In stressed rats, escitalopram (10 mg/kg; intraperitoneal injection; administered daily for 28 days) lessens cognitive impairment and specifically reduces the build-up of phosphorylated tau protein [3]. Escitalopram at doses of 2.5 mg and 5 mg per day, when taken daily and for a total of 4 months, significantly decreased plaque burden by 28% and 34%, respectively [4].

Animal/Disease Models: Male SD (SD (Sprague-Dawley)) rat [3]
Doses: 10 mg/kg
Route of Administration: intraperitoneal (ip) injection; one time/day for 28 days.
Experimental Results: It can selectively reduce the accumulation of phosphorylated tau protein in the hippocampus of stressed rats. And it can Dramatically relieve depression and resist the overactivity of the HPA axis in rats.

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Animal/Disease Models: APP-PS1 hemizygous female mice (4 months old) [4]
Doses: 2.5-5 mg/kg
Route of Administration: daily; drinking water for a total of 4 months
Experimental Results: compared with littermates who only drank water Compared to mice, mice at both doses had Dramatically diminished plaque burden in their brains. ESC 2.5 mg/day and 5 mg/day Dramatically diminished hippocampal plaque burden by 28.7% and 34.4%, respectively.

Absorption, Distribution and Excretion
Following oral administration of escitalopram, absorption is expected to be almost complete, with an absolute bioavailability of approximately 80%. The time to peak concentration (Tmax) is approximately 4–5 hours. Peak plasma concentration (Cmax) and the area under the curve (AUC) over 24 hours appear to be dose-dependent—at steady state, patients taking 10 mg escitalopram daily have a Cmax of 21 ng/mL and a 24-hour AUC of approximately 360 ngh/mL; while patients taking 30 mg daily show approximately a 3-fold increase in both Cmax and 24-hour AUC. Approximately 8% of the total dose of escitalopram is excreted unchanged in the urine, and 10% is excreted as S-desmethylcitalopram. The apparent hepatic clearance of escitalopram is approximately 90% of the total dose.
Escitalopram appears to be widely distributed in tissues, with an apparent volume of distribution of approximately 12–26 L/kg.
The oral plasma clearance of escitalopram is 600 mL/min, of which approximately 7% is cleared by the kidneys.
/Breast Milk/ Escitalopram is excreted into human breast milk. Limited data suggest that in women taking 10–20 mg of escitalopram, the dose ingested by exclusively breastfed infants is approximately 3.9% of the mother's weight-adjusted dose, and the dose of desmethylcitalopram is approximately 1.7% of the mother's weight-adjusted dose.
The absolute bioavailability of escitalopram is approximately 80% of the intravenous dose, with a volume of distribution of approximately 12 L/kg. Specific data on escitalopram are currently unavailable. Escitalopram binds to human plasma proteins at a rate of approximately 56%.
Peak plasma concentrations occur approximately 5 hours after a single oral dose of escitalopram (20 mg tablets or solution). Food does not affect the absorption of escitalopram.

