5-HT_1a Receptor ( pKi = 5.74 ); 5-HT_2A Receptor ( pKi = 7.54 ); 5-HT_2C Receptor ( pKi = 5.55 ); D2 Receptor ( pKi = 7.25 ); 5-HT_1A Receptor ( pKi = 4.77 ); D2 Receptor ( pKi = 6.33 )

喹硫平 (<100 μM；24 小时) 对细胞活力没有显着影响[2]。喹硫平 (10 μM) 抑制 NO 释放，而 LPS (0.1-100 ng/mL) 浓度调节[2]。细胞活力测定[2] 细胞系：N9小胶质细胞 浓度：0、0.1、1、10、50和100 μM 孵育时间：24小时 结果：对细胞无明显影响。 100 μM 以下的各种浓度下的活力，其中可以观察到显着的毒性。 RT-PCR[2] 细胞系：N9 小胶质细胞 浓度：10 μM 孵育时间：24 小时 结果：显着抑制 TNF-α 合成。

喹硫平 (10 mg/kg/天；认可)可以减弱铜宗 (CPZ) 感应的慢性脱髓鞘模型中小星细胞的募集和活化，促进髓鞘修复[2]。 动物模型: C57BL/ 6 只小鼠[2] 剂量：10 mg/kg/天 给药方式：摄入 结果：与 Veh 组相比，髓磷脂碱性蛋白 (MBP) 染色的光密度显着增加。

体外结合研究[1]
结合实验使用标准方法制备的膜进行，膜取自稳定表达克隆人类靶标的细胞。位移结合采用闪烁接近试验（SPA） （NET/HEK293F细胞和5‐HT2C/CHO‐K1细胞）或过滤（5‐HT转运体[SERT]/HEK293细胞，多巴胺转运体[DAT]/CHO‐S细胞，D2S/CHO‐K1细胞，5‐HT1A/CHO细胞和5‐HT2A/CHO细胞），使用tritriated放射配体（MeNER, mesulergine, MADAM[2‐（2‐二甲氨基甲基苯基磺胺）‐5‐甲基苯胺]，WIN 35428, raclopride， WAY100635和MDL100907）进行。大部分IC50值是用XLfit中的拟合模型205计算的。采用GraphPad prism软件计算5‐HT2A和5‐HT2C的IC50值。平均表观抑制常数（ki）值采用Cheng-Prusoff方程计算，数据来源于至少三个独立的实验。在大鼠大脑皮层组织中进行了谷氨酸受体体外亲和性评价。用[3H]‐CGP39653 [3H]‐TCP和[3H]‐MDL 105,519评估NMDA受体的结合，用[3H]‐kainic酸评估kainite受体的结合，用[3H]‐AMPA评估AMPA受体的结合，根据承包商定义的标准验证方案。化合物在8种浓度（0.01、0.1、0.3、1、3、10、30和100 μM）的单硅酸盐中被评估。

细胞系：N9 小胶质细胞
浓度：0、0.1、1、10、50 和 100 μM
孵育时间：24 小时
结果：100 μM 以下各浓度对细胞活力均无显着影响，其中可以观察到显着的毒性。

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体外功能研究[1]
使用稳定表达人NET、SERT和DAT的HEK293F细胞进行摄取抑制实验。冷冻保存的细胞在每孔60K下重新悬浮，在110 g下离心1分钟，在37°C下孵育3小时。使用神经递质转运蛋白染料测量摄取抑制，方法与Jorgensen等人2008年报道的方法略有改进。该方法最重要的变化是荧光强度在Envision阅读器上进行评估。通过计算相对于总（0.5% DMSO终）和背景信号的%效应来分析数据。D2S pA2通过抑制3 μM多巴胺（~EC80）的能力来测定，使用gtp - γ - s过滤结合实验，类似于Lazareno（1999）先前描述的方法；Hudzik et al., 2008)。5‐HT1A激动剂活性（效价和最大浓度[Emax]）通过gtp - γ - s SPA结合试验确定，使用的膜来自稳定表达重组人5‐HT1A受体的CHO细胞。测定条件以先前报告的条件为基础（Jerning et al., 2002），但修改为SPA格式。100%的疗效被定义为对5‐HT的最大反应。5‐HT2A和5‐HT2C拮抗剂活性采用基于FLIPR的方法测量，如先前报道（Porter et al., 1999）使用表达5‐HT2A和5‐HT2C受体的细胞系。

