5-HT ( Ki = 13 nM )
Rat brain serotonin transporter (SERT) (Ki: 0.8 nM, IC50: 1.2 nM for [³H]5-HT uptake inhibition); no significant binding to norepinephrine transporter (NET, Ki > 100 nM) or dopamine transporter (DAT, Ki > 200 nM); weak binding to 5-HT2 receptors (Ki > 50 nM) and histamine H1 receptors (Ki > 100 nM) [1]
- Human platelet SERT (IC50: 0.9 nM for [³H]5-HT uptake inhibition); no significant binding to rat brain 5-HT1A receptors (Ki > 100 nM) or muscarinic M1 receptors (Ki > 200 nM) [2]

In vitro activity: Sertraline demonstrates superior selectivity in blocking 5-HT uptake in comparison to NE uptake when compared to fluvoxamine, zimelidine, norzimelidine, fluoxetine, or chlorimipramine. Nevertheless, in comparison to these agents, sertraline is less selective in preventing 5-HT uptake than DA uptake.[1]

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Rat brain synaptosomal 5-HT uptake inhibition [1]:
- Sertraline HCl (0.1–10 nM) dose-dependently inhibited [³H]5-HT uptake, with an IC50 of 1.2 nM; maximum inhibition (>95%) was achieved at 10 nM. It had minimal effect on [³H]norepinephrine uptake (IC50 > 100 nM) and no effect on [³H]dopamine uptake (<5% inhibition at 100 nM) [1]
- Rat brain membrane SERT binding [1]:
- Sertraline HCl competitively displaced the SERT ligand [³H]imipramine from rat cortical membranes with a Ki of 0.8 nM. It showed <10% displacement of [³H]ketanserin (a 5-HT2 ligand) even at 100 nM [1]
- Human platelet SERT uptake inhibition [2]:
- Sertraline HCl (0.05–5 nM) inhibited [³H]5-HT uptake in human platelet suspensions, with an IC50 of 0.9 nM; 5 nM induced >90% inhibition. It had no significant binding to human platelet α2-adrenergic receptors (<5% binding at 100 nM) [2]
- Rat cortical 5-HT1A receptor binding [2]:
- Sertraline HCl (0.1–1000 nM) showed no significant binding to rat cortical 5-HT1A receptors labeled with [³H]8-OH-DPAT (Ki > 100 nM) and no agonist/antagonist activity on this subtype [2]

Sertraline HCl (32μmol/kg i.p.) reduces serotonin uptake by more than 50% in rat striatal synaptosomes. When it comes to reversing the 5-HT depletion induced by PCA, sertraline HCl is 60 times more potent than amitriptyline and 6 times more potent than chlorimipramine. Whole blood's serotonin content dropped after receiving repeated acute doses of sertraline. When antidepressant mice are used in the Porsolt swim test, sertraline HCl significantly decreases their immobility. Sertraline HCl reduces the binding of [3H]dihydroalprenolol to cortical membranes and the cyclic AMP response of limbic forebrain adenylate cyclase to norepinephrine in rats after repeated dosing.[1]

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Antidepressant activity in mouse models [1]:
- Forced Swim Test (FST): Intraperitoneal (i.p.) administration of Sertraline HCl at 5 mg/kg and 10 mg/kg reduced immobility time by ~30% and ~50%, respectively, compared to vehicle control. The 10 mg/kg dose had no effect on locomotor activity (open field test, total distance traveled unchanged vs. vehicle) [1]
- Rat brain 5-HT metabolism modulation [1]:
- Oral administration of Sertraline HCl (10 mg/kg) increased cortical 5-HT concentration by ~40% and decreased 5-hydroxyindoleacetic acid (5-HIAA, a 5-HT metabolite) concentration by ~25% at 2 hours post-dosing (measured via HPLC) [1]
- Antagonism of 5-HTP-induced behavior in rats [2]:
- I.p. Sertraline HCl at 2 mg/kg and 5 mg/kg antagonized 5-hydroxytryptophan (5-HTP, 100 mg/kg i.p.)-induced head-twitching behavior by ~40% and ~70%, respectively, over a 30-minute observation period [2]
- Locomotor activity in rats [2]:
- I.p. Sertraline HCl (1–20 mg/kg) had no significant effect on spontaneous locomotor activity (activity counts changed <10% vs. vehicle) [2]

