World Library  
My Account |  Register |  Help  
  
Flag as Inappropriate
Email this Article

Fluoxetine

Article Id: WHEBN0010153680
Reproduction Date:

Title: Fluoxetine  
Author: World Heritage Encyclopedia
Language: English
Subject: Selective serotonin reuptake inhibitor, Citalopram, 5-HT2C receptor, Escitalopram, Obsessive–compulsive disorder
Collection:
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Fluoxetine

Fluoxetine
Systematic (IUPAC) name
(RS)-N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine
Clinical data
Trade names Prozac, among others
AHFS/Drugs.com
MedlinePlus
Licence data US FDA:
Pregnancy cat.
Legal status
Routes Oral
Pharmacokinetic data
Bioavailability 72%[1]
Protein binding 94-95%[1][2][3][4][5]
Metabolism Hepatic (mostly CYP2D6-mediated)[1][2][3][4][5]
Onset of action ~2–4 weeks
Half-life 1–3 days (acute)
4–6 days (chronic)[1][2][3][4][5]
Excretion Urine (80%), faeces (15%)[1][2][3][4][5]
Identifiers
CAS number  YesY  YesY
ATC code N06
PubChem
IUPHAR ligand
DrugBank
ChemSpider  YesY
UNII  YesY
KEGG  N
ChEBI  YesY
ChEMBL  YesY
Chemical data
Formula C17H18F3NO 
Mol. mass 309.33 g·mol−1
Physical data
Melt. point 179–182 °C (354–360 °F)
Boiling point 395 °C (743 °F)
Solubility in water 14 mg/mL (20 °C)
 N   

Fluoxetine (also known by the trade names Prozac, Sarafem, Ladose and Fontex, among others) is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class. Fluoxetine was first documented in 1974 by scientists from Eli Lilly and Company.[6] It was approved by the U.S. Food and Drug Administration for the treatment of major depressive disorder in December 1987.[7] The U.S. fluoxetine patent expired in August 2001 and hence generic formulations are now available in the U.S..[8]

Fluoxetine is used for the treatment of health system.[13]

Medical uses

Fluoxetine is frequently used to treat major depressive disorder, obsessive-compulsive disorder, post-traumatic stress disorder, bulimia nervosa, panic disorder, premenstrual dysphoric disorder, and trichotillomania.[10][14][15][16] It has also been used for cataplexy, obesity, and alcohol dependence,[17] as well as binge eating disorder.[18] Fluoxetine has also been tried as a treatment for autism spectrum disorders with moderate success in adults.[19][20][21][22]

Depression

The effectiveness of fluoxetine and other antidepressants in the treatment of mild-to-moderate depression is controversial. A meta-analysis published by Kirsch in 2008 suggests that in those with mild or moderate symptoms, the efficacy of fluoxetine and other SSRIs is clinically insignificant.[23] A 2009 meta analysis by Fournier et al., which evaluated patient level data from 6 trials of the SSRI paroxetine and the non-SSRI antidepressant imipramine has been further cited as evidence that antidepressants exhibit minimal efficacy in mild to moderate depression.[24] A 2012 meta analysis utilizing individual patient level data from 18 randomized controlled clinical trials of fluoxetine for the treatment of depression concluded that statistically and clinically significant benefit was seen irrespective of baseline depression severity, and that there was no significant effect of baseline severity on observed efficacy.[25]

Anti-psychopharmacology activist Joanna Moncrieff has argued that any improvements in mood found in trials for fluoxetine (and other SSRIs) are simply a product of an exaggerated placebo effect (regardless of the severity of depression).[26] A 2009 systematic review by the National Institute of Care and Clinical Excellence (NICE) (which considered the Kirsch but not the later meta analyses) concluded that there was strong evidence for the efficacy of SSRIs in the treatment of moderate and severe depression, and some evidence for their efficacy in the treatment of mild depression.[27] Both the NICE and the Fournier analyses concluded that there is greater evidence for the efficacy of antidepressants in the treatment of chronic mild depression (dysthymia) than in recent onset mild depression.

NICE recommends antidepressant treatment with an SSRI in combination with psychosocial interventions as second line treatment for short term mild depression, and as a first line treatment for severe and moderate depression, as well as mild depression that is recurrent or long-standing. The American Psychiatric Association includes antidepressant therapy among it first-line options for the treatment of depression, particularly when there is "a history of prior positive response to antidepressant medications, the presence of moderate to severe symptoms, significant sleep or appetite disturbances, agitation, patient preference, and anticipation of the need for maintenance therapy".[28]

Obsessive-compulsive disorder

The efficacy of fluoxetine in the treatment of obsessive-compulsive disorder was demonstrated in two randomized multi-center phase 3 clinical trials. The pooled results of these trials demonstrated that 47% of completers treated with the highest dose were "much improved" or "very much improved" after 13 weeks of treatment, compared to 11% in the placebo arm of the trial.[29] SSRIs including fluoxetine should be used as first-line therapy, along with CBT, for the treatment of moderate to severe OCD.[30]

Panic disorder

The efficacy of fluoxetine in the treatment of panic disorder was demonstrated in two 12 week randomized multicenter phase 3 trials that enrolled patients diagnosed with panic disorder, with or without agoraphobia. In the first trial, 42% of subjects in the fluoxetine treated arm were free of panic attacks at the end of the study, vs. 28% in the placebo arm. In the second trial, 62% of fluoxetine treated patients were free of panic attacks at the end of the study, vs. 44% in the placebo arm.[29]

Bulimia nervosa

A 2011 systematic review of 7 trials which compared fluoxetine to a placebo in the treatment of bulimia nervosa; 6 of which found a statistically significant reduction in symptoms such as vomiting and binge eating.[31] However, no difference was observed between treatment arms when fluoxetine plus psychotherapy was compared to psychotherapy alone.

Special populations

In children and adolescents fluoxetine is the antidepressant of choice due to tentative evidence favoring its efficacy and tolerability.[32][33] In pregnancy, fluoxetine is considered a [34][35][36] Furthermore an association between fluoxetine use during the first trimester and an increased risk of minor fetal malformations was been observed in one study.[35]

However, a systematic review and meta-analysis of 21 studies published in the Journal of Obstetrics and Gynaecology Canada concluded that, "the apparent increased risk of fetal cardiac malformations associated with maternal use of fluoxetine has recently been shown also in depressed women who deferred SSRI therapy in pregnancy, and therefore most probably reflects an ascertainment bias. Overall, women who are treated with fluoxetine during the first trimester of pregnancy do not appear to have an increased risk of major fetal malformations." But the study found also fifteen cohort studies that evaluated cardiac malformations and yielded an overall odds ratio of 1.6 (95% CI 1.31 to 1.95).[37]