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MTT试验[2]
如前所述，通过MTT还原法评估细胞活力（Niu et al., 2010）。将细胞接种于96孔板中24 h，然后单独暴露于Quetiapine (10 μm)或Quetiapine/奎硫平与LPS (100 ng/ml) 24 h。然后在每个孔中加入MTT溶液（0.5 mg/ml），细胞在37°C和5% CO2中孵育1 h。随后，去除上清，用DMSO溶解法玛赞的形成，用SpectraMax M2e分光光度计在540 nm处测量。

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亚硝酸盐产量评价[2]
采用Griess反应法测定培养基中亚硝酸盐（NO2−）的积累量，作为NO合成酶活性的指标。将密度为3 × 104个/孔的细胞镀于96孔微滴板上。在N9小胶质细胞培养液中分别添加100 ng/ml或不添加100 ng/ml的Quetiapine/喹硫平，培养48 h。50微升培养上清与50 μl Griess试剂混合(第一部分：1%磺胺；第二部分：0.1%二氢萘二胺和2%磷酸)在室温下，在540 nm使用微孔板读取器。参照亚硝酸钠标准曲线计算亚硝酸盐浓度。

C57BL/6 mice
10 mg/kg/day
Ingested

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Once animals were trained to a stable baseline for three consecutive days, drug testing began. Norquetiapine (0.3, 1, 2, 5 and 10 mg·kg−1, n ≥ 6 per dose) was dissolved in saline and delivered s.c. at 1 mL·kg−1, 15 min before testing. Quetiapine (2.5, 5, 10 and 20 mg·kg−1, n ≥ 8 per dose) was formulated in distilled water plus lactic acid drops (pH > 2.5) to dissolution and delivered p.o. at 2 mL·kg−1, 60 min before testing. Diazepam in an Abbott's cocktail (10% ethanol, 40% propylene glycol and 50% water) stock solution of 5 mg·mL−1 was diluted to dosing volume (0.3, 1 and 3 mg·kg−1, n ≥ 3 per dose) with a 50% concentration of Abbott's cocktail and delivered 30 min before testing. In combination studies, WAY100635 was dissolved in saline and delivered at 0.1 mg·kg−1, s.c., alongside the test drug.[1]

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Elevated plus maze with rats from prenatally stressed dams [1]
The procedure used to evaluate elevated plus maze performance of rats from prenatally stressed dams is described in detail by Peters et al. (2011). In short, male Sprague–Dawley rats born in‐house to prenatally stressed dams were housed singly in an animal room with constant temperature and a 24 h light/dark cycle, on restricted food but with free access to water. On the test day, rats were placed in the centre of the maze facing an open arm, and behaviour was recorded for exactly 5 min. The % time spent in the open arms, the % entries into the open and closed arms and the total number of entries into the open and closed arms were recorded. The rats were dosed s.c. with either vehicle (saline), Quetiapine or norquetiapine (5 or 10 mg·kg−1 in saline and lactic acid to dissolve them, pH adjusted with sodium bicarbonate to pH > 5) 15 min before testing in the elevated plus maze. The effects of drug treatment in the elevated plus maze were assessed using a one‐way anova followed by Dunnett's multiple comparison. The effect of stress in the vehicle‐treated animals was assessed with a one‐tailed t‐test.

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C57BL/6 mice were randomly assigned to one of the following four groups: control (CTL), in which mice fed regular chow and drank distilled water for 12 weeks; CPZ, in which mice fed 0.2% CPZ for 12 weeks to induce a chronic demyelination (Matsushima and Morell, 2001); Veh, in which mice fed 0.2% CPZ for 12 weeks, then fed regular chow, and drank vehicle water for 2 weeks; Quetiapine, in which mice fed 0.2% CPZ for 12 weeks, and then fed regular chow, and drank Quetiapine-containing water for 2 weeks. [2]

