|Systematic (IUPAC) name|
|Trade names||Prozac, among others|
|Licence data||US FDA:|
|Pregnancy cat.||C (AU) C (US)|
|Legal status||Prescription Only (S4) (AU) ℞-only (CA) POM (UK) ℞-only (US)|
|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 tradenames 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 presented to the U.S. Food and Drug Administration in February 1977, with Eli Lilly receiving final approval to market the drug in December 1987. Fluoxetine went off-patent in August 2001.
Fluoxetine is approved in the US for the treatment of major depression (including paediatric depression), obsessive-compulsive disorder (in both adult and paediatric populations), bulimia nervosa, panic disorder and premenstrual dysphoric disorder. In addition, fluoxetine is used to treat trichotillomania if cognitive behaviour therapy is unsuccessful. In combination with the atypical antipsychotic olanzapine it is known by a few brand names,[note 1] including its US brand name Symbyax, which is approved for the treatment of depressive episodes as part of bipolar I disorder and in the treatment of treatment-resistant depression.
Despite the availability of newer agents, fluoxetine remains extremely popular. In 2010, over 24.4 million prescriptions for generic formulations of fluoxetine were filled in the United States alone, making it the third most prescribed antidepressant after sertraline (SSRI; became generic in 2006) and citalopram (SSRI; became generic in 2003). In 2011, 6 million prescriptions for fluoxetine were handed out in the UK.
- 1 Medical uses
- 2 Adverse effects
- 3 Pharmacokinetics
- 4 Mechanism of action
- 5 History
- 6 Brand names
- 7 Popular culture
- 8 Notes
- 9 References
- 10 External links
Fluoxetine is frequently used to treat major depression, obsessive compulsive disorder, post-traumatic stress disorder, bulimia nervosa, panic disorder, body dysmorphic disorder, premenstrual dysphoric disorder, and trichotillomania. A recent clinical trial found that in bipolar II disorder fluoxetine was equally effective as lithium in preventing future mood episodes. It has also been used for cataplexy, obesity, and alcohol dependence, as well as binge eating disorder. Fluoxetine has also been tried successfully a treatment for autism.
Fluoxetine was shown to be effective for depression in six-week-long double-blind controlled trials, where it also alleviated anxiety and improved sleep. Fluoxetine was better than placebo for the prevention of depression recurrence when the patients, who originally responded to fluoxetine, were treated for a further 38 weeks. Efficacy of fluoxetine for geriatric, as well as pediatric, depression was also demonstrated in placebo-controlled trials. However two meta-analyses of randomized placebo-controlled trials suggested that in patients with mild or moderate symptoms, the efficacy is clinically insignificant. It has also been 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.
Research suggests that a significant part of the resistance to the SSRIs paroxetine (Paxil) and citalopram (Celexa) can be explained by the genetic variation of Pgp transporter. Paroxetine and citalopram, which are Pgp substrates, are actively transported from the brain by this protein. Fluoxetine is not a substrate of Pgp, and thus a switch from paroxetine or citalopram to fluoxetine may be beneficial to the nonresponders.
OCD was successfully treated by fluoxetine in two adult and one pediatric placebo-controlled 13-week trials. The higher doses of fluoxetine appeared to result in better response, while the reverse relationship was observed in the treatment of depression. Fluoxetine dramatically, by 40–50%, decreased the frequency of panic attacks in two controlled trials of panic disorder patients. In three double-blind trials, fluoxetine significantly decreased the number of binge-eating and purging episodes of bulimia nervosa. Continued year-long treatment of the patients, who originally responded to fluoxetine, was more effective than placebo for the prevention of bulimia nervosa episodes.
Use in special populations
In children and adolescents fluoxetine is the antidepressant of choice due to the relative abundance of evidence favouring its efficacy and its favourable tolerability profile. In pregnancy fluoxetine's use is advised against, the evidence supporting an increased risk of major foetal 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, that is the formation of the foetus' organs) to cause a slight increase in the risk of congenital cardiac malformations in the newborn. Although an associated between fluoxetine use during the first trimester and an increased risk of minor foetal malformations was been observed in one study. Sertraline is usually the preferred SSRI during pregnancy due to the relatively minimal foetal exposure observed. It is secreted in breast milk and hence it is advised that nursing mothers taking fluoxetine should not breastfeed their children.
Adverse effects by incidence
Note: Adverse effects next to a † are serious, that is, they are either life-threatening in the short-term (matter of days or less) or are (usually) irreversible. Adverse effects written in next to a ‡ are potentially (but not usually) irreversible adverse effects. Adverse effects next to a # are those that are most often transient. Adverse effects next to ¤ indicates adverse effects that may indicate, or lead to life-threatening/irreversible conditions if they persist into the long-term.