Of note, the FDA states that infants exposed to SSRIs in late pregnancy may have an increased risk for persistent pulmonary hypertension of the newborn(PPHN). Limited data supports this risk, but the FDA recommends that physicians consider tapering SSRIs such as fluoxetine during the third trimester.[38] A review published in 2009 in the Journal of Human Lactation recommended against fluoxetine as a first-line SSRI during lactation, stating that fluoxetine "should be viewed as a less-preferred SSRI for breastfeeding mothers, particularly with newborn infants, and in those mothers who consumed fluoxetine during gestation."[39] Sertraline is often the preferred SSRI during pregnancy due to the relatively minimal fetal exposure observed and its safety profile while breastfeeding.[40]

Adverse effects

Side effects observed in fluoxetine-treated persons in clinical trial with an incidence that was >5% and at least twice as common in fluoxetine-treated persons compared to those who received a sugar pill include abnormal dreams, abnormal ejaculation, anorexia, anxiety, asthenia, diarrhea, dry mouth, dyspepsia, flu syndrome, impotence, insomnia, libido decreased, nausea, nervousness, pharyngitis, rash, sinusitis, somnolence, sweating, tremor, vasodilatation, and yawn.[41] Fluoxetine is considered the most stimulating of the SSRIs (that is it is most prone to causing insomnia and agitation).[42][42] It also appears to be the most prone of the SSRIs for producing dermatologic reactions (e.g. urticaria (hives), rash, itchiness, etc.).[35] A more detailed listing of adverse events observed in fluoxetine-treated patients is shown in the table below. Some of these adverse events were also seen in a large percentage of patients treated with a sugar pill.[41]

Sexual dysfunction

Sexual dysfunction, including loss of libido, anorgasmia, lack of vaginal lubrication, and erectile dysfunction, is one of the most commonly encountered adverse effects of treatment with fluoxetine and other SSRIs. While early clinical trials suggested a relatively low rate of sexual dysfunction, more recent studies in which the investigator actively enquires about sexual problems suggest that the incidence is >70%.[46] Symptoms of sexual dysfunction occasionally persist after discontinuing SSRIs. The incidence of this adverse effect is unknown. A limited series of published case reports describe a loss of genital sensation and other side effects continuing years after cessation of therapy.[47][48][49][50]

Fluoxetine 20 mg capsules.

Discontinuation syndrome

Several case reports in the literature describe severe withdrawal or discontinuation symptoms following an abrupt interruption of fluoxetine treatment.[51] However, various studies have shown that the side effects of the fluoxetine discontinuation are uncommon and mild, especially compared to paroxetine, venlafaxine and fluvoxamine, probably due to the relatively long pharmacological half-life of fluoxetine.[51] One of the recommended strategies for the management of discontinuation syndrome with other SSRIs is to substitute fluoxetine for the original agent, in cases where tapering off the dose of the original SSRI is ineffective.[52][53] The double-blind controlled studies support this opinion. No increase in side effects was observed in several studies when the treatment with fluoxetine was blindly interrupted for a short time (4–8 days) and then reinstated, this result being consistent with its slow elimination from the body.

More side effects occurred during the interruption of sertraline (Zoloft) in these studies, and significantly more during the interruption of paroxetine.[54] In a longer, 6‑week-long, blind discontinuation study, an insignificantly higher (32% vs 27%) overall rate of new or worsened side effects was observed in the group that discontinued fluoxetine than in the group that continued treatment. However, a significantly higher 4.2% rate of somnolence at week 2 and 5–7% rate of dizziness at weeks 4–6 were reported by the patients in the discontinuation group. This prolonged course of the discontinuation symptoms, with dizziness persisting to the end of the study, is also consistent with the long half-life of fluoxetine in the body.[55] According to a 2007 summary report of available evidence, fluoxetine has the lowest incidence of discontinuation syndrome among several antidepressants including paroxetine and venlafaxine.[56]

Suicide

The FDA now requires all antidepressants to carry a black box warning stating that antidepressants may increase the risk of suicide in people younger than 25. This warning is based on statistical analyses conducted by two independent groups of the FDA experts that found a 2-fold increase of the suicidal ideation and behavior in children and adolescents, and 1.5-fold increase of suicidality in the 18–24 age group. The suicidality was slightly decreased for those older than 24, and statistically significantly lower in the 65 and older group.[57][58][59] This analysis was criticized by Donald Klein, who noted that suicidality, that is suicidal ideation and behavior, is not necessarily a good surrogate marker for completed suicide, and it is still possible that antidepressants may prevent actual suicide while increasing suicidality.[60]

There is less data on fluoxetine than on antidepressants as a whole. For the above analysis on the antidepressant level, the FDA had to combine the results of 295 trials of 11 antidepressants for psychiatric indications to obtain statistically significant results. Considered separately, fluoxetine use in children increased the odds of suicidality by 50%,[61] and in adults decreased the odds of suicidality by approximately 30%.[58][59] Similarly, the analysis conducted by the UK MHRA found a 50% increase of odds of suicide-related events, not reaching statistical significance, in the children and adolescents on fluoxetine as compared to the ones on placebo. According to the MHRA data, for adults fluoxetine did not change the rate of self-harm and statistically significantly decreased suicidal ideation by 50%.[62][63]

Contraindications

Contraindications include prior treatment (within the past two weeks) with MAOIs such as phenelzine and tranylcypromine, due to the potential for serotonin syndrome.[2] Its use should also be avoided in those with known hypersensitivities to fluoxetine or any of the other ingredients in the formulation used.[2] Its use in those concurrently receiving pimozide or Thioridazine is also advised against.[2]

Interactions

Fluoxetine and norfluoxetine inhibit many isozymes of the cytochrome P450 system that are involved in drug metabolism. Both are potent inhibitors of CYP2D6 (which is also the chief enzyme responsible for their metabolism) and mild to moderate inhibitors of CYP1A2, CYP2B6, CYP2C9/2C19, and CYP3A4.[64] They also inhibit the activity of P-glycoprotein, a type of membrane transport protein that plays an important role in drug transport and metabolism and hence P-glycoprotein substrates such as loperamide may have their central effects potentiated.[65] This extensive effect on the body's pathways for drug metabolism creates the potential for interactions with many commonly used drugs.[65][66]

Its use should also be avoided in those receiving other serotonergic drugs such as monoamine oxidase inhibitors, tricyclic antidepressants, methamphetamine, MDMA, triptans, buspirone, serotonin-norepinephrine reuptake inhibitors and other SSRIs due to the potential for serotonin syndrome to develop as a result.[2]

There is also the potential for interaction with highly protein-bound drugs due to the potential for fluoxetine to displace said drugs from the plasma or vice versa hence increasing serum concentrations of either fluoxetine or the offending agent.[2]

Pharmacokinetics

3 dimensional representation of the cytochrome P450 isoenzyme CYP2D6. CYP2D6 is responsible for converting fluoxetine to its only active metabolite, norfluoxetine.[67] Both drugs are also potent inhibitors of CYP2D6.[68]
Norfluoxetine, fluoxetine's chief active metabolite.