Absorption, Distribution and Excretion
Quetiapine is rapidly and well absorbed after administration of an oral dose. Steady-state is achieved within 48 hours Peak plasma concentrations are achieved within 1.5 hours. The bioavailability of a tablet is 100%. The steady-state Cmax of quetiapine in Han Chinese patients with schizophrenia after a 300 mg oral dose of the extended released formulation was approximately 467 ng/mL and the AUC at steady-state was 5094 ng·h/mL. Absorption of quetiapine is affected by food, with Cmax increased by 25% and AUC increased by 15%.
After an oral dose of radiolabeled quetiapine, less than 1% of unchanged drug was detected in the urine, suggesting that quetiapine is heavily metabolized. About 73% of a dose was detected in the urine, and about 20% in the feces.
Quetiapine distributes throughout body tissues. The apparent volume of distribution of this drug is about 10±4 L/kg.
The clearance of quetiapine healthy volunteers in the fasted state during a clinical study was 101.04±39.11 L/h. Elderly patients may require lower doses of quetiapine, as clearance in these patients may be reduced by up to 50%. Those with liver dysfunction may also require lower doses.
Quetiapine fumarate is rapidly absorbed after oral administration, reaching peak plasma concentrations in 1.5 hours. The tablet formulation is 100% bioavailable relative to solution. The bioavailability of quetiapine is marginally affected by administration with food, with Cmax and AUC values increased by 25% and 15%, respectively.
Steady state concentrations are expected to be achieved within two days of dosing.
Quetiapine is widely distributed throughout the body with an apparent volume of distribution of 10 +/-4 L/kg. It is 83% bound to plasma proteins at therapeutic concentrations.
Hepatically impaired patients (n=8) had a 30% lower mean oral clearance of quetiapine than normal subjects. In two of the 8 hepatically impaired patients, AUC and C max were 3-times higher than those observed typically in healthy subjects. Since quetiapine is extensively metabolized by the liver, higher plasma levels are expected in the hepatically impaired population...
For more Absorption, Distribution and Excretion (Complete) data for QUETIAPINE (8 total), please visit the HSDB record page.

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Metabolism / Metabolites
The metabolism of quetiapine occurs mainly in the liver. Sulfoxidation and oxidation are the main metabolic pathways of this drug. According to in vitro studies, cytochrome P450 3A4 metabolizes quetiapine to an inactive sulfoxide metabolite and also participates in the metabolism of its active metabolite, N-desalkyl quetiapine. CYP2D6 also regulates the metabolism of quetiapine. In one study, three metabolites of N-desalkylquetiapine were identified. Two of the metabolites were identified as N-desalkylquetiapine sulfoxide and 7-hydroxy-N-desalkylquetiapine. CYP2D6 has been found to be responsible for metabolism of quetiapine to 7-hydroxy-N-desalkylquetiapine, a pharmacologically active metabolite. Individual differences in CYP2D6 metabolism may be present, which may affect the concentrations of the active metabolite.
Quetiapine is extensively metabolized in the liver principally via sulfoxidation and oxidation to inactive metabolites. In vitro studies suggest that the cytochrome P-450 (CYP) 3A4 isoenzyme is involved in the metabolism of quetiapine to the inactive sulfoxide metabolite, which is the principal metabolite. ... Based on in vitro studies, quetiapine and 9 of its metabolites do not appear likely to inhibit CYP isoenzymes 1A2, 3A4, 2C9, 2C19, or 2D6.
Quetiapine has known human metabolites that include 7-Hydroxy Quetiapine and Quetiapine Sulfoxide.
Hepatic. The major metabolic pathways are sulfoxidation, mediated by cytochrome P450 3A4 (CYP3A4), and oxidation of the terminal alcohol to a carboxylic acid. The major sulfoxide metabolite of quetiapine is inactive. Quetiapine also undergoes hydroxylation of the dibenzothiazepine ring, O-deakylation, N-dealkylation, and phase II conjugation. The 7-hydroxy and 7-hydroxy-
N-delakylated metabolites appear to be active, but are present in very low concentrations.
Route of Elimination: Elimination of quetiapine is mainly via hepatic metabolism. Following a single oral dose of 14C-quetiapine, less than 1% of the administered dose was excreted as unchanged drug, indicating that quetiapine is highly metabolized. Approximately 73% and 20% of the dose was recovered in the urine and feces, respectively.
Half Life: 6 hours

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Biological Half-Life
The average terminal half-life of quetiapine is about 6-7 hours.
The mean terminal half-life of quetiapine is about 6 hours.

