Sertraline

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Sertraline
Sertraline2DACS2.svg
Sertraline-A-3D-balls.png
Systematic (IUPAC) name
(1S,4S)-4-(3,4-dichlorophenyl)-N-methyl-1,2,3,4-tetrahydronaphthalen-1-amine
Clinical data
Trade names Zoloft, Lustral, Daxid, Deprax, Altruline, Besitran, Eleval, Emergen, Gladem, Implicane, Sedoran, Sealdin, Serivo, Lowfin, Stimuloton, Serimel, Seretral, Tresleen, Sertralin Bluefish
AHFS/Drugs.com monograph
MedlinePlus a697048
Pregnancy cat.
Legal status
Routes Oral
Pharmacokinetic data
Bioavailability 44%
Protein binding 98.5%
Metabolism Hepatic (N-demethylation mainly by CYP2B6)[1]
Half-life ~23-26 h (66 h [less-active[2] metabolite, norsertraline])[3]
Excretion Renal
Identifiers
CAS number 79617-96-2 YesY
ATC code N06AB06
PubChem CID 68617
DrugBank DB01104
ChemSpider 61881 YesY
UNII QUC7NX6WMB YesY
KEGG D02360 YesY
ChEBI CHEBI:9123 YesY
ChEMBL CHEMBL809 YesY
Chemical data
Formula C17H17Cl2N 
Mol. mass 306.229 g/mol
 YesY (what is this?)  (verify)

Sertraline (trade names Zoloft, Lustral) is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class. It was introduced to the market by Pfizer in 1991. Sertraline is primarily prescribed for major depressive disorder in adult outpatients as well as obsessive–compulsive, panic, and social anxiety disorders in both adults and children. In 2011, it was the second-most prescribed antidepressant on the U.S. retail market, with 37 million prescriptions.[4]

Differences with other newer antidepressants are subtle and mostly confined to side effects. Evidence suggests that sertraline may work better than fluoxetine (Prozac) for some subtypes of depression.[5] Treatment of panic disorder with sertraline results in a decrease of the number of panic attacks and an improved quality of life.[6] For obsessive-compulsive disorder, sertraline is not as effective as cognitive behavioral therapy (CBT); the best results have been achieved by combining CBT with an SSRI.[7][8] Sertraline is also effective for the treatment of social phobia and posttraumatic stress disorder.[9][10]

Medical uses[edit]

Sertraline is used for a number of conditions including: major depression, obsessive-compulsive disorder (OCD), body dysmorphic disorder (BDD), posttraumatic stress disorder (PTSD), premenstrual dysphoric disorder (PMDD), panic disorder and social phobia (social anxiety disorder).[11] It has also been used for premature ejaculation and vascular headaches but evidence of the effectiveness in treating those conditions is not robust.[11]

Depression[edit]

The original pre-marketing clinical trials demonstrated only weak-to-moderate efficacy of sertraline for depression. A 2008 review found that only 51% of studies of various SSRI's yielded positive outcomes.[12] Sertraline may be more effective for severe depression.[13]

Evidence does not show a benefit in children with depression.[14]

With depression in dementia, there is no benefit compared to either placebo or mirtazapine.[15]

Comparison with other antidepressants[edit]

Tricyclic antidepressants (TCAs) as a group are considered to work better than selective serotonin reuptake inhibitors for melancholic depression[16] and in inpatients,[17] but not necessarily for simply more severe depression.[18] In line with this generalization, sertraline was no better than placebo in inpatients (see History) and as effective as the TCA clomipramine for severe depression.[13] The comparative efficacy of sertraline and TCAs for melancholic depression has not been studied. A 1998 review suggested that, due to its pharmacology, sertraline may be more efficacious than other SSRIs and equal to TCAs for the treatment of melancholic depression.[19]

A meta-analysis of 12 new-generation antidepressants, sertraline and escitalopram are the best in terms of efficacy and acceptability in the acute-phase treatment of adults with unipolar major depression. Reboxetine was significantly worse.[20]

Comparative clinical trials demonstrated that sertraline's efficacy in depression is similar to that of moclobemide,[21] nefazodone,[22] escitalopram,[23] bupropion,[24] citalopram, fluvoxamine, paroxetine and mirtazapine.[25] Meta-analysis indicated that sertraline is more efficacious for the treatment of depression than fluoxetine (Prozac), with a 1.4 times higher probability of response, and is possibly better tolerated.[26][27]

Elderly[edit]

Sertraline used for the treatment of depression in elderly (older than 60) patients was superior to placebo and comparable to another SSRI fluoxetine, and TCAs amitriptyline, nortriptyline (Pamelor) and imipramine. Sertraline had much lower rates of adverse effects than these TCAs, with the exception of nausea, which occurred more frequently with sertraline. In addition, sertraline appeared to be more effective than fluoxetine or nortriptyline in the older-than-70 subgroup.[28] A 2003 trial of sertraline vs. placebo in elderly patients showed a statistically significant (that is, unlikely to occur by chance), but clinically very modest improvement in depression and no improvement in quality of life.[29]

Obsessive-compulsive disorder[edit]

Sertraline is effective for the treatment of OCD in adults and children.[30] It was better tolerated and, based on intention to treat analysis, performed better than the gold standard of OCD treatment clomipramine.[31] It is generally accepted that the sertraline dosages necessary for the effective treatment of OCD are higher than the usual dosage for depression.[32] The onset of action is also slower for OCD than for depression. The treatment recommendation is to start treatment with a half of maximal recommended dose for at least two months. After that, the dose can be raised to the maximal recommended in the cases of unsatisfactory response.[33]

Cognitive behavioral therapy alone was superior to sertraline in both adults and children; however, the best results were achieved using a combination of these treatments.[7][8] Sertraline may be useful for the treatment of OCD co-morbid with Tourette syndrome.[34]

Panic disorder[edit]

In four double-blind studies sertraline was shown to be superior to placebo for the treatment of panic disorder. The response rate was independent of the dose. In addition to decreasing the frequency of panic attacks by about 80% (vs. 45% for placebo) and decreasing general anxiety, sertraline resulted in improvement of quality of life on most parameters. The patients rated as "improved" on sertraline reported better quality of life than the ones who "improved" on placebo. The authors of the study argued that the improvement achieved with sertraline is different and of a better quality than the improvement achieved with placebo.[6][35] Sertraline was equally effective for men and women.[35] While imprecise, comparison of the results of trials of sertraline with separate trials of other anti-panic agents (clomipramine, imipramine, clonazepam, alprazolam, fluvoxamine and paroxetine) indicates approximate equivalence of these medications.[6]

Social phobia[edit]

Sertraline has been successfully used for the treatment of social phobia (social anxiety disorder).[36] In a flexible dosing study, it appeared that a higher dose range was needed for adequate response. The response was higher among the patients with later onset, especially adult onset, of the disorder.[37] In addition to psychological components of social phobia, such as fear and avoidance, sertraline also ameliorated some physiological components, such as blushing and palpitations but not sweating and trembling.[38]

Premenstrual dysphoric disorder[edit]

SSRIs, including sertraline, reduce the symptoms of premenstrual syndrome.[39] Side effects such as nausea are common.[39]

Sertraline is effective in alleviating the symptoms of PMDD, a severe form of premenstrual syndrome. Significant improvement was observed in 50–60% of cases treated with sertraline vs. 20–30% of cases on placebo. The improvement began during the first week of treatment, and in addition to mood, irritability, and anxiety, improvement was reflected in better family functioning, social activity and general quality of life. Work functioning and physical symptoms, such as swelling, bloating and breast tenderness, were less responsive to sertraline.[40][41] Taking sertraline only during the luteal phase, that is, the 12–14 days before menses, was shown to work as well as continuous treatment.[39]