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Metabolism/Metabolites
Escitalopram is primarily metabolized in the liver, mainly mediated by CYP2C19 and CYP3A4, with CYP2D6 playing a minor role. The CYP enzyme system oxidatively N-demethylates citalopram to produce S-demethylcitalopram (S-DCT) and S-didemethylcitalopram (S-DDCT). These metabolites do not contribute to the pharmacological activity of escitalopram and are present in plasma at relatively low levels compared to the parent compound (28-31% and <5%, respectively). Further evidence suggests that escitalopram is metabolized in the brain by monoamine oxidases A and B to propionic acid metabolites, and these enzymes constitute the main metabolic pathway of escitalopram in the brain. The antidepressant escitalopram is primarily metabolized by the polymorphic CYP2C19 enzyme. This study investigated the impact of CYP2C19 genotype on escitalopram exposure and treatment failure in a large patient cohort study. The study retrospectively collected 4228 escitalopram serum concentration measurements from the drug surveillance database of 2087 patients who underwent CYP2C19 genotyping, all performed within 10–30 hours after medication administration. Patients were divided into two groups based on CYP2C19 genotype: those carrying the inactive (CYP2C19Null) and gain-of-function (CYP2C1917) variant alleles. A multivariate mixed model and chi-square test were used to assess differences between the two groups in escitalopram exposure (endpoint: dose-corrected serum concentration) and treatment failure rate (endpoint: switching to another antidepressant within one year of the last escitalopram measurement). Compared with the CYP2C191/1 group, the serum concentration of escitalopram was significantly increased by 3.3 times in the CYP2C19Null/Null group, significantly increased by 1.6 times in the CYP2C19Null/1 group, significantly decreased by 10% in the CYP2C19Null/17 group, and significantly decreased by 20% in the CYP2C1917/17 group. Compared with the CYP2C191/1 group, the CYP2C19Null/Null, CYP2C191/17, and CYP2C1917/17 groups were 3.3 times, 1.6 times, and 3.0 times more likely, respectively, to switch from escitalopram to other antidepressants within one year. The CYP2C19 genotype significantly influenced escitalopram exposure and treatment failure (measured by antidepressant switching). These results support the potential clinical value of CYP2C19 genotyping in personalized escitalopram therapy. Escitalopram is metabolized into S-demethylcitalopram (S-DCT) and S-didemethylcitalopram (S-DDCT). In humans, the predominant compound in plasma is unmetabolized escitalopram. At steady state, the plasma concentration of the escitalopram metabolite S-DCT is approximately one-third that of escitalopram. S-DDCT was undetectable in most subjects. In vitro studies have shown that escitalopram is at least 7-fold and 27-fold more potent than S-DCT and S-DDCT in inhibiting serotonin reuptake, respectively, suggesting that the metabolites of escitalopram contribute little to its antidepressant effect. S-DCT and S-DDCT have very low or no affinity for serotonergic receptors (5-HT1-7) or other receptors, including α- and β-adrenergic receptors, dopamine receptors (D1-5), histamine receptors (H1-3), muscarinic receptors (M1-5), and benzodiazepine receptors. S-DCT and S-DDCT also do not bind to various ion channels, including Na+, K+, Cl-, and Ca++ channels. In vitro human liver microsomal studies have shown that CYP3A4 and CYP2C19 are the main isoenzymes involved in escitalopram N-demethylation. This process mainly occurs in the liver. Escitalopram is N-demethylated to produce S-demethylcitalopram (S-DCT) and S-didemethylcitalopram (S-DDCT). CYP3A4 and CYP2C19 are the enzymes responsible for this N-demethylation reaction. Elimination pathway: After oral administration of escitalopram, approximately 8% of the drug is recovered in the urine as escitalopram and 10% as S-desmethylcitalopram (S-DCT). The oral clearance of escitalopram is 600 mL/min, of which approximately 7% is cleared by the kidneys. Escitalopram is metabolized to S-DCT and S-didesmethylcitalopram (S-DDCT). Half-life: 27-32 hours. The elimination half-life of escitalopram is 27-32 hours, but it is prolonged by approximately 50% in elderly patients and doubled in patients with impaired hepatic function. The elimination half-life of S-desmethylcitalopram, the major metabolite of escitalopram, is approximately 54 hours at steady state.
The biotransformation of escitalopram mainly occurs in the liver, with an average terminal half-life of approximately 27-32 hours.

