risperidone, but the stability of the block is poorer than risperidone, so the anti-positive symptoms of piperopilone is not as effective as risperidone. The potency of perospirone is lower than that of risperidone, so the therapeutic dose is higher than that of risperidone (16-48mg/d: 2-6mg/d). 2, negative, cognitive and depressive symptoms: perospirone partially agonized 5-HT1A receptors, increasing dopamine release, further anti-negative, cognitive and depressive symptoms, while risperidone does not have this effect, so the anti-negative, cognitive and depressive symptoms of perospirone effect is stronger than that of risperidone. 3, extrapyramidal response: paropiron binding D2 receptor is transient, while risperidone binding D2 receptor is persistent; perospirone partially agonized 5-HT1A receptor, causing dopamine deinhibitory release, while risperidone does not have this effect. Therefore, the extrapyramidal reaction tendency of piperopilone is lighter than that of risperidone. 4, weight gain: although perospirone highly blocked H1 receptors, but part of the agonist 5-HT1A receptor, causing dopamine de-inhibitory release, offset the weight gain effect, so did not see the weight gain effect. Risperidone moderately blocked the H1 receptor effect, with a significant weight gain effect. 5, pharmacokinetics: the half-life of perospirone is only 2 hours, it is appropriate to take the drug three times a day; while the half-life of risperidone is 12 hours, only need to take the drug twice a day. Perospirone is mainly metabolized by 3A4 enzyme, risperidone is mainly metabolized by 2D6 enzyme. The active metabolite of perospirone, hydroxyperospirone, is primarily anti-5-HT2A receptor and is used to counteract negative, cognitive, and depressive symptoms, whereas the active sub-metabolite of risperidone, 9-hydroxyrisperidone, is primarily anti-D2 receptor and is used to counteract positive symptoms.