Other indications[edit]

Sertraline when taken daily can be useful for the treatment of some aspects of premature ejaculation.[42] A disadvantage of SSRIs is that they require continuous daily treatment to delay ejaculation significantly.[43] And it is not clear how they affect psychological distress of those with the condition or the persons control over ejaculation timing.[44]

The benefit of sertraline in PTSD is not significant per the National Institute of Clinical Excellence.[45] Others however do feel that there is a benefit from their use.[46]

Adverse effects[edit]

Zoloft 50 mg & 25 mg tablets (US)
Zoloft 100 mg tablets (AU)

Compared to other SSRIs sertraline tends to be associated with a higher rate of psychiatric side effects and diarrhea.[47][48] It tends to be more activating (that is, associated with a higher rate of anxiety, agitation, insomnia, etc.) than other SSRIs, aside from fluoxetine.[49]

Over more than six months of sertraline therapy for depression, patients showed an insignificant weight increase of 0.1%.[50] Similarly, a 30-month-long treatment with sertraline for OCD resulted in a mean weight gain of 1.5% (1 kg).[51] Although the difference did not reach statistical significance, the weight gain was lower for fluoxetine (Prozac) (1%) but higher for citalopram (Celexa), fluvoxamine (Luvox) and paroxetine (Paxil) (2.5%). Only 4.5% of the sertraline group gained a large amount of weight (defined as more than 7% gain). This result compares favorably with placebo, where, according to the literature, 3–6% of patients gained more than 7% of their initial weight. The large weight gain was observed only among female members of the sertraline group; the significance of this finding is unclear because of the small size of the group.[51]

Over a two-week treatment of healthy volunteers, sertraline slightly improved verbal fluency but did not affect word learning, short-term memory, vigilance, flicker fusion time, choice reaction time, memory span, or psychomotor coordination.[52][53] In spite of lower subjective rating, that is, feeling that they performed worse, no clinically relevant differences were observed in the objective cognitive performance in a group of people treated for depression with sertraline for 1.5 years as compared to healthy controls.[54] In children and adolescents taking sertraline for six weeks for anxiety disorders, 18 out of 20 measures of memory, attention and alertness stayed unchanged. Divided attention was improved and verbal memory under interference conditions decreased marginally. Because of the large number of measures taken, it is possible that these changes were still due to chance.[55] The unique effect of sertraline on dopaminergic neurotransmission may be related to these effects on cognition and vigilance.[56][57]

Sexual side effects[edit]

Like other SSRIs, sertraline is associated with sexual side effects, including sexual arousal disorder and difficulty achieving orgasm. The observed frequency of sexual side effects depends greatly on whether they are reported by patients spontaneously, as in the manufacturer's trials, or actively solicited by the physicians. There have been several double-blind studies of sexual side effects comparing sertraline with placebo or other antidepressants.[58] While nefazodone (Serzone) and bupropion (Wellbutrin) did not have negative effects on sexual functioning, 67% of men on sertraline experienced ejaculation difficulties vs. 18% before the treatment[58] (or 61% vs. 0% according to another paper).[24] Similarly, in a group of women who initially did not have difficulties achieving orgasm, 41% acquired this problem during treatment with sertraline.[24] A 40% rate of orgasm dysfunction (vs. 9% for placebo) on sertraline was observed in a mixed group in another study.[59] Sexual arousal disorder, defined as "inadequate lubrication and swelling for women and erectile difficulties for men", occurred in 12% of patients on sertraline as compared with 1% of patients on placebo. The mood improvement resulting from the treatment with sertraline sometimes counteracted these side effects, so that sexual desire and overall satisfaction with sex stayed the same as before the sertraline treatment. However, under the action of placebo the desire and satisfaction slightly improved.[59]

Genital anesthesia,[60] loss of or decreased response to sexual stimuli, and ejaculatory anhedonia are also possible. Although usually reversible, for some people these effects are long-term and may persist after drug treatment is discontinued.[61]

Suicide[edit]

The FDA requires all antidepressants, including sertraline, to carry a black box warning stating that antidepressants may increase the risk of suicide in persons younger than 25. This warning is based on statistical analyses conducted by two independent groups of FDA experts that found a twofold increase of suicidal ideation and behavior in children and adolescents, and a 1.5-fold increase of suicidal behavior in the 18–24 age group.[62][63][64]

Suicidal ideation and behavior in clinical trials are rare. For the above analysis, the FDA combined the results of 295 trials of 11 antidepressants for psychiatric indications in order to obtain statistically significant results. Considered separately, sertraline use in adults decreased the odds of suicidal behavior with a marginal statistical significance by 37%[64] or 50%[63] depending on the statistical technique used. The authors of the FDA analysis note that "given the large number of comparisons made in this review, chance is a very plausible explanation for this difference".[63] The more complete data submitted later by the sertraline manufacturer Pfizer indicated increased suicidal behavior.[65] Similarly, the analysis conducted by the UK MHRA found a 50% increase of odds of suicide-related events, not reaching statistical significance, in the patients on sertraline as compared to the ones on placebo.[66][67]

Overdose[edit]

Acute overdosage is often manifested by emesis, lethargy, ataxia, tachycardia and seizures. Plasma, serum or blood concentrations of sertraline and norsertraline, its major active metabolite, may be measured to confirm a diagnosis of poisoning in hospitalized patients or to aid in the medicolegal investigation of fatalities.[68] As with most other SSRIs its toxicity in overdose is considered relatively low.[47][69]

Pregnancy and lactation[edit]

The studies comparing the levels of sertraline and its principal metabolite, desmethylsertraline, in mother's blood to their concentration in umbilical cord blood at the time of delivery indicated that foetal exposure to sertraline and its metabolite is approximately a third of the maternal exposure.[70][71] The use of sertraline during the first trimester of pregnancy was associated with increased odds of the following birth defects: omphalocele (six-fold), anal atresia and limb reduction defects (four-fold), and septal defects (two-fold); however these specific defects themselves are rare and therefore the absolute risks are small.[72] Concentration of sertraline and desmethylsertraline in breast milk is highly variable and, on average, is of the same order of magnitude as their concentration in the blood plasma of the mother. As a result, more than half of breast-fed babies receive less than 2 mg/day of sertraline and desmethylsertraline combined, and in most cases these substances are undetectable in their blood.[73] No changes in serotonin uptake by the platelets of breast-fed infants were found, as measured by their blood serotonin levels before and after their mothers began sertraline treatment.[74]

Withdrawal syndrome[edit]

Abrupt interruption of sertraline treatment may result in withdrawal or discontinuation syndrome. This syndrome occurred in 60% of the remitted depressed patients taking sertraline in a blind discontinuation study, as compared to 14% of patients on fluoxetine and 66% of patients on paroxetine.[75] During the 5–8-day period when sertraline was temporarily replaced by placebo, the most frequent symptoms (reported by more than a quarter of patients) were irritability, agitation, dizziness, headache, nervousness, crying, emotional lability, bad dreams and anger. Around a third experienced mood worsening to the level generally associated with a major depressive episode.[75] In a double-blind study of remitted panic disorder patients, abrupt discontinuation of sertraline treatment resulted in insomnia and dizziness (both 16–17% vs. 4% for continuing treatment), although headache, depression and malaise did not increase significantly.[76] In another double-blind study of recovered panic disorder patients, the withdrawal syndrome was completely avoided when sertraline was gradually discontinued over three weeks, while patients stopping paroxetine treatment still suffered from it.[77] There is at least one report of orthostatic hypotension as a result of sertraline withdrawal.[78]