The bioavailability of fluoxetine is relatively high (72%), and peak plasma concentrations are reached in 6 to 8 hours. It is highly bound to plasma proteins, mostly albumin and α1-glycoprotein.[2]

Fluoxetine is metabolized in the liver by isoenzymes of the cytochrome P450 system, including CYP2D6.[9] The role of CYP2D6 in the metabolism of fluoxetine may be clinically important, as there is great genetic variability in the function of this enzyme among people. Only one metabolite of fluoxetine, norfluoxetine (N-demethylated fluoxetine), is biologically active.[2]

The extremely slow elimination of fluoxetine and its active metabolite norfluoxetine from the body distinguishes it from other antidepressants. With time, fluoxetine and norfluoxetine inhibit their own metabolism, so fluoxetine elimination half-life changes from 1 to 3 days, after a single dose, to 4 to 6 days, after long-term use.[2] Similarly, the half-life of norfluoxetine is longer (16 days) after long-term use.[9][69][70] Therefore, the concentration of the drug and its active metabolite in the blood continues to grow through the first few weeks of treatment, and their steady concentration in the blood is achieved only after four weeks.[71][72] Moreover, the brain concentration of fluoxetine and its metabolites keeps increasing through at least the first five weeks of treatment.[73] That means that the full benefits of the current dose a patient receives are not realized for at least a month since its initiation. For example, in one 6-week study, the median time to achieving consistent response was 29 days.[71] Likewise, complete excretion of the drug may take several weeks. During the first week after the treatment discontinuation, the brain concentration of fluoxetine decreases only by 50%,[73] The blood level of norfluoxetine 4 weeks after the treatment discontinuation is about 80% of the level registered by the end of the first treatment week, and 7 weeks after the discontinuation norfluoxetine is still detectable in the blood.[69]

A PET study compared the action of a single dose of fluoxetine on exclusively heterosexual and exclusively homosexual men who attested that their past and present sexual behavior, desires, and fantasies were directed entirely toward women or men, respectively. The study found that in some areas of the brain the metabolic response in these two groups was different. "Both groups, however, did exhibit similar widespread lateralized metabolic responses to fluoxetine (relative to placebo), with most areas of the brain responding in the same direction." They "did not differ on behavioral measures or blood levels of fluoxetine".[74]

Measurement in body fluids

Fluoxetine and norfluoxetine may be quantitated in blood, plasma or serum to monitor therapy, confirm a diagnosis of poisoning in hospitalized patients or assist in a medicolegal death investigation. Blood or plasma fluoxetine concentrations are usually in a range of 50–500 μg/L in persons taking the drug for its antidepressant effects, 900–3000 μg/L in survivors of acute overdosage and 1000–7000 μg/L in victims of fatal overdosage. Norfluoxetine concentrations are approximately equal to those of the parent drug during chronic therapy, but may be substantially less following acute overdosage, since it requires at least 1–2 weeks for the metabolite to achieve equilibrium.[75][76][77]

Pharmacodynamics

Fluoxetine is a selective serotonin reuptake inhibitor and does not appreciably inhibit norepinephrine and dopamine reuptake. Nevertheless, Eli Lilly researchers found that a single injection of a large dose of fluoxetine given to a rat also resulted in a significant increase of brain concentrations of norepinephrine and dopamine.[78][79][80] This effect may be mediated by 5HT2A and, in particular, 5HT2C receptors, which are inhibited by higher concentrations of fluoxetine. The Eli Lilly scientists also suggested that the effects on dopamine and norepinephrine may contribute to the antidepressant action of fluoxetine.[80]

In the opinion of other researchers, however, the magnitude of this effect is unclear.[73] The dopamine and norepinephrine increase was not observed at a smaller, more clinically relevant dose of fluoxetine.[81] Similarly, in electrophysiological studies only larger and not smaller doses of fluoxetine changed the activity of rat's norepinephrinergic neurons. Some authors, however, argue that these findings may still have clinical relevance for the treatment of severe illness with supratherapeutic doses (60–80 mg) of fluoxetine.[82] Among SSRIs, 'fluoxetine is the least "selective" of all the SSRIs, with a 10-fold difference in binding affinity between its first and second neural targets (i.e., the serotonin and norepinephrine uptake pumps, respectively)'. Anything greater than a 10-fold difference results in insignificant activation of the secondary neuronal targets.[83]

Besides its well-known effects on serotonin, fluoxetine also increases density of endogenous opioid receptors in the brains of rats. It is unclear if this occurs in humans, but if so it might account for some of fluoxetine's antidepressant and/or side effect profile.[84]

Fluoxetine's mechanism of action is predominantly that of a serotonin reuptake inhibitor.[85][86] Fluoxetine delays the reuptake of serotonin, resulting in serotonin persisting longer when it is released. Fluoxetine may also produce some of its effects via its weak 5-HT2C receptor antagonist effects.[87] In addition, fluoxetine has been found to act as an agonist of the σ1-receptor, with a potency greater than that of citalopram but less than that of fluvoxamine. However, the significance of this property is not fully clear.[88][89] Fluoxetine also functions as a channel blocker of anoctamin 1, a calcium-activated chloride channel.[90][91]

Table 1: Binding affinity (Ki [nM]) of fluoxetine and norfluoxetine towards their molecular targets[92]
Molecular Target Fluoxetine Norfluoxetine
SERT 1.0 19
NET 660 2700
DAT 4180 420
5-HT2A 200 300
5-HT2B ≥5000 ≥5100
5-HT2C 260 91
M1 870 1200
M2 2700 4600
M3 1000 760
M4 2900 2600
M5 2700 2200

History

Chart showing increase (in red) over baseline (in blue) between 1987 and 2003
Number of Americans who received SSDI and SSI for mental illness in 1987 (blue) when Eli Lilly and Company introduced the antidepressive drug Prozac, compared to 2003 (red).

