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 )

Quetiapine (<100 μM; 24 hours) has no significant effect on cell viability [2]. Quetiapine (10 μM) inhibits NO release, while LPS (0.1-100 ng/mL) concentration modulates [2]. Cell viability assay [2] Cell line: N9 microglia Concentration: 0, 0.1, 1, 10, 50 and 100 μM Incubation time: 24 hours Results: No significant effect on cells. viability at various concentrations below 100 μM, where significant toxicity was observed. RT-PCR[2] Cell line: N9 microglia Concentration: 10 μM Incubation time: 24 hours Results: Significantly inhibited TNF-α synthesis.

Quetiapine (10 mg/kg/day; approved) can attenuate the recruitment and activation of astrocytes and promote myelin repair in a cuprizone (CPZ)-induced chronic demyelination model [2]. Animal model: C57BL/ 6 mice [2] Dosage: 10 mg/kg/day Administration method: Ingestion Results: Compared with the Veh group, the optical density of myelin basic protein (MBP) staining increased significantly.

In vitro binding studies [1]
Binding assays were performed using membranes prepared by standard methods from cells stably expressing cloned human targets. Displacement binding was performed using either scintillation proximity assay (SPA) (NET/HEK293F cells and 5‐HT2C/CHO‐K1 cells) or filtration (5‐HT transporter [SERT]/HEK293 cells, dopamine transporter [DAT]/CHO‐S cells, D2S/CHO‐K1 cells, 5‐HT1A/CHO cells and 5‐HT2A/CHO cells) using tritiated radioligands (MeNER, mesulergine, MADAM [2‐(2‐dimethylaminomethyl‐phenylsulphanyl)‐5‐methyl‐phenylamine], WIN 35428, raclopride, WAY100635 and MDL100907 respectively). The majority of IC50 values were calculated with fitting model 205 in XLfit. 5‐HT2A and 5‐HT2C IC50 values were calculated using prism software by GraphPad. Mean apparent inhibition constant (K i) values were calculated using the Cheng–Prusoff equation from data derived from at least three independent experiments. In vitro assessment of affinity at glutamate receptors was performed on preparations of rat cerebral cortex tissue. Binding at NMDA receptors was evaluated with [3H]‐CGP39653 [3H]‐TCP and [3H]‐MDL 105,519 binding at kainite receptors was evaluated with [3H]‐kainic acid and binding at AMPA receptors was evaluated with [3H]‐AMPA according to standard validated protocols under conditions defined by the contractor. Compounds were evaluated in singlicate across eight concentrations (0.01, 0.1, 0.3, 1, 3, 10, 30 and 100 μM).

Cell Line: N9 microglial cells
Concentration: 0, 0.1, 1, 10, 50, and 100 μM
Incubation Time: 24 hours
Result: Had no significant effect on cell viabilities at various concentrations under 100 μM, in which significant toxicity could be observed.

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In vitro functional studies [1]
Uptake inhibition assays were performed using HEK293F cells stably expressing human NET, SERT and DAT. Cryopreserved cells were re‐suspended at 60K per well, centrifuged at 110 g for 1 min and incubated at 37°C for 3 h. Uptake inhibition was measured using the neurotransmitter transporter dye by a method slightly modified from that reported by Jorgensen et al. 2008. The most significant alteration to the method is that fluorescence intensity was evaluated on an Envision reader. Data were analysed by calculating the % effect with respect to total (0.5% DMSO final) and background signals. D2S pA2 was measured by the ability of a compound to inhibit the response to 3 μM dopamine (~EC80), using a GTPγS filtration binding assay similar to the method previously described by Lazareno (1999; Hudzik et al., 2008). 5‐HT1A agonist activity (potency and maximal concentration [Emax]) was determined with a GTPγS SPA binding assay using membranes derived from CHO cells stably expressing recombinant human 5‐HT1A receptors. Assay conditions are based on those previously reported (Jerning et al., 2002), though modified to an SPA format. An efficacy of 100% was defined as the maximal response to 5‐HT. 5‐HT2A and 5‐HT2C antagonist activity was measured with a FLIPR‐based method, as previously reported (Porter et al., 1999) using cell lines expressing 5‐HT2A and 5‐HT2C receptors. MTT Assay [2]
Cell viability was evaluated by the MTT reduction assay as described previously (Niu et al., 2010). The cells were seeded in a 96-well plate for 24 h before being exposed to Quetiapine alone (10 μm) orQuetiapine with LPS (100 ng/ml) for 24 h. MTT solution (0.5 mg/ml) was then added to each well and the cells were incubated for 1 h at 37°C and in 5% CO2. Subsequently, the supernatant was removed and the formation of farmazan was solubilized with DMSO and measured at 540 nm with SpectraMax M2e spectrophotomete. Nitrite Production Assessment [2]
Accumulation of nitrite (NO2−) in the culture media, an indicator of NO synthase activity, was measured by Griess Reaction. Cells at density of 3 × 104 cells/well were plated onto 96-well microtiter plates. Quetiapine with or without LPS (100 ng/ml) were added to the culture medium of N9 microglial cells for 48 h. Fifty microliters of culture supernatants were mixed with 50 μl Griess reagents (Part I: 1% sulfanilamide; Part II: 0.1% naphthylethylene diamide dihydrochlride and 2% phosphoric acid) at room temperature at 540 nm using the microplate reader. Nitrite concentration was calculated with reference to a standard curve of sodium nitrite.

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

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)