Interactions[edit]

Sertraline is a moderate inhibitor of CYP2D6 and CYP2B6 in vitro.[79] Accordingly, in human trials it caused increased blood levels of CYP2D6 substrates such as metoprolol, dextromethorphan, desipramine, imipramine and nortriptyline, as well as the CYP3A4/CYP2D6 substrate haloperidol.[80][81][82] This effect is dose-dependent; for example, co-administration with 50 mg of sertraline resulted in 20% greater exposure to desipramine, while 150 mg of sertraline led to a 70% increase.[83][84] In a placebo-controlled study, the concomitant administration of sertraline and methadone caused a 40% increase in blood levels of the latter, which is primarily metabolized by CYP2B6.[85] Sertraline is often used in combination with stimulant medication for the treatment of co-morbid depression and/or anxiety in ADHD[86] Sertraline reduces amphetamine metabolism as a result of CYP2D6 inhibition.[87]

Sertraline had a slight inhibitory effect on the metabolism of diazepam, tolbutamide and warfarin, which are CYP2C9 or CYP2C19 substrates; this effect was not considered to be clinically relevant.[83] As expected from in vitro data, sertraline did not alter the human metabolism of the CYP3A4 substrates erythromycin, alprazolam, carbamazepine, clonazepam, and terfenadine; neither did it affect metabolism of the CYP1A2 substrate clozapine.

Sertraline had no effect on the actions of digoxin and atenolol, which are not metabolized in the liver.[79][83][88][89] Case reports suggest that taking sertraline with phenytoin or zolpidem may induce sertraline metabolism and decrease its efficacy,[90][91] and that taking sertraline with lamotrigine may increase the blood level of lamotrigine, possibly by inhibition of glucuronidation.[92]

Clinical reports indicate that interaction between sertraline and the MAOIs isocarboxazid and tranylcypromine may cause serotonin syndrome. In a placebo-controlled study in which sertraline was co-administered with lithium, 35% of the subjects experienced tremors, while none of those taking placebo did.[83]

According to Pfizer, sertraline is contraindicated in individuals taking monoamine oxidase inhibitors or the antipsychotic pimozide (Orap). Sertraline concentrate contains alcohol, and is therefore contraindicated with disulfiram (Antabuse). The prescribing information recommends that treatment of the elderly and patients with liver impairment "must be approached with caution." Due to the slower elimination of sertraline in these groups, their exposure to sertraline may be as high as three times the average exposure for the same dose.[88]

Grapefruit juice should be avoided, as this may increase the levels of Sertraline in the body ( see Grapefruit–drug interactions ).

Mechanism of action[edit]

Sertraline is primarily a serotonin reuptake inhibitor (SRI) with a binding affinity towards the serotonin transporter of Ki=2.0μM.[93] Therapeutic doses of sertraline (25–200 mg/day) taken by patients for four weeks resulted in 80–90% inhibition of serotonin transporter (SERT) in striatum as measured by positron emission tomography. A daily 9 mg dose was sufficient to inhibit 50% of SERT.[94]

Sertraline molecule

Sertraline is also a dopamine reuptake inhibitor, (<50 nmol/L). However, this is not considered a tight binding, and this action is only 10% of its potency as a monoamine reuptake inhibitor.[95] It is a σ1 receptor agonist with 5% of its SRI potency,[96] and an α1-adrenoreceptor antagonist with 1–10% of its SRI potency.[97] However, though confirming sertraline's high affinity for σ1 receptors, different studies suggest that the drug actually behaves as an antagonist at those.[98]

Sertraline demonstrated anti-fungal activity against Candida and Aspergillus species in vitro and in vivo.[99][100]

Pharmacokinetics[edit]

Norsertraline, sertraline's chief active metabolite

Sertraline is absorbed slowly when taken orally, achieving its maximal concentration in the plasma 4–6 hours after ingestion. In the blood, it is 98.5% bound to plasma proteins. Its half-life in the body is 13–45 hours and, on average, is about 1.5 times longer in women (32 hours) than in men (22 hours), leading to a 1.5-times-higher exposure in women.[83] According to in vitro studies, sertraline is metabolized by multiple cytochrome 450 isoforms: CYP2D6, CYP2C9, CYP2B6, CYP2C19 and CYP3A4. It appeared unlikely that inhibition of any single isoform could cause clinically significant changes in sertraline pharmacokinetics.[1][101] No differences in sertraline pharmacokinetics were observed between people with high and low activity of CYP2D6;[102] however, poor CYP2C19 metabolizers had a 1.5-times-higher level of sertraline than normal metabolizers.[103] In vitro data also indicate that the inhibition of CYP2B6 should have even greater effect than the inhibition of CYP2C19, while the contribution of CYP2C9 and CYP3A4 to the metabolism of sertraline would be minor. These conclusions have not been verified in human studies.[1] Sertraline can be deaminated in vitro by monoamine oxidases; however, this metabolic pathway has never been studied in vivo.[1] The major metabolite of sertraline, desmethylsertraline, is about 50 times weaker as a serotonin transporter inhibitor than sertraline and its clinical effect is negligible.[97]

Non-amine metabolites may also contribute to the antidepressant effects of this medication. Sertraline deaminated is O-2098, a compound that has been found to inhibit the dopamine reuptake transporter proteins in spite of its lack of a nitrogen atom.[104]

Its chief active metabolite is norsertraline (N-desmethylsertraline) which is significantly less biologically active than its parent compound.[105]

History[edit]

Skeletal formulae of chlorprothixene and tametraline, from which sertraline was derived

The history of sertraline dates back to the early 1970s, when Pfizer chemist Reinhard Sarges invented a novel series of psychoactive compounds based on the structures of neuroleptics chlorprothixene and thiothixene.[106][107] Further work on these compounds led to tametraline, a norepinephrine and weaker dopamine reuptake inhibitor. Development of tametraline was soon stopped because of undesired stimulant effects observed in animals. A few years later, in 1977, pharmacologist Kenneth Koe, after comparing the structural features of a variety of reuptake inhibitors, became interested in the tametraline series. He asked another Pfizer chemist, Willard Welch, to synthesize some previously unexplored tametraline derivatives. Welch generated a number of potent norepinephrine and triple reuptake inhibitors, but to the surprise of the scientists, one representative of the generally inactive cis-analogs was a serotonin reuptake inhibitor. Welch then prepared stereoisomers of this compound, which were tested in vivo by animal behavioral scientist Albert Weissman. The most potent and selective (+)-isomer was taken into further development and eventually named sertraline. Weissman and Koe recalled that the group did not set up to produce an antidepressant of the SSRI type—in that sense their inquiry was not "very goal driven", and the discovery of the sertraline molecule was serendipitous. According to Welch, they worked outside the mainstream at Pfizer, and even "did not have a formal project team". The group had to overcome initial bureaucratic reluctance to pursue sertraline development, as Pfizer was considering licensing an antidepressant candidate from another company.[106][108][109]

Sertraline was approved by the U.S. Food and Drug Administration (FDA) in 1991 based on the recommendation of the Psychopharmacological Drugs Advisory Committee; it had already become available in the United Kingdom the previous year.[110] The FDA committee achieved a consensus that sertraline was safe and effective for the treatment of major depression.