Hoping to find a derivative inhibiting only serotonin reuptake, an Eli Lilly scientist, David T. Wong, proposed to retest the series for the in vitro reuptake of serotonin, norepinephrine and dopamine. This test, carried out by Jong-Sir Horng in May 1972,[93] showed the compound later named fluoxetine to be the most potent and selective inhibitor of serotonin reuptake of the series.[6] Wong published the first article about fluoxetine in 1974.[6] A year later, it was given the official chemical name fluoxetine and the Eli Lilly and Company gave it the trade name Prozac. In February 1977, Dista Products Company, a division of Eli Lilly & Company, file an Investigational New Drug application to the U.S. Food and Drug Administration (FDA) for fluoxetine.[94]

Fluoxetine appeared on the Belgian market in 1986.[95] In the U.S., the FDA gave its final approval in December 1987,[96] and a month later Eli Lilly began marketing Prozac; annual sales in the U.S. reached $350 million within a year.[94]

Eli Lilly's U.S. patent on Prozac (fluoxetine) expired in August 2001,[97] prompting an influx of generic drugs onto the market. Prozac was rebranded "Sarafem" for the treatment of PMDD in an attempt to stem the post-patent decrease in Eli Lilly's sales of fluoxetine.[98]

As of April 2, 2010, fluoxetine is one of four antidepressant drugs that the FAA allows pilots to take. The others are sertraline (Zoloft), citalopram (Celexa), and escitalopram (Lexapro).[99]

There has been research on possible effects of fluoxetine on marine life.[100]

Society and culture

Violence

Neither the American Psychiatric Association,[101] the National Institute for Health and Care Excellence (NICE),[102] nor the American College of Physicians[103] list violence among the potential side effects of treatment with serotonin selective reuptake inhibitors. Similarly, the World Health Organization and the European Psychiatric Association do not list violence among the potential side effects of SSRIs.[104][105]

Psychiatrist David Healy and certain patient activist groups have compiled case reports of violent acts committed by individuals taking fluoxetine or other SSRIs,[106][107] and have argued that these drugs predispose susceptible individuals to commit violent acts.

Serial case report studies of this type have been criticized as being subject to "confounding by indication", in which effects due to an underlying disease state are mistakenly attributed to the effects of treatment.[108] Other studies, including randomized clinical trials and observational studies, have suggested that fluoxetine and other SSRIs may reduce the propensity for violence. A randomized clinical trial performed by the US National Institutes for Mental Health found that fluoxetine reduced acts of domestic violence in alcoholics with a history of such behavior[109] A second clinical trial performed at the University of Chicago found that fluoxetine reduced aggressive behavior in patients in intermittent aggressive disorder.[110] A clinical trial found that fluoxetine reduced aggressive behavior in patients with borderline personality disorder.[111] These results are indirectly supported by studies demonstrating that other SSRIs can reduce violence and aggressive behavior.[112][113][114][115] A NBER study examining international trends in antidepressant use and crime rates in the 1990s found that increases in antidepressant drug prescriptions were associated with reductions in violent crime.[116]

Brand names

Fluoxetine is available under many brand names internationally. The table below provides a listing of these and the countries they are marketed in.

Table of brand names for fluoxetine pills
( † indicates discontinued brands):[35][117]
  • Actan (CL)
  • Adofen (ES)
  • Affex (IE)
  • Alental (AR)
  • Alentol (CL)
  • Andepin (PL)
  • Animex-On (AR)
  • Anismol (CL)
  • Ansilan (CO)
  • Anxetin (TN)
  • Ao Mai Lun (CN)
  • Apinrol (CL)
  • Apo-fluoxetine (CN, RU, TW)
  • Auscap (AU)
  • Bellzac (IE)
  • Bioxetin (PL)
  • Biozac (BG, IE)
  • Daforin (BR)
  • Dawnex (IN)
  • Deprexetin (BG, PL, LT)
  • Deprimaks (LT)
  • Depten (IN)
  • Depten-AZ (IN)
  • Depten-OZ (IN)
  • Depzac (IN)
  • Dinalexin (TN)
  • Doc Fluoxetine (LU)
  • Dominium (EC, CL)
  • Eburnate (AR)
  • Felicium (AT, UK†)
  • Felixina (AR)
  • Floccin (AT)
  • Florak (TR)
  • Floxet (BG)
  • Fluctine (AT, MX†, CH)
  • Fludac (GE, IN)
  • Fludawn (IN)
  • Fludep (IN)
  • Fludep (IN)
  • Fludep Plus (IN)
  • Flumed (TH)
  • Flunil-20 (GE)
  • Flunirin (RS)
  • Flunisan (MK, RS)
  • Fluocim (CH†)
  • Fluohexal (AU†)
  • Fluoksetin (MK, RS)
  • Fluovex (MY)
  • Fluox (BE, NZ, KR)
  • Fluoxac (MX)
  • FluoxeLich (DE)
  • Fluoxemed (BE†)
  • Fluoxe-Q (DE†)
  • Fluoxeren (IT)
  • Fluoxgamma (DE)
  • Fluoxin (RO)
  • Fluoxiram (AR)
  • Fluoxone (BE)
  • Fluronin (TW)
  • Flusac (TH)
  • Flusetin (HR)
  • Flustad (NL)
  • Flutin (DK, OM)
  • Flutine (IL, TH)
  • Fluval (HR)
  • Flux Hexal (AT)
  • Flux (EE, LT, TW)
  • Fluxadir (GR)
  • Fluxemed (EE, LT)
  • Fluxen (TW)
  • Fluxene (BR)
  • Fluxet (DE)
  • Fluxetil (MY, SG†, TH)
  • Fluxetin (HK, SG)
  • Fluxetin Atlantic (TH)
  • Fluxil (AT†, HK, SG)
  • Fluxomed (AT)
  • Fluzac (IE, VE)
  • Fluzac-20 (TH)
  • Fluzak (CZ)
  • Fluzyn (OM)
  • Fokeston (GR)
  • Fontex D.A.C. (BE, DK, FL†, IS, LU, NO, SE)
  • Fontex (DK)
  • Fonzac (TW)
  • Foxetin (AR, KR)
  • Framex (RS)
  • Fropine (KR)
  • Fulsac (TR)
  • FXT (CA†)
  • Gerozac (IE)
  • Hapilux (GR)
  • Indozul (MX)
  • Jin Kai Ke (CN)
  • Juxac (TW)
  • Kai Ke (CN)
  • Kalxetin (ID)
  • Ladose (GR)
  • Lapsus (AR)
  • Lebensart (MX)
  • Lecimar (ES)
  • Linz (BH, OM)
  • Lorien (ZA)
  • Lovan (AU, NZ†)
  • Luramon (ES)
  • Magrilan (CZ, HK†, MT, RO, SG, SK, TH)
  • Mitilase (AR)
  • Modipran (BD)
  • Moltoben (CO, DO, GT, HN, PA, SV)
  • Mutan (AT)
  • Nerbet (CL)
  • Nervosal (AR)
  • Neupax (AR, CR, DO, EC, GT, HN, PA, SV)
  • Neuxetin (PH)
  • Nodep (BD)
  • Nortec (BR)
  • Norzac (IE)
  • Noxetine (ID)
  • Nuzak (ZA)
  • Nycoflox (EE, LT)
  • Orthon (GR)
  • Ovisen (MX)
  • Oxactin (UK, MT)
  • Oxedep (VN)
  • Oxetine (TH)
  • Oxipres (ID)
  • Oxsac (TH)
  • Pisaurit (MX)
  • Plazeron (MT)
  • Portal (HU, LT, CZ, HR)
  • Positivum (AT)
  • Pragmaten (CL)
  • Prizma (IL)
  • Proctin (KR)
  • Prodep (RU)
  • Prodin (PH)
  • Profluzac (RU)
  • Prohexal (ZA)
  • Prolert (BD)
  • Proren (KR)
  • Prozac (AR, AU, BE, BR, CA, CL, CN, CZ, FR, HK, HU, ID, IE, IT, MY, MX, NL, NZ, PH, PT, RU, ZA, SG, TH, TR, UK, US, VE)
  • Prozac Bb Farma (IT)
  • Prozac Dispersable (MX)
  • Prozamel (IE)
  • Prozatan (IE†)
  • Prozen (BR)
  • Prozit (IE, UK)
  • Prozep (IE, UK)
  • Psipax (PT)
  • Psiquial (BR)
  • Qualisac (HK)
  • Ranflocs (ZA)
  • Ranflutin (BG)
  • Reconcile (US) (only used for veterinary use)
  • Reneuron (ES)
  • Roxetin (KR)
  • Salipax (LT, MY, PL, SI)
  • Sarafem (US)
  • Sartuzin (GR)
  • Saurat (AR)
  • Selectine (KR)
  • Selectus (PT)
  • Serol (IS)
  • Seromex (FL)
  • Seronil (FL, PL)
  • Sinzac (MY)
  • Sofelin (GR)
  • Sofluxen (BG)
  • Stapiadilat (GR)
  • Stapiadilat-S (GR)
  • Stressless (GR)
  • Thiramil (GR)
  • Trizac (ET)
  • T-Zac (TW)
  • Ultiflox (CL)
  • Unprozy (TH)
  • U-Zet (TW)
  • Verotina (BR)
  • Xeredien (IT)
  • Xetiran (PL)
  • Youke (CN)
  • Zac (ID)
  • Zactin (AU, CN, ID†, SG, TW)
  • Zedprex (TR)
  • Zinovat (GR)
  • Zyfloxin (BR)