Effects During Pregnancy and Lactation
◉ Overview of Use During Lactation
Escitalopram is the active S-isomer of the antidepressant citalopram. Limited information suggests that even with maternal daily intake of up to 20 mg of escitalopram, low concentrations in breast milk are not expected to have any adverse effects on breastfed infants, especially those older than 2 months. If a mother needs to take escitalopram, this is not a reason to discontinue breastfeeding. A safety rating system considers the use of escitalopram during lactation to be feasible. There has been a reported case of a mother taking escitalopram during pregnancy and lactation, resulting in necrotizing enterocolitis in her breastfed newborn, but a causal relationship has not been established. One infant experienced seizure-like events after exposure to bupropion in breast milk. In addition, there have been several other reports of minor behavioral problems. Closely monitor infants for lethargy, irritability, restlessness, feeding difficulties, and poor weight gain, especially younger exclusively breastfed infants and those using multiple psychotropic medications. Mothers taking selective serotonin reuptake inhibitors (SSRIs) (such as escitalopram) during pregnancy and postpartum may find breastfeeding more difficult, but this may reflect their medical condition. These mothers may require additional breastfeeding support. Infants exposed to SSRIs in late pregnancy have a lower risk of neonatal maladaptive disorder if breastfed compared to formula-fed infants. ◉ Impact on Breastfed Infants
A pediatrician assessed eight breastfed infants whose mothers were taking an average dose of escitalopram at 199 mcg/kg daily due to postpartum depression. The median postpartum escitalopram use for these mothers was 55 days (range 23 to 240 days). The infants scored 110% of the normal range on the scale.
A woman started taking escitalopram 5 mg daily immediately after delivery. Seven weeks postpartum, her dose was increased to 10 mg daily, and valproic acid was added to her regimen at 1200 mg daily. Her breastfed infant was assessed by a general practitioner at 7.5 weeks of age and was in good health with normal neuropsychological development.
A woman was taking escitalopram 20 mg and reboxetine 4 mg orally while breastfeeding (duration unspecified). She had been taking reboxetine for 1.5 months, but the start date of escitalopram was not specified. At 9.5 months of age, her breastfed infant had normal weight gain and a Denver Developmental Significance score of 105% of chronological age.
A breastfeeding mother started taking escitalopram 10 mg daily three weeks postpartum to treat depression, gradually increasing to 20 mg daily. At four months of age, her exclusively breastfed infant was hospitalized with irritability, vomiting, and fever for four days. According to the mother, the baby had been irritable and crying incessantly for the past three months, gaining only 400 grams per month since birth. Liver enzymes were moderately elevated. The baby was discharged after a five-day hospital stay and continued breastfeeding, but only twice a day for two weeks, then stopped at 4.5 months of age. Symptoms improved at 5 months, and serum liver enzymes returned to normal at 6 months. The authors noted that the timing of the adverse reactions coincided with the treatment with escitalopram. One mother started taking 20 mg of escitalopram every morning on day 15 postpartum. She exclusively breastfed her baby on demand. No adverse reactions were reported by the pediatrician when the baby was 3 months old. Five days after birth, the baby was readmitted to the neonatal intensive care unit due to necrotizing enterocolitis. The baby had been treated in the ICU for respiratory distress for the first two days after birth. The mother had taken 20 mg of escitalopram daily throughout pregnancy and lactation (specific medication details not specified). The authors speculate that escitalopram may have caused enterocolitis in the infant due to its effect on platelet aggregation. The drug may be the cause of the adverse reaction. One author reported a case of a newborn born to a mother taking escitalopram (dosage and duration not mentioned). This infant was extremely irritable, crying loudly every afternoon for two hours after breastfeeding, approximately 5 to 6 hours after the mother took escitalopram. Adjusting the timing of the mother's escitalopram administration changed the timing of the infant's crying, but the intervals between crying episodes remained the same as after the mother took the medication. The infant's symptoms improved after partially replacing breast milk with formula and completely disappeared after being exclusively formula-fed on day 11. A non-controlled online survey collected data from 930 breastfeeding mothers taking antidepressants. Approximately 10% of the infants reported discontinuation symptoms (e.g., irritability, hypothermia, uncontrollable crying, feeding and sleep disturbances). Mothers who take antidepressants only while breastfeeding are less likely to notice withdrawal symptoms in their infants than mothers who take the medication during both pregnancy and breastfeeding. A 6.5-month-old infant experienced severe vomiting and marked tonic-clonic seizures after breastfeeding. The mother had been taking 10 mg escitalopram daily since birth and had started taking 150 mg extended-release bupropion daily three weeks prior. The seizures occurred eight hours after the mother took bupropion in the morning. Previously, the mother had repeatedly noticed sleep-behavioral disturbances, abnormal movements, and unresponsive sleep in the infant. The infant was partially breastfed and also fed expressed breast milk, formula, and complementary foods. After breastfeeding was discontinued, the infant was discharged 48 hours later without symptoms. The seizures are likely drug-related, most likely caused by bupropion and hydroxybupropion in breast milk, but the influence of escitalopram cannot be ruled