Sertraline entered the Australian market in 1994 and became the most often prescribed antidepressant in 1996 (2004 data).[111] It was measured as among the top ten drugs ranked by cost to the Australian government in 1998 and 2000–01, having cost $45 million and $87 million in subsidies respectively.[112][113] Sertraline is less popular in the UK (2003 data) and Canada (2006 data)—in both countries it was fifth (among drugs marketed for the treatment of MDD, or antidepressants), based on the number of prescriptions.[114][115]

Until 2002, sertraline was only approved for use in adults ages 18 and over; that year, it was approved by the FDA for use in treating children aged 6 or older with severe obsessive-compulsive disorder (OCD). In 2003, the UK Medicines and Healthcare products Regulatory Agency issued a guidance that, apart from fluoxetine (Prozac), SSRIs are not suitable for the treatment of depression in patients under 18.[116][117] However, sertraline can still be used in the UK for the treatment of OCD in children and adolescents.[118] In 2005, the FDA added a black box warning concerning pediatric suicidal behavior to all antidepressants, including sertraline. In 2007, labeling was again changed to add a warning regarding suicidal behavior in young adults ages 18 to 24.[119]

The U.S. patent for Zoloft expired in 2006,[120] and sertraline is now available in generic form.

Pfizer advertisements[edit]

The brand-name form of sertraline, Zoloft, was advertised to consumers by Pfizer using the following wording: "While the cause is unknown, depression may be related to an imbalance of natural chemicals between nerve cells in the brain. Prescription Zoloft works to correct this imbalance. You just shouldn't have to feel this way anymore." An essay published in the journal PLoS Medicine criticized these advertisements for their reliance on the "serotonin imbalance" theory of depression, although the monoamine hypothesis of antidepressant action was a leading theory at the time.[121] When asked to comment, the FDA answered that such "reductionist statements" are acceptable to explain the neurochemistry of depression "to the fraction of the public that functions at no higher than a 6th-grade reading level."[122]

An FDA Warning Letter was issued when a Zoloft advertisement omitted information about the risk of suicidal behavior.[123]

References[edit]