Rat brain membrane SERT binding assay [1]:
- Rat cortical membranes were prepared by homogenization in ice-cold 50 mM Tris-HCl buffer (pH 7.4, containing 120 mM NaCl and 5 mM KCl) and centrifugation (12,000×g for 20 minutes). The membrane pellet was resuspended in the same buffer. Membranes were mixed with [³H]imipramine (final concentration: 1 nM) and Sertraline HCl (0.01–100 nM) and incubated at 25°C for 90 minutes. Bound ligand was separated from free ligand by filtration through glass fiber filters pre-soaked in 0.5% polyethyleneimine (PEI). Filters were washed 3 times with ice-cold buffer, and radioactivity was measured via liquid scintillation counting. Ki values were calculated using the Cheng-Prusoff equation [1]
- Human platelet SERT uptake assay [2]:
- Human platelet suspensions (1×10⁸ cells/mL) were prepared from fresh blood. Sertraline HCl (0.05–50 nM) was added to the suspensions and pre-incubated for 10 minutes at 37°C. [³H]5-HT (final concentration: 2 nM) was then added, and incubation continued for 5 minutes. The reaction was terminated by centrifugation (3,000×g for 5 minutes), and the platelet pellet was lysed. Radioactivity in the lysate was measured via liquid scintillation counting to determine [³H]5-HT uptake. IC50 values were derived from dose-response curves [2]

Cell-based assays for sertraline are primarily conducted using human neuroblastoma SH-SY5Y cells and primary mouse cortical neurons . For the oxygen-glucose deprivation model, primary cortical neurons from C57BL/6J mouse embryos (E14-E17) are cultured in neurobasal medium with B27 supplement. OGD injury is induced by washing cells with glucose-free buffer and incubating in glucose-free, serum-free DMEM under 95% N₂/5% CO₂ at 37°C for 2 hours, followed by 24 hours reoxygenation with sertraline treatment . The antimicrobial activity test for sertraline uses spot inoculation, broth, and agar dilution methods with 161 clinical isolates of Gram-negative and Gram-positive bacteria, as well as Candida species, to determine minimum inhibitory concentrations .

Aromatase-knockout (Ar −/− ) mice
10 mg/kg
A single i.p. administration

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Mouse Forced Swim Test (FST) and open field test [1]:
- Male ICR mice (20–25 g) were randomly divided into 3 groups (n=8/group): vehicle (0.5% methylcellulose, i.p.), Sertraline HCl 5 mg/kg (i.p.), Sertraline HCl 10 mg/kg (i.p.). Sertraline HCl was dissolved in the vehicle. Thirty minutes post-dosing, mice were placed in a cylindrical tank (25 cm diameter) filled with 25°C water (15 cm depth) for 6 minutes, and immobility time was recorded during the last 4 minutes. For the open field test, the same mice were placed in a 30×30 cm arena 1 hour post-dosing, and total distance traveled was recorded for 30 minutes via video tracking [1]
- Rat 5-HTP-induced head-twitching assay [2]:
- Male Wistar rats (220–250 g) were divided into 3 groups (n=6/group): vehicle (saline, i.p.), Sertraline HCl 2 mg/kg (i.p.), Sertraline HCl 5 mg/kg (i.p.). Sertraline HCl was dissolved in saline. Twenty minutes post-dosing, rats received an i.p. injection of 5-HTP (100 mg/kg). Rats were placed in individual cages, and the number of head-twitch responses was counted for 30 minutes [2]
- Rat brain neurotransmitter measurement [1]:
- Male Sprague-Dawley rats (250–300 g) were divided into 2 groups (n=6/group): vehicle (0.5% methylcellulose, oral), Sertraline HCl 10 mg/kg (oral). Two hours post-dosing, rats were euthanized, and cortical tissue was dissected. Tissue was homogenized in 0.1 M perchloric acid, centrifuged (15,000×g for 15 minutes), and the supernatant was analyzed via HPLC to measure 5-HT and 5-HIAA concentrations [1]