In combination with the atypical antipsychotic olanzapine it is known by a few brand names,including,

Table of brand names for fluoxetine/olanzapine combination pill
( † indicates discontinued brands):[35][118]
  • Symbyax
  • Alamflu
  • Alp-FT
  • Altin
  • Ateez-F
  • Azo-F
  • Cinol Forte
  • Cinol Plus
  • Cooltime
  • Coral-F
  • Depten-AZ
  • Depten-OZ
  • Depwell
  • Exiten Plus
  • Faa Plus
  • Faxtin-A
  • Fiden-AZ
  • Fludep Plus
  • Fludep-AZ
  • Flumusa
  • Fluwel
  • Fluxin-AL
  • Fluzolam
  • Kurelam-F
  • L-Peez F
  • M-Olan Plus
  • Oladay-F
  • Olanex-F
  • Olapin Forte
  • Olapin Plus
  • Olorest-F
  • Symbyax

See also

References

  1. ^ a b c d e Altamura, AC; Moro, AR; Percudani, M (March 1994). "Clinical Pharmacokinetics of Fluoxetine" (PDF). Clinical Pharmacokinetics 26 (3): 201–214.  
  2. ^ a b c d e f g h i j k l m "PROZAC® Fluoxetine Hydrochloride" (PDF). TGA eBusiness Services. Eli Lilly Australia Pty. Limited. 9 October 2013. Retrieved 23 November 2013. 
  3. ^ a b c d e "FLUOXETINE HYDROCHLORIDE capsule [Sandoz Inc]". DailyMed. Sandoz Inc. January 2013. Retrieved 23 November 2013. 
  4. ^ a b c d e "Fluoxetine 20 mg Capsules - Summary of Product Characteristics (SPC)". electronic Medicines Compendium. Accord Healthcare Limited. 21 November 2012. Retrieved 23 November 2013. 
  5. ^ a b c d e "Prozac, Sarafem (fluoxetine) dosing, indications, interactions, adverse effects, and more". Medscape Reference. WebMD. Retrieved 23 November 2013. 
  6. ^ a b c Wong, David T.; Horng, Jong S.; Bymaster, Frank P.; Hauser, Kenneth L.; Molloy, Bryan B. (1974). "A selective inhibitor of serotonin uptake: Lilly 110140, 3-(p-Trifluoromethylphenoxy)-n-methyl-3-phenylpropylamine". Life Sciences 15 (3): 471–9.  
  7. ^ "Drugs@FDA: FDA Approved Drug Products". 
  8. ^ Generic Prozac' expected to be cleared for sale"'". CNN. 1 Aug 2001. Retrieved 27 Dec 2012. 
  9. ^ a b c "Prozac Pharmacology, Pharmacokinetics,Studies, Metabolism". RxList.com. 2007. Retrieved April 14, 2007. 
  10. ^ a b Randi Jenssen Hagerman (16 September 1999). Neurodevelopmental Disorders: Diagnosis and Treatment.  
  11. ^ a b Verispan. "Top 200 Generic Drugs by Units in 2010" (PDF). Drug Topics. 
  12. ^ Patrisha Macnair (September 2012). "BBC - Health: Prozac". BBC. Archived from the original on 2012-12-11. In 2011 over 43 million prescriptions for antidepressants were handed out in the UK and about 14 per cent (or nearly 6 million prescriptions) of these were for a drug called fluoxetine, better known as Prozac. 
  13. ^ "WHO Model List of Essential Medicines" (PDF). World Health Organization. October 2013. Retrieved 22 April 2014. 
  14. ^ Truven Health Analytics, Inc. DrugPoint® System (Internet) [cited 2013 Oct 4]. Greenwood Village, CO: Thomsen Healthcare; 2013.
  15. ^ Australian Medicines Handbook 2013. The Australian Medicines Handbook Unit Trust; 2013.
  16. ^ British National Formulary (BNF) 65. Pharmaceutical Pr; 2013.
  17. ^ "Fluoxetine Hydrochloride". The American Society of Health-System Pharmacists. Retrieved April 3, 2011. 
  18. ^ "NIMH•Eating Disorders". The National Institute of Mental Health. National Institute of Health. 2011. Retrieved 25 November 2013. 
  19. ^ Williams, K. (August 2010). "Selective serotonin reuptake inhibitors (SSRIs) for autism spectrum disorders (ASD)". Cochrane Database Systematic Review 8: CD004677.  
  20. ^ Myers, SM (August 2007). "The status of pharmacotherapy for autism spectrum disorders". Expert Opinion on Pharmacotherapy 8 (11): 1579–1603.  
  21. ^ Doyle, CA; McDougle, CJ (August 2012). "Pharmacotherapy to control behavioral symptoms in children with autism". Expert Opinion on Pharmacotherapy 13 (11): 1615–1629.  
  22. ^ Benvenuto, A; Battan, B; Porfirio, MC; Curatolo, P (February 2013). "Pharmacotherapy of autism spectrum disorders". Brain and Development 35 (2): 119–127.  
  23. ^ Kirsch, Irving; Deacon, BJ; Huedo-Medina, TB; Scoboria, A; Moore, TJ; Johnson, BT (2008). "Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration". PLoS Medicine (PLoS Med) 5 (2): e45.  
  24. ^ Fournier, Jay C.; Jay C. Fournier, MA; Robert J. DeRubeis, PhD; Steven D. Hollon, PhD; Sona Dimidjian, PhD; Jay D. Amsterdam, MD; Richard C. Shelton, MD; Jan Fawcett, MD (2010). "Antidepressant Drug Effects and Depression Severity". The Journal of the American Medical Association 303 (1): 47–53.  
  25. ^ Gibbons RD, Hur K, Brown CH, Davis JM, Mann JJ (June 2012). "Benefits from antidepressants: synthesis of 6-week patient-level outcomes from double-blind placebo-controlled randomized trials of fluoxetine and venlafaxine". Arch. Gen. Psychiatry 69 (6): 572–9.  
  26. ^ Moncrieff, Joanna (2009). The Myth of the Chemical Cure: A Critique of Psychiatric Drug Treatment (Revised Edition). Basingstoke, UK: Palgrave Macmillan.  
  27. ^ "CG90 Depression in adults: full guidance". 
  28. ^ "PsychiatryOnline | APA Practice Guidelines | Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition". 
  29. ^ a b "www.accessdata.fda.gov". 
  30. ^ "Practice parameter for the assessment and treatment of children and adolescents with obsessive-compulsive disorder.". J Am Acad Child Adolesc Psychiatry 51 (1): 98–113. January 2012.  
  31. ^ "www.wfsbp.org". 