  1. ^ a b c d Obach RS, Cox LM, Tremaine LM (2005). "Sertraline is metabolized by multiple cytochrome P450 enzymes, monoamine oxidases, and glucuronyl transferases in human: an in vitro study". Drug Metab. Dispos. 33 (2): 262–70. doi:10.1124/dmd.104.002428. PMID 15547048. 
  2. ^ Sertraline FDA Label. http://www.fda.gov/ohrms/dockets/ac/04/briefing/4006b1_06_zoloft-label.pdf
  3. ^ Brunton L, Chabner B, Knollman B. Goodman and Gilman’s The Pharmacological Basis of Therapeutics, Twelfth Edition. McGraw Hill Professional; 2010.
  4. ^ John M. Grohol (2012). "Top 25 Psychiatric Medication Prescriptions for 2011". Psych Central. Retrieved 9 January 2013. 
  5. ^ Flament MF, Lane RM, Zhu R, Ying Z (1999). "Predictors of an acute antidepressant response to fluoxetine and sertraline". Int Clin Psychopharmacol 14 (5): 259–75. doi:10.1097/00004850-199914050-00001. PMID 10529069. 
  6. ^ a b c Hirschfeld RM (2000). "Sertraline in the treatment of anxiety disorders". Depress Anxiety 11 (4): 139–57. doi:10.1002/1520-6394(2000)11:4<139::AID-DA1>3.0.CO;2-C. PMID 10945134. 
  7. ^ a b Pediatric OCD Treatment Study (POTS) Team (2004). "Cognitive-behavior therapy, sertraline, and their combination for children and adolescents with obsessive-compulsive disorder: the Pediatric OCD Treatment Study (POTS) randomized controlled trial". JAMA 292 (16): 1969–76. doi:10.1001/jama.292.16.1969. PMID 15507582. 
  8. ^ a b Sousa MB, Isolan LR, Oliveira RR, Manfro GG, Cordioli AV (2006). "A randomized clinical trial of cognitive-behavioral group therapy and sertraline in the treatment of obsessive-compulsive disorder". The Journal of Clinical Psychiatry 67 (7): 1133–9. doi:10.4088/JCP.v67n0717. PMID 16889458. 
  9. ^ Hansen RA, Gaynes BN, Gartlehner G, Moore CG, Tiwari R, Lohr KN (May 2008). "Efficacy and tolerability of second-generation antidepressants in social anxiety disorder". Int Clin Psychopharmacol 23 (3): 170–9. doi:10.1097/YIC.0b013e3282f4224a. PMC 2657552. PMID 18408531. 
  10. ^ Watts BV, Schnurr PP, Mayo L, Young-Xu Y, Weeks WB, Friedman MJ (June 2013). "Meta-analysis of the efficacy of treatments for posttraumatic stress disorder". J Clin Psychiatry 74 (6): e541–50. doi:10.4088/JCP.12r08225. PMID 23842024. 
  11. ^ a b "Sertraline hydrochloride". The American Society of Health-System Pharmacists. Retrieved 3 April 2011. 
  12. ^ Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R (2008). "Selective publication of antidepressant trials and its influence on apparent efficacy". N. Engl. J. Med. 358 (3): 252–60. doi:10.1056/NEJMsa065779. PMID 18199864. 
  13. ^ a b Lépine JP, Goger J, Blashko C, Probst C, Moles MF, Kosolowski J, Scharfetter B, Lane RM (2000). "A double-blind study of the efficacy and safety of sertraline and clomipramine in outpatients with severe major depression". International Clinical Psychopharmacology 15 (5): 263–71. doi:10.1097/00004850-200015050-00003. PMID 10993128. 
  14. ^ Cohen D (2007). "Should the use of selective serotonin reuptake inhibitors in child and adolescent depression be banned?". Psychotherapy and psychosomatics 76 (1): 5–14. doi:10.1159/000096360. PMID 17170559. 
  15. ^ Banerjee S, Hellier J, Romeo R, Dewey M, Knapp M, Ballard C, Baldwin R, Bentham P, Fox C, Holmes C, Katona C, Lawton C, Lindesay J, Livingston G, McCrae N, Moniz-Cook E, Murray J, Nurock S, Orrell M, O'Brien J, Poppe M, Thomas A, Walwyn R, Wilson K, Burns A (2007). "Study of the use of antidepressants for depression in dementia: the HTA-SADD trial – a multicentre, randomised, double-blind, placebo-controlled trial of the clinical effectiveness and cost-effectiveness of sertraline and mirtazapine". Health Technol Assess 17 (7): 1–116. doi:10.3310/hta17070. PMID 23438937. 
  16. ^ Parker G, Roy K, Wilhelm K, Mitchell P (2001). "Assessing the comparative effectiveness of antidepressant therapies: a prospective clinical practice study". J Clin Psychiatry 62 (2): 117–25. doi:10.4088/JCP.v62n0209. PMID 11247097. 
  17. ^ Anderson IM (1998). "SSRIS versus tricyclic antidepressants in depressed inpatients: a meta-analysis of efficacy and tolerability". Depress Anxiety 7 (S1): 11–7. doi:10.1002/(SICI)1520-6394(1998)7:1+<11::AID-DA4>3.0.CO;2-I. PMID 9597346. 
  18. ^ Hirschfeld RM (1999). "Efficacy of SSRIs and newer antidepressants in severe depression: comparison with TCAs". J Clin Psychiatry 60 (5): 326–35. doi:10.4088/JCP.v60n0511. PMID 10362442. 
  19. ^ Amsterdam JD (1998). "Selective serotonin reuptake inhibitor efficacy in severe and melancholic depression". J. Psychopharmacol. (Oxford) 12 (3 Suppl B): S99–111. doi:10.1177/0269881198012003061. PMID 9808081. 
  20. ^ Cipriani A, Furukawa TA, Salanti G, Geddes JR, Higgins JP, Churchill R, Watanabe N, Nakagawa A, Omori IM, McGuire H, Tansella M, Barbui C (2009). "Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis". The Lancet 373 (9665): 746–758. doi:10.1016/S0140-6736(09)60046-5. PMID 19185342. Lay summaryThe Washington Post (29 January 2009). 
  21. ^ Papakostas GI, Fava M (2006). "A metaanalysis of clinical trials comparing moclobemide with selective serotonin reuptake inhibitors for the treatment of major depressive disorder". Canadian Journal of Psychiatry 51 (12): 783–90. PMID 17168253. 
  22. ^ Feiger A, Kiev A, Shrivastava RK, Wisselink PG, Wilcox CS (1996). "Nefazodone versus sertraline in outpatients with major depression: focus on efficacy, tolerability, and effects on sexual function and satisfaction". The Journal of Clinical Psychiatry. 57. Suppl 2: 53–62. PMID 8626364. 
  23. ^ Ventura D, Armstrong EP, Skrepnek GH, Haim Erder M (2007). "Escitalopram versus sertraline in the treatment of major depressive disorder: a randomized clinical trial". Current Medical Research and Opinion 23 (2): 245–50. doi:10.1185/030079906X167273. PMID 17288677. 
  24. ^ a b c Kavoussi RJ, Segraves RT, Hughes AR, Ascher JA, Johnston JA (1997). "Double-blind comparison of bupropion sustained release and sertraline in depressed outpatients". The Journal of Clinical Psychiatry 58 (12): 532–7. doi:10.4088/JCP.v58n1204. PMID 9448656. 
  25. ^ For the review, see:Hansen RA, Gartlehner G, Lohr KN, Gaynes BN, Carey TS (2005). "Efficacy and safety of second-generation antidepressants in the treatment of major depressive disorder". Ann. Intern. Med. 143 (6): 415–26. doi:10.7326/0003-4819-143-6-200509200-00006. PMID 16172440. 
  26. ^ Cipriani A, Brambilla P, Furukawa T, Geddes J, Gregis M, Hotopf M, Malvini L, Barbui C (2005). "Fluoxetine versus other types of pharmacotherapy for depression". In Cipriani, Andrea. Cochrane Database of Systematic Reviews (Online) (4): CD004185. doi:10.1002/14651858.CD004185.pub2. PMID 16235353. 
  27. ^ "Sertraline versus other antidepressive agents for depression". Cochrane Database of Systematic Reviews: CD006117 (4th rev.). 14 April 2010. doi:10.1002/14651858.CD006117.pub4.
  28. ^ Muijsers RB, Plosker GL, Noble S (2002). "Sertraline: a review of its use in the management of major depressive disorder in elderly patients". Drugs & Aging 19 (5): 377–92. doi:10.2165/00002512-200219050-00006. PMID 12093324. 
  29. ^ Schneider LS, Nelson JC, Clary CM, Newhouse P, Krishnan KR, Shiovitz T, Weihs K (2003). "An 8-week multicenter, parallel-group, double-blind, placebo-controlled study of sertraline in elderly outpatients with major depression". Am J Psychiatry 160 (7): 1277–85. doi:10.1176/appi.ajp.160.7.1277. PMID 12832242. 