Rat pharmacokinetics[1]: - Oral administration (10 mg/kg): peak plasma concentration (Cmax) = 45 ng/mL, time to peak concentration (Tmax) = 1.5 h, elimination half-life (t1/2) = 4.2 h, oral bioavailability (F) = 65%[1] - Intravenous administration (2 mg/kg): t1/2 = 3.8 h, clearance (CL) = 18 mL/min/kg, volume of distribution (Vd) = 5.1 L/kg[1] - Human plasma protein binding[2]: - Sertraline hydrochloride has a plasma protein binding rate of 98% in human plasma (determined by equilibrium dialysis) in the concentration range of 10–1000 ng/mL; binding is concentration-independent[2] - Rat excretion and metabolism[2]: - After rats were orally administered ¹⁴C-labeled sertraline hydrochloride (10 mg/kg), approximately 40% of the radioactive material was excreted in the urine (as a metabolite) within 24 hours, and approximately 55% was excreted in the feces (as a metabolite). Unmetabolized sertraline hydrochloride accounted for <5% of the total excretion [2]

Effects During Pregnancy and Lactation
◉ Overview of Medication Use During Lactation
Because sertraline is present in low concentrations in breast milk, the amount ingested by the infant is very small and usually undetectable in the infant's serum. However, its less active metabolite, norsertraline (desmethylsertraline), is often detectable at low concentrations in the infant's serum. In rare cases, premature infants with impaired metabolism may accumulate the drug and experience symptoms similar to neonatal withdrawal. Most authoritative reviewers consider sertraline to be the first-line antidepressant during lactation.
Mothers who take selective serotonin reuptake inhibitors (SSRIs) during pregnancy and postpartum may find breastfeeding more difficult, but this may reflect their medical condition. These mothers may require additional breastfeeding support. Breastfed infants exposed to SSRIs in late pregnancy have a lower risk of neonatal maladaptive disorder than formula-fed infants.
◉ Effects on Breastfed Infants
A 4-month-old infant presented with benign neonatal sleep myoclonus and restlessness, which resolved spontaneously; the mother was taking 75 mg of sertraline daily.
26 infants with a mean age of 16.6 weeks (range 4 to 28 weeks), whose mothers were taking an average of 124 mg of sertraline daily, showed no sertraline-related acute adverse reactions detected in the breast milk of any of the infants. All infants had been breastfed for at least 3 weeks.
Whole blood serotonin levels were measured in 14 mothers and their breastfed infants after 6 to 16 weeks of sertraline treatment. The mothers' daily dose ranged from 25 to 200 mg. Although sertraline treatment reduced maternal serotonin levels from 159 μg/L to 19 μg/L, infants' serotonin levels were 227 μg/L before treatment and 224 μg/L after treatment. The authors concluded that these results indicate that the dose of sertraline ingested by infants is insufficient to affect platelet uptake of serotonin in breastfed infants. Since platelets and neurons share the same serotonin transporter, this lack of effect is considered indirect evidence of the safety of sertraline use during breastfeeding. No adverse reactions to sertraline in breast milk were observed in any of the infants, including six exclusively breastfed infants under 3 months of age. The 25 mothers received an average daily dose of 82.4 mg of sertraline, exclusively breastfed their infants for 4 months, and breastfed at least 50% of their infants in the 5th and 6th months. These infants' weight gain at 6 months met national growth standards, and the mothers did not report any adverse reactions in their infants. In six infants aged 5 to 34 weeks, whose mothers received 50 to 100 mg of sertraline daily, no clinical adverse reactions were observed during the study. In seven infants aged 4 weeks, whose mothers received 50 mg of sertraline daily from day 4 postpartum, no adverse reactions were also observed.
A study on the side effects of selective serotonin reuptake inhibitors (SSRIs) in breastfeeding mothers found that none of the breastfeeding mothers experienced adverse reactions requiring medical attention. Two infants were born to mothers taking sertraline. Specific information regarding the mothers' sertraline dosage, breastfeeding frequency, or infant age was not reported in the study.
A small study compared pain responses in infants born to mothers with depression who took SSRIs alone during pregnancy or both during pregnancy and breastfeeding with those born to non-depressed mothers who had not been exposed to SSRIs. Infants who were exposed to SSRIs alone during pregnancy or through breast milk during pregnancy and postpartum showed a dulled pain response compared to the control group. Four out of 30 infants were exposed to sertraline. Because the control group consisted of mothers without depression but not taking the medication, the influence of maternal behavior due to depression could not be ruled out. The authors emphasize that these findings do not imply that medication for depression should be avoided during pregnancy or that breastfeeding should be avoided during SSRI treatment.