  32. ^ Taurines, R; Gerlach, M; Warnke, A; Thome, J; Wewetzer, C (September 2011). "Pharmacotherapy in depressed children and adolescents". The World Journal of Biological Psychiatry 12 (Suppl 1): 11–15.  
  33. ^ 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.  
  34. ^ Morrison, JL; Riggs, KW; Rurak, DW (March 2005). "Fluoxetine during pregnancy: impact on fetal development". Reproduction, Fertility and Development 17 (6): 641–650.  
  35. ^ a b c d e Brayfield, A, ed. (13 August 2013). Fluoxetine Hydrochloride. Martindale: The Complete Drug Reference (London, UK: Pharmaceutical Press). Retrieved 24 November 2013. 
  36. ^ "Fluoxetine in pregnancy: slight risk of heart defects in unborn child" (PDF). MHRA. Medicines and Healthcare Products Regulatory Agency. 10 September 2011. Retrieved 23 November 2013. 
  37. ^ http://www.jogc.com/abstracts/full/201304_DrugsinPregnancy_1.pdf
  38. ^ http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/018936s091lbl.pdf
  39. ^ http://jhl.sagepub.com.proxy1.lib.tju.edu/content/26/2/187.full.pdf+html
  40. ^ Taylor, D; Paton, C; Shitij, K (2012). The Maudsley prescribing guidelines in psychiatry. West Sussex: Wiley-Blackwell.  
  41. ^ a b Bland RD, Clarke TL, Harden LB, et al. (February 1976). "Rapid infusion of sodium bicarbonate and albumin into high-risk premature infants soon after birth: a controlled, prospective trial". Am. J. Obstet. Gynecol. 124 (3): 263–7.  
  42. ^ a b Koda-Kimble, MA; Alldredge, BK (2012). Applied therapeutics: the clinical use of drugs (10th ed.). Baltimore: Wolters Kluwer Health/Lippincott Williams & Wilkins.  
  43. ^ a b Leo, Raphael J. (1996). "Movement Disorders Associated with the Serotonin Selective Reuptake Inhibitors". The Journal of Clinical Psychiatry 57 (10): 449–54.  
  44. ^ a b Gerber, P.; Lynd, LD (1998). "Selective serotonin-reuptake inhibitor-induced movement disorders". Annals of Pharmacotherapy 32 (6): 692–8.  
  45. ^ a b Caley, CF (1997). "Extrapyramidal reactions and the selective serotonin-reuptake inhibitors". The Annals of pharmacotherapy 31 (12): 1481–9.  
  46. ^ Clark MS, Jansen K, Bresnahan M (November 2013). "Clinical inquiry: How do antidepressants affect sexual function?". J Fam Pract 62 (11): 660–1.  
  47. ^ Csoka AB, Csoka A, Bahrick A, Mehtonen OP (2008). "Persistent sexual dysfunction after discontinuation of selective serotonin reuptake inhibitors". The Journal of Sexual Medicine 5 (1): 227–33.  
  48. ^ Kauffman, Robert P; Amanda Murdock (2007). "Prolonged Post-Treatment Genital Anesthesia and Sexual Dysfunction Following Discontinuation of Citalopram and the Atypical Antidepressant Nefazodone". The Open Women's Health Journal 1: 1–3.  
  49. ^ Csoka AB, Shipko S (2006). "Persistent sexual side effects after SSRI discontinuation". Psychotherapy and Psychosomatics 75 (3): 187–8.  
  50. ^ Bolton JM, Sareen J, Reiss JP (September 2006). "Genital Anaesthesia Persisting Six Years after Sertraline Discontinuation". Journal of Sex & Marital Therapy 32 (4): 327–330.  
  51. ^ a b Blum, Diana; Maldonado, José; Meyer, Everett; Lansberg, Maarten (2008). "Delirium following abrupt discontinuation of fluoxetine". Clinical Neurology and Neurosurgery 110 (1): 69–70.  For the earlier case reports see the references cited therein.
  52. ^ Rosenbaum, JF; Zajecka, J (1997). "Clinical management of antidepressant discontinuation". The Journal of clinical psychiatry. 58 Suppl 7: 37–40.  
  53. ^ Schatzberg, AF; Blier, P; Delgado, PL; Fava, M; Haddad, PM; Shelton, RC (2006). "Antidepressant discontinuation syndrome: Consensus panel recommendations for clinical management and additional research". The Journal of clinical psychiatry. 67 Suppl 4: 27–30.  
  54. ^ Fava, M (2006). "Prospective studies of adverse events related to antidepressant discontinuation". The Journal of clinical psychiatry. 67 Suppl 4: 14–21.  
  55. ^ Zajecka, John; Fawcett, Jan; Amsterdam, Jay; Quitkin, Frederic; Reimherr, Frederick; Rosenbaum, Jerrold; Michelson, David; Beasley, Charles (1998). "Safety of Abrupt Discontinuation of Fluoxetine". Journal of Clinical Psychopharmacology 18 (3): 193–7.  
  56. ^ Gartlehner, G; Hansen, RA; Thieda, P; Deveaugh-Geiss, AM; Gaynes, BN; Krebs, EE; Lux, LJ; Morgan, LC; Shumate, JA (January 2007). Comparative Effectiveness of Second-Generation Antidepressants in the Pharmacologic Treatment of Adult Depression (PDF). Comparative Effectiveness Reviews (7). Rockville, MD: Agency for Healthcare Research and Quality (US).  
  57. ^ Levenson M, Holland C. "Antidepressants and Suicidality in Adults: Statistical Evaluation. (Presentation at Psychopharmacologic Drugs Advisory Committee; December 13, 2006)". Retrieved May 13, 2007. 
  58. ^ a b Stone MB, Jones ML (November 17, 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 September 22, 2007. 
  59. ^ a b Levenson M, Holland C (November 17, 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 September 22, 2007. 
  60. ^ Klein, Donald F (2005). "The Flawed Basis for FDA Post-Marketing Safety Decisions: The Example of Anti-Depressants and Children". Neuropsychopharmacology 31 (4): 689–99.  
  61. ^ Tarek A. Hammad (September 13, 2004). "Results of the Analysis of Suicidality in Pediatric Trials of Newer Antidepressants" (PDF). Presentation at the Meeting of Psychopharmacologic Drugs Advisory Committee and the Pediatric Advisory Committee on September 13, 2004. FDA. Pages 25, 28. Retrieved 2008-01-06.