  30. ^ Geller DA, Biederman J, Stewart SE, Mullin B, Martin A, Spencer T, Faraone SV (2003). "Which SSRI? A meta-analysis of pharmacotherapy trials in pediatric obsessive-compulsive disorder". The American Journal of Psychiatry 160 (11): 1919–28. doi:10.1176/appi.ajp.160.11.1919. PMID 14594734. 
  31. ^ Flament MF, Bisserbe JC (1997). "Pharmacologic treatment of obsessive-compulsive disorder: comparative studies". The Journal of Clinical Psychiatry. 58. Suppl 12: 18–22. PMID 9393392. 
  32. ^ Math SB, Janardhan Reddy YC (19 July 2007). "Issues In The Pharmacological Treatment of Obsessive-Compulsive Disorder: First-Line Treatment Options for OCD". medscape.com. Retrieved 28 July 2009. 
  33. ^ Blier P, Habib R, Flament MF (2006). "Pharmacotherapies in the management of obsessive-compulsive disorder" (PDF). Can J Psychiatry 51 (7): 417–30. PMID 16838823. 
  34. ^ Jiménez-Jiménez FJ, García-Ruiz PJ (2001). "Pharmacological options for the treatment of Tourette's disorder". Drugs 61 (15): 2207–20. doi:10.2165/00003495-200161150-00005. PMID 11772131. 
  35. ^ a b Clayton AH, Stewart RS, Fayyad R, Clary CM (2006). "Sex differences in clinical presentation and response in panic disorder: pooled data from sertraline treatment studies". Arch Womens Ment Health 9 (3): 151–7. doi:10.1007/s00737-005-0111-y. PMID 16292466. 
  36. ^ Review: Davidson JR (2006). "Pharmacotherapy of social anxiety disorder: what does the evidence tell us?". J Clin Psychiatry. 67. Suppl 12: 20–6. PMID 17092192. 
  37. ^ The BSPS15 criterion identified 28 (21%) of sertraline-treated patients and 4 (6%) of placebo-treated patients as responders. The 50% reduction in BSPS criterion identified 47 (35%) of sertraline-treated patients and 9 (13%) of placebo-treated patients as responders. Finally, the 50% reduction in MFQ-SP criterion identified 53 (39%) of sertraline-treated patients and 9 (13%) of placebo-treated patients as responders. Van Ameringen M, Oakman J, Mancini C, Pipe B, Chung H (2004). "Predictors of response in generalized social phobia: effect of age of onset". J Clin Psychopharmacol 24 (1): 42–8. doi:10.1097/01.jcp.0000104909.75206.6f. PMID 14709946. 
  38. ^ Connor KM, Davidson JR, Chung H, Yang R, Clary CM (2006). "Multidimensional effects of sertraline in social anxiety disorder". Depress Anxiety 23 (1): 6–10. doi:10.1002/da.20086. PMID 16216019. 
  39. ^ a b c Marjoribanks J, Brown J, O'Brien PM, Wyatt K (7 June 2013). "Selective serotonin reuptake inhibitors for premenstrual syndrome.". The Cochrane database of systematic reviews 6: CD001396. doi:10.1002/14651858.cd001396.pub3. PMID 23744611. 
  40. ^ Pearlstein T (2002). "Selective serotonin reuptake inhibitors for premenstrual dysphoric disorder: the emerging gold standard?". Drugs 62 (13): 1869–85. doi:10.2165/00003495-200262130-00004. PMID 12215058. 
  41. ^ Ackermann RT, Williams JW (2002). "Rational treatment choices for non-major depressions in primary care: an evidence-based review". J Gen Intern Med 17 (4): 293–301. doi:10.1046/j.1525-1497.2002.10350.x. PMC 1495030. PMID 11972726. 
  42. ^ Abdel-Hamid IA (September 2006). "Pharmacologic treatment of rapid ejaculation: levels of evidence-based review.". Current clinical pharmacology 1 (3): 243–54. doi:10.2174/157488406778249352. PMID 18666749. 
  43. ^ Waldinger MD (2007). "Premature ejaculation: state of the art". Urol. Clin. North Am. 34 (4): 591–9, vii–viii. doi:10.1016/j.ucl.2007.08.011. PMID 17983899. 
  44. ^ McMahon CG, Porst H (October 2011). "Oral agents for the treatment of premature ejaculation: review of efficacy and safety in the context of the recent International Society for Sexual Medicine criteria for lifelong premature ejaculation.". The journal of sexual medicine 8 (10): 2707–25. doi:10.1111/j.1743-6109.2011.02386.x. PMID 21771283. 
  45. ^ Pratchett LC, Daly K, Bierer LM, Yehuda R (October 2011). "New approaches to combining pharmacotherapy and psychotherapy for posttraumatic stress disorder.". Expert opinion on pharmacotherapy 12 (15): 2339–54. doi:10.1517/14656566.2011.604030. PMID 21819273. 
  46. ^ Davis LL, Frazier EC, Williford RB, Newell JM (2006). "Long-term pharmacotherapy for post-traumatic stress disorder". CNS Drugs 20 (6): 465–76. doi:10.2165/00023210-200620060-00003. PMID 16734498. 
  47. ^ a b Taylor, D; Paton, C; Shitij, K (2012). The Maudsley prescribing guidelines in psychiatry (in English). West Sussex: Wiley-Blackwell. ISBN 978-0-470-97948-8. 
  48. ^ Brayfield, A, ed. (13 August 2013). "Fluoxetine Hydrochloride". Martindale: The Complete Drug Reference (London, UK: Pharmaceutical Press). Retrieved 27 November 2013. 
  49. ^ "Side effects of antidepressant medications". UpToDate. Wolters Kluwer Health. Retrieved 27 November 2013. 
  50. ^ Fava M, Judge R, Hoog SL, Nilsson ME, Koke SC (2000). "Fluoxetine versus sertraline and paroxetine in major depressive disorder: changes in weight with long-term treatment". The Journal of Clinical Psychiatry 61 (11): 863–7. doi:10.4088/JCP.v61n1109. PMID 11105740. 
  51. ^ a b Maina G, Albert U, Salvi V, Bogetto F (2004). "Weight gain during long-term treatment of obsessive-compulsive disorder: a prospective comparison between serotonin reuptake inhibitors". The Journal of Clinical Psychiatry 65 (10): 1365–71. doi:10.4088/JCP.v65n1011. PMID 15491240. 
  52. ^ Schmitt JA, Kruizinga MJ, Riedel WJ (2001). "Non-serotonergic pharmacological profiles and associated cognitive effects of serotonin reuptake inhibitors". J. Psychopharmacol. (Oxford) 15 (3): 173–9. doi:10.1177/026988110101500304. PMID 11565624. 
  53. ^ Siepmann M, Grossmann J, Mück-Weymann M, Kirch W (2003). "Effects of sertraline on autonomic and cognitive functions in healthy volunteers". Psychopharmacology (Berl.) 168 (3): 293–8. doi:10.1007/s00213-003-1448-4. PMID 12692706. 
  54. ^ Gorenstein C, de Carvalho SC, Artes R, Moreno RA, Marcourakis T (2006). "Cognitive performance in depressed patients after chronic use of antidepressants". Psychopharmacology (Berl.) 185 (1): 84–92. doi:10.1007/s00213-005-0274-2. PMID 16485140. 
  55. ^ Günther T, Holtkamp K, Jolles J, Herpertz-Dahlmann B, Konrad K (2005). "The influence of sertraline on attention and verbal memory in children and adolescents with anxiety disorders". J Child Adolesc Psychopharmacol 15 (4): 608–18. doi:10.1089/cap.2005.15.608. PMID 16190792. 
  56. ^ Borkowska A, Pilaczyńska E, Araszkiewicz A, Rybakowski J (2002). "The effect of sertraline on cognitive functions in patients with obsessive-compulsive disorder". Psychiatria polska 36 (6 Suppl): 289–95. PMID 12647451. 
  57. ^ Schmitt JA, Ramaekers JG, Kruizinga MJ, van Boxtel MP, Vuurman EF, Riedel WJ (2002). "Additional dopamine reuptake inhibition attenuates vigilance impairment induced by serotonin reuptake inhibition in man". Journal of psychopharmacology (Oxford, England) 16 (3): 207–214. doi:10.1177/026988110201600303. PMID 12236626. 
  58. ^ a b Ferguson JM (2001). "The effects of antidepressants on sexual functioning in depressed patients: a review". The Journal of Clinical Psychiatry. 62. Suppl 3: 22–34. PMID 11229450. 