A non-controlled online survey collected data from 930 mothers who were taking antidepressants and breastfeeding. Approximately 10% of infants reported discontinuation symptoms (e.g., irritability, hypothermia, uncontrollable crying, eating and sleeping disturbances). Infants of mothers who took antidepressants only while breastfeeding were far less likely to experience discontinuation symptoms than those of mothers who took the medication during both pregnancy and breastfeeding. In a telephone follow-up study, 124 mothers who took benzodiazepines while breastfeeding reported any signs of sedation in their infants. One mother, taking 50 mg of sertraline daily, 2.5 mg of zopiclone approximately every 3 days as needed, and twice taking 0.25 mg of alprazolam, reported sedation in her breastfed infant. Another mother, who took 150 mg of sertraline daily during pregnancy, labor, and postpartum, and exclusively breastfed her infant, had a premature infant born by cesarean section at 33 weeks of gestation who developed high fever, dystonia, and high-pitched crying within 24 hours of birth. Symptoms worsened on day 4, but breastfeeding continued. On day 5, the infant's serum concentrations of sertraline and its metabolites reached adult therapeutic ranges. Breastfeeding was discontinued on day 9 postpartum, the infant's symptoms subsided, serum drug concentrations decreased, and the infant grew healthily over the following months. It was later discovered that the infant possessed a genetic intermediate capacity for metabolizing two CYP450 enzymes involved in sertraline metabolism. The authors believe that the infant's symptoms were due to persistently elevated sertraline levels caused by breastfeeding and excessive serotonergic stimulation resulting from slowed metabolism. This response may be sertraline-induced.
One mother started taking sertraline (50 mg daily) and methylphenidate 5 weeks postpartum and continued breastfeeding (the extent of breastfeeding was not specified). The initial dose was 10 mg daily in an immediate-release formulation, gradually increased to 72 mg daily in a sustained-release formulation. The infant was developing normally at 14 weeks of age with no feeding difficulties. No developmental problems were found at 6 months and 1 year of age.
In a study of sertraline for postpartum depression, 11 out of 36 participants completed the full 7-week study. Six mothers reported breastfeeding (the extent of breastfeeding was not specified), and five mothers did not breastfeed. The mean dose of sertraline at week 7 was 100 mg daily. Currently, no side effects have been reported in any infants in either the sertraline or placebo groups. A meta-analysis of sertraline reported that 25 infants were breastfed by mothers taking sertraline. Of these, 10 were exclusively breastfed, 2 were 80% breastfed, and the breastfeeding status of the remaining infants was not reported. No adverse reactions occurred. A cohort study of 247 infants exposed to antidepressants in utero during late pregnancy assessed the incidence of neonatal maladaptive disorder (PNA). Of these 247 infants, 154 experienced PNA. The risk of PNA was approximately three times higher in formula-fed infants than in exclusively or partially breastfed infants. 68 infants were exposed to sertraline in utero. A retrospective study included 30 breastfeeding mothers who visited a psychiatric outpatient clinic, were followed up for at least 8 weeks, and were taking sertraline. Five infants (13%) experienced adverse reactions. One mother took 25 mg daily, three took 50 mg daily, and one took 100 mg daily. The most common adverse reactions in infants were insomnia and irritability; persistent crying and feeding difficulties were less common. All adverse reactions occurred within the first two weeks after the mother started medication and disappeared within 3 days after discontinuation. One infant's adverse reaction persisted even after the mother reduced the dose from 50 mg daily to 25 mg daily. The incidence of adverse reactions was not different in these infants compared to infants whose mothers in the same study were taking paroxetine. A 12-day-old exclusively breastfed male infant experienced severe weight loss and hypernatremic dehydration due to insufficient milk intake, resulting in a 30% weight loss since birth. The infant's mother was receiving treatment for bipolar disorder, taking lamotrigine 250 mg once daily, aripiprazole 15 mg once daily, and sertraline 100 mg once daily. She was also taking levothyroxine 50 mcg once daily, as well as prenatal multivitamins and folic acid. At initial assessment in the emergency department, the infant was pale, with marbled skin, dry mucous membranes, decreased skin elasticity, and cyanotic feet with prolonged capillary refill time. The patient's right foot gradually darkened, the toes turned black, and gangrene developed in the right lower extremity. Drug treatment was ineffective, ultimately requiring amputation of all five toes and metatarsal debridement. The necrosis was thought to be due to arterial microthrombosis caused by disseminated intravascular coagulation following severe dehydration. The authors believe that the mother's medications may have contributed to the dehydration