out. A study of 247 infants exposed to antidepressants in utero during late pregnancy evaluated neonatal maladaptive disorder (PNA). Of the 247 infants, 154 developed polyacrylamide (PNA). The risk of PNA was approximately three times higher in formula-fed infants than in exclusively breastfed or partially breastfed infants. None of the infants were exposed to escitalopram in utero, but 51 infants were exposed to citalopram (the racemic form of the drug). An Israeli case-control study compared infants born to 280 breastfeeding mothers on long-term use of psychotropic drugs with infants born to 152 mothers on antibiotics. Three mothers who took escitalopram during pregnancy and breastfeeding reported that their children developed drowsiness three days after birth, while none of the mothers on antibiotics reported drowsiness. The drowsiness subsided within 24 hours and did not affect development. A mother with mixed anxiety and depression was taking sertraline and breastfeeding her 9-month-old infant. Due to side effects, sertraline was discontinued, and citalopram was started at 10 mg daily. Two weeks after treatment, she reported that her baby had developed teeth grinding symptoms. The baby was breastfed 5 to 6 times a day and supplemented with fruits, vegetables, meat, and biscuits. The baby exhibited intermittent, pulsating, and brief movements of the lower jaw, usually beginning with head movements, especially during sleep. Additionally, the mother mentioned that her child had a habit of clenching and grinding their teeth when awake. Pediatric and dental examinations revealed no abnormalities, but the dentist observed the teeth grinding symptoms during an examination. The teeth grinding symptoms disappeared 72 hours after citalopram was discontinued. The mother resumed breastfeeding, and the symptoms did not recur; the baby did not experience teeth grinding symptoms for the next two years. The bruxism was most likely caused by citalopram in the breast milk.
◉ Effects on Lactation and Breast Milk
Selective serotonin reuptake inhibitors (SSRIs), including escitalopram, can cause elevated prolactin levels and galactorrhea in non-pregnant, non-lactating patients. Norprolactinemia-related galactorrhea has also been reported. For established lactating mothers, prolactin levels may not affect their breastfeeding ability. In a small prospective study, researchers compared eight primiparous women taking serotonin reuptake inhibitors (SRIs; three took fluoxetine, and the remaining one took citalopram, duloxetine, escitalopram, paroxetine, or sertraline, respectively) with 423 mothers not taking SRIs. The results showed that the onset of lactation activation (stage II) was delayed by an average of 16.7 hours in the SRI-treated group compared to the control group (85.8 hours postpartum vs. 69.1 hours postpartum), effectively doubling the risk of delayed breastfeeding in the untreated group. However, this delay in stage II lactation may not be clinically significant, as there was no statistically significant difference in the proportion of mothers experiencing feeding difficulties after day 4 postpartum between the two groups. A case-control study compared breastfeeding rates at two weeks postpartum. Participants included mothers who took selective serotonin reuptake inhibitors (SSRIs) throughout pregnancy and delivery (n = 167), mothers who took SSRIs only during pregnancy (n = 117), and a control group of mothers who did not take any antidepressants (n = 182). Among the mothers taking SSRIs, 33 took citalopram, 18 took escitalopram, 63 took fluoxetine, 2 took fluvoxamine, 78 took paroxetine, and 87 took sertraline. Breastfeeding rates at two weeks postpartum were 27% to 33% lower in women taking SSRIs than in those not taking antidepressants, but there was no statistically significant difference in breastfeeding rates between the SSRI exposure groups. An observational study investigated the outcomes of 2859 women who had taken antidepressants in the two years prior to pregnancy. Compared to women who did not take antidepressants during pregnancy, mothers who took antidepressants in all three stages of pregnancy were 37% less likely to breastfeed at discharge. Mothers who took antidepressants only in the third trimester were 75% less likely to breastfeed at discharge. Mothers who took antidepressants only in the first and second trimesters were not less likely to breastfeed at discharge. The specific antidepressants used by the mothers were not specified.
A retrospective cohort study analyzed hospital electronic medical records from 2001 to 2008, comparing women who took antidepressants in the third trimester (n = 575), women with mental illness but not taking antidepressants (n = 1552), and mothers who were not diagnosed with mental illness (n = 30,535). The results showed that women who took antidepressants were 37% less likely to breastfeed at discharge than women who were not diagnosed with mental illness, but there was no significant difference in the likelihood of breastfeeding compared to mothers with untreated mental illness. None of the mothers were taking escitalopram. A study of 80,882 Norwegian mother-infant pairs between 1999 and 2008 showed that 392 women reported starting antidepressants postpartum, and another 201 women reported starting antidepressants during pregnancy. Compared to a control group unexposed to antidepressants, antidepressant use in late pregnancy was associated with a 7% decrease in breastfeeding initiation rates, but had no effect on the duration of breastfeeding or exclusive breastfeeding rates. Compared to a control group unexposed to antidepressants, starting or restarting antidepressants postpartum was associated with a 63% decrease in primary breastfeeding rates at 6 months, a 51% decrease in any form of breastfeeding, and a 2.6-fold increased risk of abrupt cessation of breastfeeding. No specific antidepressant was mentioned.
Protein Binding
Escitalopram has a relatively low protein binding rate, approximately 55-56%.