Toxicity Summary
IDENTIFICATION AND USE: Quetiapine fumarate is used for the symptomatic management of psychotic disorders. Short-term efficacy of quetiapine for the management of schizophrenia has been established by placebo-controlled studies of 6 weeks' duration principally in hospitalized patients with schizophrenia. Quetiapine is used alone or in conjunction with lithium or divalproex sodium for the management of acute manic episodes associated with bipolar I disorder. Quetiapine also is used for the treatment of depressive episodes associated with bipolar disorder. HUMAN EXPOSURE AND TOXICITY: The most common adverse effects reported in 5% or more of patients receiving quetiapine therapy for schizophrenia or bipolar disorder and at a frequency twice that reported among patients receiving placebo in clinical trials include somnolence, sedation, asthenia, lethargy, dizziness, dry mouth, constipation, increased ALT, weight gain, dyspepsia, abdominal pain, postural hypotension, and pharyngitis. The development of cataracts in association with quetiapine was observed in animal studies. Lens changes also have been reported in some patients receiving long-term quetiapine therapy, although a causal relationship has not been established. Seizures occurred in 0.6% of patients receiving quetiapine in controlled clinical trials. Geriatric patients with dementia-related psychosis treated with atypical antipsychotic drugs appear to be at an increased risk of death compared with that among patients receiving placebo. Worsening of depression and/or the emergence of suicidal ideation and behavior (suicidality) or unusual changes in behavior may occur in both adult and pediatric patients with major depressive disorder and other psychiatric disorders, whether or not they are taking antidepressants. Neuroleptic malignant syndrome (NMS), a potentially fatal syndrome requiring immediate discontinuance of the drug and intensive symptomatic treatment, has been reported in patients receiving antipsychotic agents, including quetiapine. Contact dermatitis, maculopapular rash, and photosensitivity reactions were reported infrequently during clinical trials. Anaphylaxis and Stevens-Johnson syndrome have been reported during postmarketing surveillance. Quetiapine appears to be distributed into human milk in relatively small amounts. The effect of quetiapine on labor and delivery is unknown. Safety and efficacy of quetiapine in pediatric patients younger than 18 years of age with bipolar depression have not been established. Quetiapine overdose causes central nervous system depression and sinus tachycardia. In large overdoses, patients may require intubation and ventilation for associated respiratory depression. Although a prolonged QTc occurs, its clinical significance is unclear because it is most likely caused by an overcorrection caused by the tachycardia. No evidence of clastogenic potential was obtained in an in vitro chromosomal aberration assay in cultured human lymphocytes. ANIMAL STUDIES: Quetiapine caused a dose-related increase in pigment deposition in thyroid gland in a mouse 2 year carcinogenicity study. Doses were 75-750 mg/kg. The identity of the pigment could not be determined, but was found to be co-localized with quetiapine in thyroid gland follicular epithelial cells. The functional effects and the relevance of this finding to human risk are unknown. In dogs receiving quetiapine for 6 or 12 months, but not for 1 month, focal triangular cataracts occurred at the junction of posterior sutures in the outer cortex of the lens at a dose of 100 mg/kg. This finding may be due to inhibition of cholesterol biosynthesis by quetiapine. Quetiapine caused a dose related reduction in plasma cholesterol levels in repeat-dose dog and monkey studies; however, there was no correlation between plasma cholesterol and the presence of cataracts in individual dogs. The appearance of delta-8-cholestanol in plasma is consistent with inhibition of a late stage in cholesterol biosynthesis in these species. There also was a 25% reduction in cholesterol content of the outer cortex of the lens observed in a special study in quetiapine treated female dogs. The teratogenic potential of quetiapine was studied in rats and rabbits dosed during the period of organogenesis. No evidence of a teratogenic effect was detected in rats at doses of 25 to 200 mg/kg or in rabbits at 25 to 100 mg/kg. There was, however, evidence of embryo/fetal toxicity. Delays in skeletal ossification were detected in rat fetuses at doses of 50 and 200 mg/ kg and in rabbits at 50 and 100 mg/kg. Fetal body weight was reduced in rat fetuses at 200 mg/kg and rabbit fetuses at 100 mg/kg. There was an increased incidence of a minor soft tissue anomaly (carpal/tarsal flexure) in rabbit fetuses at a dose of 100 mg/kg. Evidence of maternal toxicity (i.e., decreases in body weight gain and/or death) was observed at the high dose in the rat study and at all doses in the rabbit study. In a peri/ postnatal reproductive study in rats, no drug-related effects were observed at doses of 1, 10, and 20 mg/kg. However, in a preliminary peri/postnatal study, there were increases in fetal and pup death, and decreases in mean litter weight at 150 mg/kg. The mutagenic potential of quetiapine was tested in six in vitro bacterial gene mutation assays and in an in vitro mammalian gene mutation assay in Chinese Hamster Ovary cells. However, sufficiently high concentrations of quetiapine may not have been used for all tester strains. Quetiapine did produce a reproducible increase in mutations in one Salmonella typhimurium tester strain in the presence of metabolic activation. No evidence of clastogenic potential was obtained in the in vivo micronucleus assay in rats.
The mechanism of action of quetiapine, as with other drugs used to treat schizophrenia, is unknown. However, it is thought that the drug's therapeutic activity in schizophrenia is mediated through a combination of dopamine type 2 (D2) and serotonin type 2 (5HT₂) receptor antagonism. Although quetiapine is known to bind other receptors with similar affinity, only the dopamine D2 and serotonin 5HT₂ receptor binding is responsible for quetiapine's therapeutic activity in schizophrenia.