and related problems. A mother of a two-month-old exclusively breastfed infant began taking sertraline 50 mg daily for the treatment of depression. Six days later, the infant developed irritability and a sharp decrease in sleep duration. Symptoms completely disappeared within three days after sertraline was discontinued. Physical examination and laboratory tests revealed no abnormalities. The infant subsequently developed severe constipation due to the mother's paroxetine use but tolerated citalopram well. A mother three months postpartum was treated for depression, taking 50 mg of sertraline in the morning and 1.25 mg of olanzapine in the evening for sleep. Two weeks later, the sertraline dose was increased to 25 mg in the morning and 50 mg in the evening. Five days after the dose increase, her breastfed infant began experiencing diarrhea approximately 15 minutes after each feeding. She continued taking sertraline and gave the infant oral rehydration salts. The diarrhea resolved after two weeks. The diarrhea was likely due to sertraline in the breast milk. Nine women took 25 to 75 mg of sertraline daily during late pregnancy and lactation (seven of whom took 50 mg daily). Pediatric evaluations, including neurological assessments and brain ultrasound, were performed within 24 hours postpartum. Further follow-up was conducted when the infants were 6 months or older. The infants' clinical condition was comparable to that of infants in the same pediatric department who had not been exposed to the medication. A case-control study in Israel compared infants born to 280 breastfeeding mothers on long-term use of psychotropic drugs with infants born to 152 mothers on antibiotics. One mother who took sertraline during pregnancy and breastfeeding reported her infant experiencing lethargy at 3 days of age, while none of the mothers taking antibiotics reported lethargy. The lethargy resolved within 24 hours and did not affect development. A prospective study in Poland of breastfeeding mothers who called lactation counseling services found that four mothers' breastfed infants experienced adverse reactions to sertraline. These cases included three suspected cases of infantile colic and one case of sinus tachycardia possibly related to sertraline in a 3-week-old exclusively breastfed infant whose mother was taking 50 mg of sertraline daily.
◉ Effects on Lactation and Breast Milk
Sertraline can cause galactorrhea in non-pregnant, non-lactating patients, sometimes with normal serum prolactin levels. However, a study of cases of hyperprolactinemia and its symptoms (such as gynecomastia) reported by the French Pharmacovigilance Center showed that sertraline did not increase the risk of hyperprolactinemia compared to other drugs. Prolactin levels in established lactating mothers may not affect their ability to breastfeed.
A midwife observed six patients reporting decreased milk production (dose not reported) after starting sertraline. One of the mothers started taking sertraline in the sixth month of pregnancy. She reported an increase in milk production one week after discontinuing sertraline four months postpartum. Upon resuming sertraline, milk production reportedly decreased. In all women, milk production increased within 2 to 3 days after increasing fluid intake and breastfeeding frequency. In a small prospective study, researchers compared eight primiparous women taking serotonin reuptake inhibitors (SRIs; three taking fluoxetine, and one taking citalopram, duloxetine, escitalopram, paroxetine, or sertraline, respectively) with 423 mothers not taking SRIs. The onset of lactation activation (stage II lactation) 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 in the untreated group), effectively doubling the risk of delayed breastfeeding in the untreated group. However, this delay in stage II lactation may not have been 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; sertraline n = 200), women with mental illness but not taking antidepressants (n = 1552), and mothers not diagnosed with mental illness (n = 30,535). Women treated with antidepressants were 37% less likely to breastfeed at discharge than women not diagnosed with mental illness, but there was no difference in the likelihood of breastfeeding compared to mothers who were diagnosed with mental illness but not treated.
A study of 80,882 Norwegian mothers and infants between 1999 and 2008 showed that 392 women reported starting antidepressants postpartum and 201 women reported starting antidepressants during pregnancy. Compared with the control group that had not been exposed to antidepressants, taking antidepressants in late pregnancy was associated with a 7% lower likelihood of initiating breastfeeding, but had no effect on the duration of breastfeeding or the rate of exclusive breastfeeding. Compared with the control group that had not been exposed to antidepressants, starting or restarting antidepressants was associated with a 63% lower likelihood of primary breastfeeding at 6 months and a 51% lower likelihood of any breastfeeding, and was associated with a 2.6-fold increased risk of abrupt cessation of breastfeeding. No specific antidepressant was mentioned.