  62. ^  
  63. ^ 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.  
  64. ^ Ciraulo, DA; Shader, RI, ed. (2011). Pharmacotherapy of Depression. SpringerLink (2nd ed.) (New York, NY: Humana Press).  
  65. ^ a b Sandson, Neil B.; Armstrong, Scott C.; Cozza, Kelly L. (2005). "An Overview of Psychotropic Drug-Drug Interactions". Psychosomatics 46 (5): 464–94.  
  66. ^ An extensive list of possible interactions is available in Lexi-Comp (September 2008). "Fluoxetine".   Retrieved on December 28, 2008.
  67. ^ Mandrioli, R.; Forti, G. C.; Raggi, M. A. (2006). "Fluoxetine Metabolism and Pharmacological Interactions: The Role of Cytochrome P450". Current Drug Metabolism 7 (2): 127–33.  
  68. ^ Hiemke, Christoph; Härtter, Sebastian (2000). "Pharmacokinetics of selective serotonin reuptake inhibitors". Pharmacology & Therapeutics 85: 11.  
  69. ^ a b Burke, William J.; Hendricks, Shelton E.; McArthur-Miller, Delores; Jacques, Daniel; Bessette, Diane; McKillup, Tracy; Stull, Todd; Wilson, James (2000). "Weekly Dosing of Fluoxetine for the Continuation Phase of Treatment of Major Depression: Results of a Placebo-Controlled, Randomized Clinical Trial". Journal of Clinical Psychopharmacology 20 (4): 423–7.  
  70. ^ "Drug Treatments in Psychiatry: Antidepressants".  
  71. ^ a b Pérez, Victor; Puiigdemont, Dolors; Gilaberte, Inmaculada; Alvarez, Enric; Artigas, Francesc; Grup de Recerca en Trastorns Afectius (2001). "Augmentation of Fluoxetine's Antidepressant Action by Pindolol: Analysis of Clinical, Pharmacokinetic, and Methodologic Factors". Journal of Clinical Psychopharmacology 21 (1): 36–45.  
  72. ^ Brunswick, David J.; Amsterdam, Jay D.; Fawcett, Jan; Quitkin, Frederic M.; Reimherr, Frederick W.; Rosenbaum, Jerrold F.; Beasley Jr, Charles M. (2002). "Fluoxetine and norfluoxetine plasma concentrations during relapse-prevention treatment". Journal of Affective Disorders 68 (2–3): 243–9.  
  73. ^ a b c Henry, Michael E; Schmidt, Mark E; Hennen, John; Villafuerte, Rosemond A; Butman, Michelle L; Tran, Pierre; Kerner, Lynn T; Cohen, Bruce; Renshaw, Perry F (2005). "A Comparison of Brain and Serum Pharmacokinetics of R-Fluoxetine and Racemic Fluoxetine: A 19-F MRS Study". Neuropsychopharmacology 30 (8): 1576–83.  
  74. ^ Kinnunen, Leann H.; Moltz, Howard; Metz, John; Cooper, Malcolm (2004). "Differential brain activation in exclusively homosexual and heterosexual men produced by the selective serotonin reuptake inhibitor, fluoxetine". Brain Research 1024 (1–2): 251–4.  
  75. ^ Lemberger, L; Bergstrom, RF; Wolen, RL; Farid, NA; Enas, GG; Aronoff, GR (1985). "Fluoxetine: Clinical pharmacology and physiologic disposition". The Journal of clinical psychiatry 46 (3 Pt 2): 14–9.  
  76. ^ Pato, MT; Murphy, DL; Devane, CL (1991). "Sustained plasma concentrations of fluoxetine and/or norfluoxetine four and eight weeks after fluoxetine discontinuation". Journal of Clinical Psychopharmacology 11 (3): 224–5.  
  77. ^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 645–648.
  78. ^ Perry, K. W.; Fuller, R. W. (1997). "Fluoxetine increases norepinephrine release in rat hypothalamus as measured by tissue levels of MHPG-SO4 and microdialysis in conscious rats". Journal of Neural Transmission 104 (8–9): 953–66.  
  79. ^ Bymaster, Frank; Zhang, Wei; Carter, Petra; Shaw, Janice; Chernet, Eyassu; Phebus, Lee; Wong, David; Perry, Kenneth (2002). "Fluoxetine, but not other selective serotonin uptake inhibitors, increases norepinephrine and dopamine extracellular levels in prefrontal cortex". Psychopharmacology 160 (4): 353–61.  
  80. ^ a b Koch, S; Perry, KW; Nelson, DL; Conway, RG; Threlkeld, PG; Bymaster, FP (2002). "R-fluoxetine Increases Extracellular DA, NE, As Well As 5-HT in Rat Prefrontal Cortex and Hypothalamus an in vivo Microdialysis and Receptor Binding Study". Neuropsychopharmacology 27 (6): 949–59.  
  81. ^ Bymaster, Frank; Zhang, Wei; Carter, Petra; Shaw, Janice; Chernet, Eyassu; Phebus, Lee; Wong, David; Perry, Kenneth (2002). "Fluoxetine, but not other selective serotonin uptake inhibitors, increases norepinephrine and dopamine extracellular levels in prefrontal cortex". Psychopharmacology 160 (4): 353–61.  
  82. ^ Miguelez, C.; Fernandez-Aedo, I.; Torrecilla, M.; Grandoso, L.; Ugedo, L. (2009). "Α2-Adrenoceptors mediate the acute inhibitory effect of fluoxetine on locus coeruleus noradrenergic neurons". Neuropharmacology 56 (6–7): 1068–73.  
  83. ^ De-Spinning In Vitro Data.
  84. ^ De Gandarias, Juan Manuel; Echevarría, Enrique; Acebes, Iñaky; Abecia, Luis C; Casis, Oscar; Casis, Luis (1999). "Effects of fluoxetine administration on mu-opioid receptor immunostaining in the rat forebrain". Brain Research 817 (1–2): 236–40.  
  85. ^ Fuller RW, Perry KW, Molloy BB (September 1974). "Effect of an uptake inhibitor on serotonin metabolism in rat brain: studies with 3-(p-trifluoromethylphenoxy)-N-methyl-3-phenylpropylamine (Lilly 110140)". Life Sciences 15 (6): 1161–71.  
  86. ^ Tatsumi M, Groshan K, Blakely RD, Richelson E (December 1997). "Pharmacological profile of antidepressants and related compounds at human monoamine transporters". European Journal of Pharmacology 340 (2–3): 249–58.  
  87. ^ Pälvimäki EP, Roth BL, Majasuo H, et al. (August 1996). "Interactions of selective serotonin reuptake inhibitors with the serotonin 5-HT2c receptor". Psychopharmacology 126 (3): 234–40.  