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Interactions
Coadministration of quetiapine (250 mg) and phenytoin (100 mg) increased the mean oral clearance of quetiapine by 5-fold. Increased doses of quetiapine may be required to maintain control of symptoms of schizophrenia in patients receiving quetiapine and phenytoin, or other hepatic enzyme inducers (e.g., carbamazepine, barbiturates, rifampin, glucocorticoids). Caution should be taken if phenytoin is withdrawn and replaced with a non-inducer (e.g., valproate)
Coadministration of quetiapine (150 mg) and divalproex (500 mg) increased the mean maximum plasma concentration of quetiapine at steady state by 17% without affecting the extent of absorption or mean oral clearance.
Thioridazine (200 mg) increased the oral clearance of quetiapine (300 mg) by 65%.
Administration of multiple daily doses of cimetidine (400 mg) resulted in a 20% decrease in the mean oral clearance of quetiapine (150 mg).
For more Interactions (Complete) data for QUETIAPINE (10 total), please visit the HSDB record page.

[1]. Quetiapine and its metabolite norquetiapine: translation from in vitro pharmacology to in vivo efficacy in rodent models. Br J Pharmacol. 2016 Jan;173(1):155-66.

[2]. Quetiapine Inhibits Microglial Activation by Neutralizing Abnormal STIM1-Mediated Intercellular Calcium Homeostasis and Promotes Myelin Repair in a Cuprizone-Induced Mouse Model of Demyelination. Front Cell Neurosci. 2015 Dec 21;9:492.

Therapeutic Uses
Antipsychotic Agents
Quetiapine also is used for the treatment of depressive episodes associated with bipolar disorder.
Quetiapine is used alone or in conjunction with lithium or divalproex sodium for the management of acute manic episodes associated with bipolar I disorder.
Short-term efficacy of quetiapine for the management of schizophrenia has been established by placebo-controlled studies of 6 weeks' duration principally in hospitalized patients with schizophrenia.
Quetiapine fumarate is used for the symptomatic management of psychotic disorders (e.g., schizophrenia).

