|Systematic (IUPAC) name|
|Trade names||Prozac, among others|
|Licence data||US FDA:|
|Metabolism||Hepatic (mostly CYP2D6-mediated)|
|Half-life||1–3 days (acute)
4–6 days (chronic)
|Excretion||Urine (80%), faeces (15%)|
|Mol. mass||309.33 g·mol−1|
|Melt. point||179–182 °C (354–360 °F)|
|Boiling point||395 °C (743 °F)|
|Solubility in water||14 mg/mL (20 °C)|
|(what is this?)|
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. It was approved by the U.S. Food and Drug Administration for the treatment of major depressive disorder in December 1987. The U.S. fluoxetine patent expired in August 2001 and hence generic formulations are now available in the U.S..
Fluoxetine is used for the treatment of major depressive disorder (including pediatric depression), obsessive-compulsive disorder (in both adults and children), bulimia nervosa, panic disorder and premenstrual dysphoric disorder. In addition, fluoxetine is used to treat trichotillomania if cognitive behaviour therapy has been unsuccessful.
In 2010, over 24.4 million prescriptions for generic formulations of fluoxetine were filled in the United States, making it the third most prescribed antidepressant after sertraline and citalopram. In 2011, 6 million prescriptions for fluoxetine were filled in the United Kingdom. It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.
- 1 Medical uses
- 2 Adverse effects
- 3 Pharmacokinetics
- 4 Pharmacodynamics
- 5 Mechanism of action
- 6 History
- 7 Society and culture
- 8 Notes
- 9 See also
- 10 References
- 11 External links
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. It has also been used for cataplexy, obesity, and alcohol dependence, as well as binge eating disorder. Fluoxetine has also been tried as a treatment for autism spectrum disorders with moderate success in adults.
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. 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. 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.
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). 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. 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".
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. SSRIs including fluoxetine should be used as first-line therapy, along with CBT, for the treatment of moderate to severe OCD.
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.
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. However, no difference was observed between treatment arms when fluoxetine plus psychotherapy was compared to psychotherapy alone.
In children and adolescents fluoxetine is the antidepressant of choice due to tentative evidence favoring its efficacy and tolerability. In pregnancy, fluoxetine is considered a category C drug. Evidence supporting an increased risk of major fetal malformations resulting from fluoxetine exposure is limited, although the MHRA of the UK has warned prescribers and patients of the potential for fluoxetine exposure in the first trimester (during organogenesis, formation of the fetal organs) to cause a slight increase in the risk of congenital cardiac malformations in the newborn. Furthermore an association between fluoxetine use during the first trimester and an increased risk of minor fetal malformations was been observed in one study.
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).
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. 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." Sertraline is often the preferred SSRI during pregnancy due to the relatively minimal fetal exposure observed and its safety profile while breastfeeding.
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. Fluoxetine is considered the most stimulating of the SSRIs (that is it is most prone to causing insomnia and agitation). It also appears to be the most prone of the SSRIs for producing dermatologic reactions (e.g. urticaria (hives), rash, itchiness, etc.). 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.
|Detailed list of adverse effects by incidence|
Very common (>10% incidence) adverse effects include:
Common (1-10% incidence) adverse effects include:
Unknown frequency adverse effects include:
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%. 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.
Several case reports in the literature describe severe withdrawal or discontinuation symptoms following an abrupt interruption of fluoxetine treatment. 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. 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. 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. 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. According to a 2007 summary report of available evidence, fluoxetine has the lowest incidence of discontinuation syndrome among several antidepressants including paroxetine and venlafaxine.
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. 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.
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%, and in adults decreased the odds of suicidality by approximately 30%. 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%.
Contraindications include prior treatment (within the past two weeks) with MAOIs such as phenelzine and tranylcypromine, due to the potential for serotonin syndrome. Its use should also be avoided in those with known hypersensitivities to fluoxetine or any of the other ingredients in the formulation used. Its use in those concurrently receiving pimozide or Thioridazine is also advised against.
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. 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. This extensive effect on the body's pathways for drug metabolism creates the potential for interactions with many commonly used drugs.
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.
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.
Fluoxetine is metabolized in the liver by isoenzymes of the cytochrome P450 system, including CYP2D6. 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.
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. Similarly, the half-life of norfluoxetine is longer (16 days) after long-term use. 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. Moreover, the brain concentration of fluoxetine and its metabolites keeps increasing through at least the first five weeks of treatment. 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. 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%, 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.
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".
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.
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. 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.
In the opinion of other researchers, however, the magnitude of this effect is unclear. The dopamine and norepinephrine increase was not observed at a smaller, more clinically relevant dose of fluoxetine. 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. 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.
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.
Mechanism of action
Fluoxetine's mechanism of action is predominantly that of a serotonin reuptake inhibitor. 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. 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.
Table 1: Binding affinity (Ki [nM]) of fluoxetine and norfluoxetine towards their molecular targets
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, showed the compound later named fluoxetine to be the most potent and selective inhibitor of serotonin reuptake of the series. Wong published the first article about fluoxetine in 1974. 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.
Fluoxetine appeared on the Belgian market in 1986. In the U.S., the FDA gave its final approval in December 1987, and a month later Eli Lilly began marketing Prozac; annual sales in the U.S. reached $350 million within a year.
A controversy ensued after Lilly researchers published a paper titled "Prozac (fluoxetine, Lilly 110140), the first selective serotonin uptake inhibitor and an antidepressant drug" claiming fluoxetine to be the first selective serotonin reuptake inhibitor (SSRI). Two years later they had to issue a correction, admitting that the first SSRI was zimelidine developed by Arvid Carlsson and colleagues.
Eli Lilly's U.S. patent on Prozac (fluoxetine) expired in August 2001, 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.
There has been research on possible effects of fluoxetine on marine life.
Society and culture
Neither the American Psychiatric Association, the National Institute for Health and Care Excellence (NICE), nor the American College of Physicians 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.
Psychiatrist David Healy and certain patient activist groups have compiled case reports of violent acts committed by individuals taking fluoxetine or other SSRIs, 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. 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 A second clinical trial performed at the University of Chicago found that fluoxetine reduced aggressive behavior in patients in intermittent aggressive disorder. A clinical trial found that fluoxetine reduced aggressive behavior in patients with borderline personality disorder. These results are indirectly supported by studies demonstrating that other SSRIs can reduce violence and aggressive behavior. 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.
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):
|Table of brand names for fluoxetine/olanzapine combination pill|
|( † indicates discontinued brands):
Prozac has had numerous references to it in popular culture, including many books, movies, and songs.
- The book Listening to Prozac was written in 1993 by psychiatrist Peter D. Kramer.
- The memoir Prozac Nation was written in 1994 by Elizabeth Wurtzel; it was made into a film of the same name in 2001, starring Christina Ricci as Wurtzel.
- A well-known book critical of the drug, Talking Back to Prozac, was written by psychiatrist Peter Breggin and published in 1994 (ISBN 0312114869)
- It is mentioned in the Superman graphic novel Red Son, where Brainiac uses it to control people's mood in the Superman's Empire.
- Prozac Diary is a 1998 confessional memoir by Lauren Slater.
- Prosac (a play on Prozac) is among the more notable works by progressive house artist Tomcraft. The main lyrics of the song read from the drug's pharmacological description and indication usages.
- Bernard Sumner (of New Order and Joy Division) chronicled his experience with Prozac and its influence on his creativity in the BBC documentary Prozac Diaries.
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|Wikimedia Commons has media related to Fluoxetine.|
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