  88. ^ Narita N, Hashimoto K, Tomitaka S, Minabe Y (June 1996). "Interactions of selective serotonin reuptake inhibitors with subtypes of sigma receptors in rat brain". European Journal of Pharmacology 307 (1): 117–9.  
  89. ^ Hashimoto K (September 2009). "Sigma-1 receptors and selective serotonin reuptake inhibitors: clinical implications of their relationship". Central Nervous System Agents in Medicinal Chemistry 9 (3): 197–204.  
  90. ^ "Fluoxetine". IUPHAR Guide to Pharmacology. IUPHAR. Retrieved 10 November 2014. 
  91. ^ "Calcium activated chloride channel". IUPHAR Guide to Pharmacology. IUPHAR. Retrieved 10 November 2014. 
  92. ^ Roth, BL; Driscol, J (12 January 2011). Database"i"PDSP K. Psychoactive Drug Screening Program (PDSP). University of North Carolina at Chapel Hill and the United States National Institute of Mental Health. Retrieved 24 June 2013. 
  93. ^ Wong, David T.; Bymaster, Frank P.; Engleman, Eric A. (1995). "Prozac (fluoxetine, lilly 110140), the first selective serotonin uptake inhibitor and an antidepressant drug: Twenty years since its first publication". Life Sciences 57 (5): 411–41.  
  94. ^ a b Breggin, Peter R.; Ginger Ross Breggin (1995). Talking Back to Prozac.  
  95. ^ Swiatek, Jeff (August 2, 2001). "Prozac's profitable run coming to an end for Lilly". The Indianapolis Star. 
  96. ^ "Electronic Orange Book". Food and Drug Administration. April 2007. Retrieved May 24, 2007. 
  97. ^ "Patent Expiration Dates for Common Brand-Name Drugs". Retrieved July 20, 2007. 
  98. ^ Class, Selena (December 2, 2002). "Pharma Overview". Retrieved June 15, 2009. 
  99. ^ "Press Release – FAA Proposes New Policy on Antidepressants for Pilots". Faa.gov. April 2, 2010. Retrieved February 10, 2012. 
  100. ^ Ravilious, K (July 16, 2010). "Prozac Pollution Making Shrimp Reckless". National Geographic. Retrieved 25 November 2013. 
  101. ^ "PsychiatryOnline | APA Practice Guidelines | Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition". 
  102. ^ http://guidance.nice.org.uk/CG90
  103. ^ "Annals of Internal Medicine | Comparative Benefits and Harms of Second-Generation Antidepressants: Background Paper for the American College of Physicians". 
  104. ^ "whqlibdoc.who.int". 
  105. ^ Möller HJ, Bitter I, Bobes J, Fountoulakis K, Höschl C, Kasper S (February 2012). "Position statement of the European Psychiatric Association (EPA) on the value of antidepressants in the treatment of unipolar depression". Eur. Psychiatry 27 (2): 114–28.  
  106. ^ Healy, David; Herxheimer, Andrew; Menkes, David B. (2006). "Antidepressants and Violence: Problems at the Interface of Medicine and Law". PLoS Medicine 3 (9): e372.  
  107. ^ Breggin, Peter R.; Ginger Ross Breggin (1995). Talking Back to Prozac.  
  108. ^ "Causation, bias and confounding: a hitchhiker's guide to the epidemiological galaxy". 
  109. ^ George DT, Phillips MJ, Lifshitz M, et al. (January 2011). "Fluoxetine treatment of alcoholic perpetrators of domestic violence: a 12-week, double-blind, randomized, placebo-controlled intervention study". J Clin Psychiatry 72 (1): 60–5.  
  110. ^ Coccaro EF, Lee RJ, Kavoussi RJ (May 2009). "A double-blind, randomized, placebo-controlled trial of fluoxetine in patients with intermittent explosive disorder". J Clin Psychiatry 70 (5): 653–62.  
  111. ^ Coccaro EF, Kavoussi RJ (December 1997). "Fluoxetine and impulsive aggressive behavior in personality-disordered subjects". Arch. Gen. Psychiatry 54 (12): 1081–8.  
  112. ^ Stark LJ, Spirito A, Williams CA, Guevremont DC (April 1989). "Common problems and coping strategies. I: Findings with normal adolescents". J Abnorm Child Psychol 17 (2): 203–12.  
  113. ^ Berman ME, McCloskey MS, Fanning JR, Schumacher JA, Coccaro EF (June 2009). "Serotonin augmentation reduces response to attack in aggressive individuals". Psychol Sci 20 (6): 714–20.  
  114. ^ McCloskey MS, Berman ME, Echevarria DJ, Coccaro EF (April 2009). "Effects of acute alcohol intoxication and paroxetine on aggression in men". Alcohol. Clin. Exp. Res. 33 (4): 581–90.  
  115. ^ Cherek DR, Lane SD, Pietras CJ, Steinberg JL (January 2002). "Effects of chronic paroxetine administration on measures of aggressive and impulsive responses of adult males with a history of conduct disorder". Psychopharmacology (Berl.) 159 (3): 266–74.  
  116. ^ Marcotte, DE; Markowitz, S (September 2009). "A Cure For Crime? Psycho-Pharmaceuticals and Crime Trends" (PDF). Nber Working Paper Series. Cambridge, MA: The National Bureau of Economic Research. Retrieved 25 November 2013. 
  117. ^ "Fluoxetine". Drugs.com. 2013. Retrieved 25 November 2013. 
  118. ^ "Fluoxetine". Drugs.com. 2013. Retrieved 25 November 2013. 

External links

  • Trouble in Prozac, from Fortune magazine
  • Fluoxetine, from the United States National Library of Medicine's Drug Information Portal
  • Biographies of inventors:
    • David T. Wong, from Nature
    • Bryan B. Molloy, from Invent Now
5-HT1A agonists
GABAAR PAMs
α2δ VDCC blockers
Antidepressants
Sympatholytics
Others

: PSO/PSI

(, , , , , , ), /,

proc (/), drug (/////)

Antidepressants
Others
Receptor
Ligands
Unknown
interaction
Corporate directors
Products
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 


Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.