[1]. Structure-activity relationships for a novel series of citalopram (1-(3-(dimethylamino)propyl)-1-(4-fluorophenyl)-1,3-dihydroisobenzofuran-5-carbon itrile) analogues at monoamine transporters. J Med Chem, 2010. 53(16): p. 6112-21.

[2]. Pastoor, D. and J. Gobburu, Clinical pharmacology review of escitalopram for the treatment of depression. Expert Opin Drug Metab Toxicol, 2014. 10(1): p. 121-8.

[3]. Escitalopram alleviates stress-induced Alzheimer's disease-like tau pathologies and cognitive deficits by reducing hypothalamic-pituitary-adrenal axis reactivity and insulin/GSK-3β signal pathway activity. Neurobiol Aging. 2018;67:137-147.

[4]. Effect of escitalopram on Aβ levels and plaque load in an Alzheimer mouse model. Neurology. 2020;95(19):e2666-e2674.

Escitalopram is a 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-onitrile with an S-configuration at its chiral center. It is the active enantiomer of citalopram. It is an antidepressant and an EC 3.4.21.26 (prolyl oligopeptidase) inhibitor. It is the conjugate base of escitalopram (1+) and the enantiomer of (R)-citalopram. Escitalopram is a selective serotonin reuptake inhibitor (SSRI) and is the S-enantiomer of racemic citalopram. It is used to treat depression and anxiety disorders to restore serotonergic function. Escitalopram is approximately 150 times more potent than the R-enantiomer of citalopram and is the primary source of its clinical activity. Some evidence suggests that the R-enantiomer of racemic citalopram does not merely exist as an inactive enantiomer, but actively inhibits the activity of escitalopram. Among selective serotonin reuptake inhibitors (SSRIs), escitalopram exhibits the highest selectivity for the serotonin transporter (SERT), and its incidence of adverse reactions is lower compared to other non-target drugs, which may explain its lower incidence of adverse reactions compared to other drugs in its class. Escitalopram also differs from other SSRIs in its allosteric effect on the target—this may be due to its superior efficacy and faster onset of action. Escitalopram is a serotonin reuptake inhibitor. Its mechanism of action is as a serotonin reuptake inhibitor. Escitalopram is the active S-stereoisomer of the selective serotonin reuptake inhibitor (SSRI) citalopram, and has antidepressant, anti-obsessive-compulsive, and anti-bulimia effects. Escitalopram inhibits the reuptake of the neurotransmitter serotonin (5-HT) by the serotonin reuptake pump on the presynaptic neuronal membrane, thereby increasing 5-HT levels in the synaptic cleft and enhancing the effect of serotonin on its 5-HT1A autoreceptor. Unlike other selective serotonin reuptake inhibitors (SSRIs), escitalopram appears to bind not only to a major high-affinity site on the serotonin transporter but also to a minor low-affinity allosteric site, which is thought to stabilize and prolong drug binding. Escitalopram is the S-enantiomer of citalopram and belongs to a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs). Despite significant structural differences among these compounds, SSRIs share similar pharmacological activities. As with other antidepressants, several weeks of treatment may be required to observe clinical efficacy. SSRIs are potent inhibitors of neuronal serotonin reuptake. They have little effect on the reuptake of norepinephrine or dopamine and do not antagonize α- or β-adrenergic receptors, dopamine D2 receptors, or histamine H1 receptors. In acute use, selective serotonin reuptake inhibitors (SSRIs) block serotonin reuptake and increase serotonin stimulation of somatic dendritic 5-HT1A receptors and terminal autoreceptors. Long-term use leads to desensitization of somatic dendritic 5-HT1A receptors and terminal autoreceptors. The overall clinical effect of improved mood and reduced anxiety is thought to be due to adaptive changes in neuronal function leading to enhanced serotonergic neurotransmission. Side effects include dry mouth, nausea, dizziness, drowsiness, sexual dysfunction, and headache. Side effects typically occur within the first two weeks of treatment and are generally milder and less common than those of tricyclic antidepressants. Escitalopram is used to treat major depressive disorder (MDD) and generalized anxiety disorder (GAD). Escitalopram is a furanyl nitrile compound, belonging to the class of selective serotonin reuptake inhibitors (SSRIs), and is used as an antidepressant. This drug is also effective in reducing ethanol intake in patients with alcohol dependence and is preferentially used to treat depression accompanied by tardive dyskinesia, rather than tricyclic antidepressants