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Drug Warnings
/BOXED WARNING/ WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITH DEMENTIA- RELATED PSYCHOSIS; and SUICIDAL THOUGHTS AND BEHAVIORS: Increased Mortality in Elderly Patients with Dementia-Related Psychosis: Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. Quetiapine is not approved for the treatment of patients with dementia-related psychosis. Suicidal Thoughts and Behaviors: Antidepressants increased the risk of suicidal thoughts and behavior in children, adolescents, and young adults in short-term studies. These studies did not show an increase in the risk of suicidal thoughts and behavior with antidepressant use in patients over age 24; there was a reduction in risk with antidepressant use in patients aged 65 and older. In patients of all ages who are started on antidepressant therapy, monitor closely for worsening, and for emergence of suicidal thoughts and behaviors. Advise families and caregivers of the need for close observation and communication with the prescriber. Quetiapine is not approved for use in pediatric patients under ten years of age.
Geriatric patients with dementia-related psychosis treated with atypical antipsychotic drugs appear to be at an increased risk of death compared with that among patients receiving placebo. Analyses of 17 placebo-controlled trials (average duration of 10 weeks) revealed an approximate 1.6- to 1.7-fold increase in mortality among geriatric patients receiving atypical antipsychotic drugs (i.e., quetiapine, aripiprazole, olanzapine, risperidone) compared with that in patients receiving placebo. Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5% compared with a rate of about 2.6% in the placebo group. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. The manufacturer states that quetiapine is not approved for the treatment of dementia-related psychosis.
Antidepressants increased the risk of suicidal thinking and behavior (suicidality) in short-term studies in children and adolescents with major depressive disorder (MDD) and other psychiatric disorders. Anyone considering the use of quetiapine or any other antidepressant in a child or adolescent must balance this risk with the clinical need. Patients who are started on therapy should be observed closely for clinical worsening, suicidality, or unusual changes in behavior. Families and caregivers should be advised of the need for close observation and communication with the prescriber. Quetiapine is not approved for use in pediatric patients.
Pooled analyses of short-term (4 to 16 weeks) placebo- controlled trials of 9 antidepressant drugs (SSRIs and others) in children and adolescents with major depressive disorder (MDD), obsessive compulsive disorder (OCD), or other psychiatric disorders (a total of 24 trials involving over 4400 patients) have revealed a greater risk of adverse events representing suicidal thinking or behavior (suicidality) during the first few months of treatment in those receiving antidepressants. The average risk of such events in patients receiving antidepressants was 4%, twice the placebo risk of 2%.
For more Drug Warnings (Complete) data for QUETIAPINE (31 total), please visit the HSDB record page.

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Pharmacodynamics
Quetiapine improves the positive and negative symptoms of schizophrenia and major depression by acting on various neurotransmitter receptors, such as the serotonin and dopamine receptors. In bipolar disorder, it improves both depressive and manic symptoms. **A note on suicidality in young patients and administration in the elderly** Quetiapine can cause suicidal thinking or behavior in children and adolescents and should not be given to children under 10 years of age. It is important to monitor for suicidality if this drug is given to younger patients. In addition, this drug is not indicated for the treatment of psychosis related to dementia due to an increased death rate in elderly patients taking this drug.

C21H25N3O2S

383.51

383.166

C, 65.77; H, 6.57; N, 10.96; O, 8.34; S, 8.36

111974-69-7

Quetiapine hemifumarate; 111974-72-2; Quetiapine sulfoxide dihydrochloride;329218-11-3; Quetiapine-d4 fumarate; 1287376-15-1; Quetiapine sulfoxide; 329216-63-9; 918505-61-0 (analog); Quetiapine; 111974-69-7; Quetiapine-d4 hemifumarate; 1217310-65-0; Quetiapine-d8 fumarate; 1185247-12-4; Quetiapine-d8 hemifumarate; Quetiapine hemifumarate-d8; 1435938-24-1

5002

Light yellow to yellow oil

1.3±0.1 g/cm3

556.5±60.0 °C at 760 mmHg

172 - 174ºC

290.4±32.9 °C

0.0±1.6 mmHg at 25°C

1.653

1.57

73.6

1

5

6

27

496

0

OCCOCCN(CC1)CCN1C2=NC3=CC=CC=C3SC4=C2C=CC=C4

URKOMYMAXPYINW-UHFFFAOYSA-N

InChI=1S/C21H25N3O2S/c25-14-16-26-15-13-23-9-11-24(12-10-23)21-17-5-1-3-7-19(17)27-20-8-4-2-6-18(20)22-21/h1-8,25H,9-16H2

2-[2-(4-benzo[b][1,4]benzothiazepin-6-ylpiperazin-1-yl)ethoxy]ethanol

ICI 204636; ICI-204636; ICI 204,636; 111974-69-7; Seroquel; Quetiapine fumarate; Norsic; Co-Quetiapine; quetiapina; quetiapinum; ICI204636; Quetiapine; quetiapine fumarate; brand name: Seroquel

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 77~100 mg/mL (200.8~260.8 mM)
Ethanol: ~100 mg/mL (~260.8 mM)
H2O: ~0.1 mg/mL (~0.3 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (6.52 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (6.52 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (6.52 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。