  59. ^ a b Croft H, Settle E, Houser T, Batey SR, Donahue RM, Ascher JA (1999). "A placebo-controlled comparison of the antidepressant efficacy and effects on sexual functioning of sustained-release bupropion and sertraline". Clinical Therapeutics 21 (4): 643–58. doi:10.1016/S0149-2918(00)88317-4. PMID 10363731. 
  60. ^ Bolton JM, Sareen J, Reiss JP (2006). "Genital anaesthesia persisting six years after sertraline discontinuation". J Sex Marital Ther 32 (4): 327–30. doi:10.1080/00926230600666410. PMID 16709553. 
  61. ^ Csoka AB, Csoka A, Bahrick A, Mehtonen OP (2008). "Persistent Sexual Dysfunction after Discontinuation of Selective Serotonin Reuptake Inhibitors (SSRIs)". J Sex Med. 5 (1): 227–33. doi:10.1111/j.1743-6109.2007.00630.x. PMID 18173768. 
  62. ^ Levenson M, Holland C. "Antidepressants and Suicidality in Adults: Statistical Evaluation. (Presentation at Psychopharmacologic Drugs Advisory Committee; December 13, 2006)". FDA. Retrieved 11 July 2008. 
  63. ^ a b c Stone MB, Jones ML (17 November 2006). "Clinical review: relationship between antidepressant drugs and suicidality in adults" (PDF). Overview for December 13 Meeting of Psychopharmacologic Drugs Advisory Committee (PDAC). FDA. pp. 11–74. Retrieved 11 July 2008. 
  64. ^ a b Levenson M, Holland C (17 November 2006). "Statistical Evaluation of Suicidality in Adults Treated with Antidepressants" (PDF). Overview for December 13 Meeting of Psychopharmacologic Drugs Advisory Committee (PDAC). FDA. pp. 75–140. Retrieved 11 July 2008. 
  65. ^ Pfizer Inc. (30 November 2006). "Memorandum from Pfizer Global Pharmaceuticals Re: DOCKET: 2006N-0414 –"Suicidality data from adult antidepressant trials" Background package for December 13 Advisory Committee" (PDF). FDA DOCKET 2006N-0414. FDA. Retrieved 11 July 2008. 
  66. ^ "Report of the CSM expert working group on the safety of selective serotonin reuptake inhibitor antidepressants" (PDF). MHRA. December 2004. Retrieved 11 July 2008. 
  67. ^ Gunnell D, Saperia J, Ashby D (2005). "Selective serotonin reuptake inhibitors (SSRIs) and suicide in adults: meta-analysis of drug company data from placebo controlled, randomised controlled trials submitted to the MHRA's safety review". BMJ 330 (7488): 385. doi:10.1136/bmj.330.7488.385. PMC 549105. PMID 15718537. 
  68. ^ R. Baselt (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, California: Biomedical Publications. pp. 1399–1400. 
  69. ^ White N, Litovitz T, Clancy C (December 2008). "Suicidal antidepressant overdoses: a comparative analysis by antidepressant type". Journal of Medical Toxicology 4 (4): 238–250. doi:10.1007/BF03161207. PMC 3550116. PMID 19031375. 
  70. ^ Hostetter A, Ritchie JC, Stowe ZN (2000). "Amniotic fluid and umbilical cord blood concentrations of antidepressants in three women". Biol. Psychiatry 48 (10): 1032–4. doi:10.1016/S0006-3223(00)00958-6. PMID 11082480. 
  71. ^ Hendrick V, Stowe ZN, Altshuler LL, Hwang S, Lee E, Haynes D (2003). "Placental passage of antidepressant medications". The American Journal of Psychiatry 160 (5): 993–6. doi:10.1176/appi.ajp.160.5.993. PMID 12727706. 
  72. ^ Louik C, Lin AE, Werler MM, Hernández-Díaz S, Mitchell AA (2007). "First-trimester use of selective serotonin-reuptake inhibitors and the risk of birth defects". N. Engl. J. Med. 356 (26): 2675–83. doi:10.1056/NEJMoa067407. PMID 17596601. 
  73. ^ Stowe ZN, Hostetter AL, Owens MJ, Ritchie JC, Sternberg K, Cohen LS, Nemeroff CB (2003). "The pharmacokinetics of sertraline excretion into human breast milk: determinants of infant serum concentrations". The Journal of Clinical Psychiatry 64 (1): 73–80. doi:10.4088/JCP.v64n0114. PMID 12590627. 
  74. ^ Epperson N, Czarkowski KA, Ward-O'Brien D, Weiss E, Gueorguieva R, Jatlow P, Anderson GM (2001). "Maternal sertraline treatment and serotonin transport in breast-feeding mother-infant pairs". The American Journal of Psychiatry 158 (10): 1631–7. doi:10.1176/appi.ajp.158.10.1631. PMID 11578995. 
  75. ^ a b Rosenbaum JF, Fava M, Hoog SL, Ascroft RC, Krebs WB (1998). "Selective serotonin reuptake inhibitor discontinuation syndrome: a randomized clinical trial". Biol. Psychiatry 44 (2): 77–87. doi:10.1016/S0006-3223(98)00126-7. PMID 9646889. 
  76. ^ Rapaport MH, Wolkow R, Rubin A, Hackett E, Pollack M, Ota KY (2001). "Sertraline treatment of panic disorder: results of a long-term study". Acta Psychiatr Scand 104 (4): 289–98. doi:10.1034/j.1600-0447.2001.00263.x. PMID 11722304. 
  77. ^ Bandelow B, Behnke K, Lenoir S, Hendriks GJ, Alkin T, Goebel C, Clary CM (2004). "Sertraline versus paroxetine in the treatment of panic disorder: an acute, double-blind noninferiority comparison". J Clin Psychiatry 65 (3): 405–13. doi:10.4088/JCP.v65n0317. PMID 15096081. 
  78. ^ Amsden GW, Georgian F (1996). "Orthostatic hypotension induced by sertraline withdrawal". Pharmacotherapy 16 (4): 684–6. PMID 8840377. 
  79. ^ a b Obach RS, Walsky RL, Venkatakrishnan K, Gaman EA, Houston JB, Tremaine LM (2006). "The utility of in vitro cytochrome P450 inhibition data in the prediction of drug-drug interactions". J. Pharmacol. Exp. Ther. 316 (1): 336–48. doi:10.1124/jpet.105.093229. PMID 16192315. 
  80. ^ Ozdemir V, Naranjo CA, Herrmann N, Shulman RW, Sellers EM, Reed K, Kalow W (1998). "The extent and determinants of changes in CYP2D6 and CYP1A2 activities with therapeutic doses of sertraline". Journal of Clinical Psychopharmacology 18 (1): 55–61. doi:10.1097/00004714-199802000-00009. PMID 9472843. 
  81. ^ Alfaro CL, Lam YW, Simpson J, Ereshefsky L (1999). "CYP2D6 status of extensive metabolizers after multiple-dose fluoxetine, fluvoxamine, paroxetine, or sertraline". Journal of Clinical Psychopharmacology 19 (2): 155–63. doi:10.1097/00004714-199904000-00011. PMID 10211917. 
  82. ^ Alfaro CL, Lam YW, Simpson J, Ereshefsky L (2000). "CYP2D6 inhibition by fluoxetine, paroxetine, sertraline, and venlafaxine in a crossover study: intraindividual variability and plasma concentration correlations". Journal of Clinical Pharmacology 40 (1): 58–66. doi:10.1177/00912700022008702. PMID 10631623. 
  83. ^ a b c d e DeVane CL, Liston HL, Markowitz JS (2002). "Clinical pharmacokinetics of sertraline". Clinical Pharmacokinetics 41 (15): 1247–66. doi:10.2165/00003088-200241150-00002. PMID 12452737. 
  84. ^ Preskorn SH, Greenblatt DJ, Flockhart D, Luo Y, Perloff ES, Harmatz JS, Baker B, Klick-Davis A, Desta Z, Burt T (2007). "Comparison of duloxetine, escitalopram, and sertraline effects on cytochrome P450 2D6 function in healthy volunteers". Journal of Clinical Psychopharmacology 27 (1): 28–34. doi:10.1097/00004714-200702000-00005. PMID 17224709. 
  85. ^ Hamilton SP, Nunes EV, Janal M, Weber L (2000). "The effect of sertraline on methadone plasma levels in methadone-maintenance patients". The American Journal on Addictions / American Academy of Psychiatrists in Alcoholism and Addictions 9 (1): 63–9. doi:10.1080/10550490050172236. PMID 10914294. 
  86. ^ Thomas E. Brown; Thomas E. Brown (Ph. D.) (2009). ADHD comorbidities: handbook for ADHD complications in children and adults. American Psychiatric Pub. ISBN 978-1-58562-158-3. 
  87. ^ "Adderall XR Prescribing Information". Medication Guide. United States Food and Drug Administration. Retrieved 7 October 2013. 
  88. ^ a b "Zoloft Prescribing Information for the U.S" (PDF). Pfizer. Retrieved 26 April 2008. 