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Acute toxicity in mice[1]:
-Oral LD50 = 400 mg/kg; Intraperitoneal LD50 = 150 mg/kg. Mice showed transient sedation (2-4 hours) at subLD50 doses, but no death or pathological damage to the liver, kidneys or brain tissue occurred [1]
- Subacute toxicity in rats [1]:
- Oral administration of sertraline hydrochloride (10 mg/kg/day) for 14 days had no significant effect on body weight, food intake or serum markers of liver function (ALT, AST) and kidney function (creatinine) [1]
- Chronic toxicity in rats [2]:
- Oral administration of sertraline hydrochloride (20 mg/kg/day) for 28 days had no pathological abnormalities observed in the brain, liver or kidneys. Hematological parameters (white blood cells, red blood cells, platelets) were all within the normal range [2]

[1]. J Pharmacol Exp Ther . 1983 Sep;226(3):686-700.

[2]. J Pharmacol Exp Ther . 1976 Dec;199(3):649-61.

Sertraline hydrochloride is the hydrochloride salt formed by the reaction of equimolar amounts of sertraline with hydrogen chloride. It is a selective serotonin reuptake inhibitor (SSRI) used orally to treat depression, obsessive-compulsive disorder, panic disorder, and post-traumatic stress disorder. It has a dual action of inhibiting serotonin reuptake and acting as an antidepressant. It contains the sertraline (1+) ion. Sertraline hydrochloride is the hydrochloride salt of sertraline, a synthetic derivative of naphthylamine, which has antiserotonergic and antidepressant properties. Sertraline appears to selectively inhibit the uptake of serotonin by neurons, thereby increasing serotonin levels in the central nervous system. A selective serotonin reuptake inhibitor used to treat depression. See also: Sertraline (with active fraction). Sertraline hydrochloride is a selective serotonin reuptake inhibitor (SSRI) with the chemical structure (1S,4S)-N-methyl-4-(3,4-dichlorophenyl)-1,2,3,4-tetrahydro-1-naphthylamine hydrochloride. Its key pharmacological feature is its high selectivity for SERT rather than NET and DAT, thereby reducing the anticholinergic and cardiovascular side effects associated with tricyclic antidepressants such as imipramine [1] - Literature [2] shows that sertraline hydrochloride is about 10 times more potent than imipramine in inhibiting human platelet SERT, which supports its efficacy in enhancing central serotonergic neurotransmission—the core mechanism of its antidepressant activity [2] - In animal models, sertraline hydrochloride has shown significant antidepressant activity (e.g., in the forced swimming test) without significant motor inhibition, indicating a low risk of sedative side effects [1]

C17H18CL3N

342.69

341.05

C, 59.58; H, 5.29; Cl, 31.04; N, 4.09

79559-97-0

(±)-cis-Sertraline-d3 hydrochloride; 1217741-83-7; rel-Sertraline-d3 hydrochloride; 1330180-66-9; 79617-96-2

63009

White to off-white solid powder

416.3ºC at 760 mmHg

246-249°C

205.6ºC

6.372

2

1

2

21

322

2

N([C@H]1CC[C@@H](C2C=CC(Cl)=C(Cl)C=2)C2C=CC=CC1=2)C.Cl

BLFQGGGGFNSJKA-XHXSRVRCSA-N

InChI=1S/C17H17Cl2N.ClH/c1-20-17-9-7-12(13-4-2-3-5-14(13)17)11-6-8-15(18)16(19)10-11;/h2-6,8,10,12,17,20H,7,9H2,1H3;1H/t12-,17-;/m0./s1

(1S,4S)-4-(3,4-dichlorophenyl)-N-methyl-1,2,3,4-tetrahydronaphthalen-1-amine;hydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

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

Solubility in Formulation 1: ≥ 2.5 mg/mL (7.30 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 (7.30 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 (7.30 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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Solubility in Formulation 4: 30% PEG400+0.5% Tween80+5% Propylene glycol : 5 mg/mL

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