that may worsen tardive dyskinesia. Escitalopram (brand name: Cipralex) is a drug developed by the Danish pharmaceutical company Lundbeck and belongs to the class of selective serotonin reuptake inhibitors (SSRIs). It is commonly used as an antidepressant to treat depression associated with mood disorders, but can also be used to treat body dysmorphic disorder and anxiety disorders, including obsessive-compulsive disorder (OCD). In the United States, it is marketed by Forest Laboratories, Inc. under the name Lexapro. Escitalopram is a selective serotonin reuptake inhibitor (SSRI). It is commonly used as an antidepressant to treat depression associated with mood disorders, but can also be used to treat body dysmorphic disorder and anxiety disorders, including obsessive-compulsive disorder. Discontinuation of antidepressants, especially abrupt discontinuation, is known to cause certain withdrawal symptoms. One possible symptom of discontinuing escitalopram is spontaneous nerve throbbing, called paresthesia or "electric shock," which some patients describe as a mild electric shock and may be accompanied by dizziness. These throbbing episodes are very short, lasting only a few milliseconds, can affect any part of the body, and can occur several times per minute at all times of wakefulness. Physical activity can exacerbate these throbbing episodes, but they are not entirely related to muscle activity. Other withdrawal symptoms include extreme sensitivity to loud noises and bright lights, chills, hot flashes, night sweats, facial flushing, abdominal pain, weight gain, and extreme mental fatigue.
Citalopram is the S-enantiomer. It belongs to the class of selective serotonin reuptake inhibitors and is used to treat depression and generalized anxiety disorder.
See also: escitalopram oxalate (salt form); citalopram (note moved to). Drug Indications Escitalopram is indicated for the acute and maintenance treatment of major depressive disorder (MDD) in adults and children aged 12 years and older, and for the acute treatment of generalized anxiety disorder (GAD) in adults and children aged 7 years and older. Additionally, in Canada, it is approved for the relief of symptoms of obsessive-compulsive disorder (OCD). Mechanism of Action Like other selective serotonin reuptake inhibitors (SSRIs), escitalopram enhances serotonergic activity by binding to the ortho- (i.e., major) binding site on the serotonin transporter (SERT), which is also the binding site for endogenous serotonin (5-HT), thereby preventing the reuptake of serotonin by presynaptic neurons. Like paroxetine, escitalopram is also considered an allosteric serotonin reuptake inhibitor—it binds to a minor allosteric site on the SERT molecule, thus more effectively inhibiting 5-HT reuptake. Compared to other SSRIs, its combined ortho- and allosteric activity against SERT can increase extracellular 5-HT levels, resulting in faster onset and better efficacy. Sustained increases in synaptic cleft 5-HT levels eventually lead to desensitization to 5-HT_sub>1A autoreceptors, which typically inhibit the release of endogenous 5-HT in cases of 5-HT overdose—this desensitization may be necessary for SSRIs to achieve their full clinical efficacy, and may also explain their typically slower onset of action. Escitalopram has very low or no binding affinity for some other receptors (such as histamine and muscarinic receptors), and its mild activity against these non-target sites may explain some of its adverse reactions. Escitalopram is the S-enantiomer of racemic citalopram, and its antidepressant mechanism is thought to be related to enhanced serotonergic activity in the central nervous system (CNS), which is attributed to its inhibition of serotonin (5-HT) reuptake by CNS neurons.

C19H18FN2O

309.36

309.14

128196-01-0

Escitalopram oxalate;219861-08-2

146570

Colorless to light yellow ointment

1.2±0.1 g/cm3

428.3±45.0 °C at 760 mmHg

147-152C

212.8±28.7 °C

0.0±1.0 mmHg at 25°C

1.591

2.51

0

4

5

24

466

1

FC1=CC=C([C@@]2(CCCN(C)C)C(C=CC(C#N)=C3)=C3CO2)C=C1

WSEQXVZVJXJVFP-FQEVSTJZSA-N

InChI=1S/C20H21FN2O/c1-23(2)11-3-10-20(17-5-7-18(21)8-6-17)19-9-4-15(13-22)12-16(19)14-24-20/h4-9,12H,3,10-11,14H2,1-2H3/t20-/m0/s1

(1S)-1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-3H-2-benzofuran-5-carbonitrile

Seroplex Escitalopram

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 : ~100 mg/mL (~308.27 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (7.71 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 (7.71 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 (7.71 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.)