  89. ^ DeVane CL, Donovan JL, Liston HL, Markowitz JS, Cheng KT, Risch SC, Willard L (2004). "Comparative CYP3A4 inhibitory effects of venlafaxine, fluoxetine, sertraline, and nefazodone in healthy volunteers". Journal of Clinical Psychopharmacology 24 (1): 4–10. doi:10.1097/01.jcp.0000104908.75206.26. PMID 14709940. 
  90. ^ Allard S, Sainati SM, Roth-Schechter BF (1999). "Coadministration of short-term zolpidem with sertraline in healthy women". Journal of clinical pharmacology 39 (2): 184–91. doi:10.1177/00912709922007624. PMID 11563412. 
  91. ^ Haselberger MB, Freedman LS, Tolbert S (1997). "Elevated serum phenytoin concentrations associated with coadministration of sertraline". Journal of Clinical Psychopharmacology 17 (2): 107–9. doi:10.1097/00004714-199704000-00008. PMID 10950473. 
  92. ^ Kaufman KR, Gerner R (1998). "Lamotrigine toxicity secondary to sertraline". Seizure 7 (2): 163–5. doi:10.1016/S1059-1311(98)80074-5. PMID 9627209. 
  93. ^ http://www.abcam.com/Sertraline-hydrochloride-ab141068.pdf
  94. ^ Meyer JH, Wilson AA, Sagrati S, Hussey D, Carella A, Potter WZ, Ginovart N, Spencer EP, Cheok A, Houle S (2004). "Serotonin transporter occupancy of five selective serotonin reuptake inhibitors at different doses: an [11C]DASB positron emission tomography study". The American Journal of Psychiatry 161 (5): 826–35. doi:10.1176/appi.ajp.161.5.826. PMID 15121647. 
  95. ^ Owens JM, Knight DL, Nemeroff CB (2002). "Second generation SSRIS: human monoamine transporter binding profile of escitalopram and R-fluoxetine". Encephale 28 (4): 350–5. PMID 12232544. 
  96. ^ Narita N, Hashimoto K, Tomitaka S, Minabe Y (1996). "Interactions of selective serotonin reuptake inhibitors with subtypes of sigma receptors in rat brain". Eur. J. Pharmacol. 307 (1): 117–9. doi:10.1016/0014-2999(96)00254-3. PMID 8831113. 
  97. ^ a b Owens MJ, Morgan WN, Plott SJ, Nemeroff CB (1997). "Neurotransmitter receptor and transporter binding profile of antidepressants and their metabolites". J. Pharmacol. Exp. Ther. 283 (3): 1305–22. PMID 9400006. 
  98. ^ Hashimoto, K (2009). "Sigma-1 Receptors and Selective Serotonin Reuptake Inhibitors: Clinical Implications of their Relationship". Central Nervous System Agents in Medicinal Chemistry 2009 (Sept): 197–204.  [1] PDF
  99. ^ Lass-Flörl C, Ledochowski M, Fuchs D, Speth C, Kacani L, Dierich MP, Fuchs A, Würzner R (2003). "Interaction of sertraline with Candida species selectively attenuates fungal virulence in vitro". FEMS Immunol. Med. Microbiol. 35 (1): 11–5. doi:10.1111/j.1574-695X.2003.tb00643.x. PMID 12589952. 
  100. ^ Young TJ, Oliver GP, Pryde D, Perros M, Parkinson T (April 2003). "Antifungal activity of selective serotonin reuptake inhibitors attributed to non-specific cytotoxicity". Journal of Antimicrobial Chemotherapy 51 (4): 1045–1047. doi:10.1093/jac/dkg184. PMID 12654745. 
  101. ^ Kobayashi K, Ishizuka T, Shimada N, Yoshimura Y, Kamijima K, Chiba K (1999). "Sertraline N-demethylation is catalyzed by multiple isoforms of human cytochrome P-450 in vitro". Drug Metab. Dispos. 27 (7): 763–6. PMID 10383917. 
  102. ^ Hamelin BA, Turgeon J, Vallée F, Bélanger PM, Paquet F, LeBel M (1996). "The disposition of fluoxetine but not sertraline is altered in poor metabolizers of debrisoquin". Clin. Pharmacol. Ther. 60 (5): 512–21. doi:10.1016/S0009-9236(96)90147-2. PMID 8941024. 
  103. ^ Wang JH, Liu ZQ, Wang W, Chen XP, Shu Y, He N, Zhou HH (2001). "Pharmacokinetics of sertraline in relation to genetic polymorphism of CYP2C19". Clin. Pharmacol. Ther. 70 (1): 42–7. doi:10.1067/mcp.2001.116513. PMID 11452243. 
  104. ^ Madras BK, Fahey MA, Miller GM, De La Garza R, Goulet M, Spealman RD, Meltzer PC, George SR, O'Dowd BF, Bonab AA, Livni E, Fischman AJ (2003). "Non-amine-based dopamine transporter (reuptake) inhibitors retain properties of amine-based progenitors". Eur. J. Pharmacol. 479 (1–3): 41–51. doi:10.1016/j.ejphar.2003.08.055. PMID 14612136. 
  105. ^ Ciraulo, DA; Shader, RI, ed. (2011). "Pharmacotherapy of Depression". SpringerLink (2nd ed.) (New York, NY: Humana Press). doi:10.1007/978-1-60327-435-7. ISBN 978-1-60327-434-0. 
  106. ^ a b The most complete account of sertraline discovery, targeted at chemists, see: Welch WM (1995). "Discovery and Development of Sertraline". Advances in Medicinal Chemistry. Advances in Medicinal Chemistry 3: 113–148. doi:10.1016/S1067-5698(06)80005-2. ISBN 978-1-55938-798-9. 
  107. ^ Sarges R, Tretter JR, Tenen SS, Weissman A (1973). "5,8-Disubstituted 1-Aminotetralins. A Class of Compounds with a Novel Profile of Central Nervous System Activity". Journal of Medicinal Chemistry 16 (9): 1003–1011. doi:10.1021/jm00267a010. PMID 4795663. 
  108. ^ See also: Mullin R (2006). "ACS Award for Team Innovation". Chemical & Engineering News 84 (5): 45–52. doi:10.1021/cen-v084n010.p045. 
  109. ^ A short blurb on the history of sertraline, see: Couzin J (2005). "The brains behind blockbusters". Science 309 (5735): 728. doi:10.1126/science.309.5735.728. PMID 16051786. 
  110. ^ Healy, David (1999). The Antidepressant Era. Cambridge, Massachusetts: Harvard University Press. p. 168. ISBN 0-674-03958-0. 
  111. ^ Mant A, Rendle VA, Hall WD, Mitchell PB, Montgomery WS, McManus PR, Hickie IB (2004). "Making new choices about antidepressants in Australia: the long view 1975–2002". Med. J. Aust. 181 (7 Suppl): S21–4. PMID 15462638. 
  112. ^ "Top 10 drugs – 1998". Australian Prescriber 22: 119. 1999. Retrieved 30 April 2008. 
  113. ^ "Top 10 drugs – 2000–01". Australian Prescriber 24: 136. 2001. Retrieved 30 April 2008. 
  114. ^ "Prescribing trends for SSRIs and related antidepressants" (PDF). UK MHRA. 2004. Retrieved 30 April 2008. 
  115. ^ Skinner BJ, Rovere M (31 July 2007). "Canada's Drug Price Paradox 2007" (PDF). The Fraser Institute. pp. 21–29. Retrieved 11 July 2008. 
  116. ^ "Safety review of antidepressants used by children completed". MHRA. 10 December 2003. Retrieved 11 July 2008. 
  117. ^ Boseley, Sarah (10 December 2003). "Drugs for depressed children banned". The Guardian. Retrieved 19 April 2007. 
  118. ^ "Overview of regulatory status and CSM advice relating to major depressive disorder (MDD) in children and adolescents". MHRA. Retrieved 17 April 2008. 
  119. ^ Food and Drug Administration (2 May 2007). "FDA Proposes New Warnings About Suicidal Thinking, Behavior in Young Adults Who Take Antidepressant Medications". Retrieved 11 July 2008. 
  120. ^ Smith, Aaron (17 July 2006). "Pfizer needs more drugs". CNNMoney.com. Retrieved 27 January 2007. 
  121. ^ Owens MJ (2004). "Selectivity of antidepressants: from the monoamine hypothesis of depression to the SSRI revolution and beyond". J Clin Psychiatry. 65 Suppl 4: 5–10. PMID 15046536. 
  122. ^ Lacasse JR, Leo J (2005). "Serotonin and depression: a disconnect between the advertisements and the scientific literature". PLoS Med 2 (12): e392. doi:10.1371/journal.pmed.0020392. PMC 1277931. PMID 16268734.  Free full text, open-access source
  123. ^ "Food and Drug Administration Division of Drug Marketing Advertising and Communications. (2005) Zoloft warning letter" (PDF). FDA. Archived from the original on 25 June 2008. Retrieved 11 July 2008. 

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