Very common (>10% incidence) adverse effects include:
- Insomnia# (sleeplessness)
- Anorexia (appetite loss). This may be a desirable effect in obese patients but in children, the underweight, the pregnant and in those affected by the eating disorder, anorexia nervosa, this may be an undesirable effect.
- Asthenia# (weakness)
- Somnolence# (drowsiness)
Common (1-10% incidence) adverse effects include:
- Dry mouth¤ (can lead to dental carries if left uncontrolled)
- Dyspepsia (indigestion)
- Decreased libido‡
- Dysgeusia (abnormal taste)
- QTc interval prolongation†
- Chest pain
- Ear pain
- Hypertension¤ (high blood pressure)
- Increased appetite
- Abnormal/blurred vision#
- Urticaria (hives)
- Pruritus (itchiness)
- Hyperhidrosis (excess sweating)
- Abnormal dreams (including nightmares)
- Sleep disorder
- Tinnitus (hearing ringing in the ears)
- Urinary frequency
- Weight gain or loss
- Arthralgia (joint pain)
- Gynaecological bleeding
- Erectile dysfunction‡ (impotence)
- Ejaculation disorder‡
- Feeling jittery#
- Epistaxis (nose bleed; only common in children and adolescents treated with fluoxetine)
Uncommon (0.1-1% incidence) adverse effects include:
- Elevated mood
- Euphoric mood
- Abnormal thoughts
- Abnormality in or difficulty achieving an orgasm‡ (anorgasmia)
- Bruxism¤ (teeth grinding)
- Dyskinesia (a movement disorder characterized by either a lack of voluntary movement or the presence of involuntary movements)
- Balance disorder
- Akathisia/psychomotor restlessness An inner sense of restlessness that presents itself with the patient's inability to stay still. Usually transient at the beginning of therapy or after an escalation of dosage. It is possible that this symptom may cause sufficient distress to contribute to some of the suicide attempts associated with fluoxetine.
- Mania† (a dangerously elated/irritable mood)
- Buccoglossal syndrome[note 2]
- Myoclonus (spasmodic, jerky movement of muscle groups)
- Mydriasis (dilation of the pupils)
- Hypotension (low blood pressure)
- Dyspnea (air hunger)
- Dysphagia (difficulty/discomfort from swallowing)
- Alopecia (hair loss)
- Increased tendency to bruise/ecchymosis
- Cold sweat
- Feeling abnormal
- Feeling hot or cold
- Dysuria (painful or difficult urination)
Rare (0.01-0.1% incidence) adverse effects include:
- Anaphylactic reaction†
- Serum sickness
- Hyponatremia† (low blood sodium)
- Panic attacks
- Esophageal pain
- Photosensitivity reaction
- Urinary retention† (being unable to pass urine)
- Galactorrhea (lactation that is unrelated to pregnancy or breastfeeding)
- Priapism† (a persistent and painful erection)
Very rare (<0.01% incidence) adverse effects include:
- Thrombocytopaenia† (a drop in platelet count leading to an increased risk of bleeds)
- Serotonin syndrome†
- Orthostatic hypotension (a drop in blood pressure that occurs when one stands up)
Unknown frequency adverse effects include:
- Syndrome of inappropriate secretion of antidiuretic hormone† (SIADH)
- Suicidal thoughts and/or behavior†
- Dysphemia (stuttering)
- Memory impairment
- Pulmonary events
- Gastrointestinal hemorrhage† (bleeding into the digestive tract)
- Hepatitis† (inflammation [swelling] of the liver)
- Erythema multiforme† (a potentially fatal skin reaction)
- Myalgia (muscle ache)
- Micturition disorder (problems with urination)
- Mucosal hemorrhage†
- Tardive dyskinesia† (an often irreversible movement disorder)
- Abnormal liver function tests
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.). Chronic SSRI treatment may also be associated with deficits in concentration and intellectual ability. Flattening of affect can also occur in an otherwise successfully treated with SSRIs patient, whether or not this is due to the drug or the underlying depression is yet to be determined. The aforementioned sexual side effects, although usually reversible, can persist for months, years, or permanently after the drug has been completely withdrawn. This is known as Post SSRI Sexual Dysfunction.
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%.
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.
Contraindications include prior treatment (within the past fortnight) with MAOIs such as phenelzineand 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 is also advised against.
Fluoxetine and norfluoxetine inhibit many isozymes of the cytochrome P450 system that are involved in drug metabolism possible. 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 forinteractions 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".
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.
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.
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 potencygreater 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, presented a new drug request to the U.S. Food and Drug Administration (FDA) for fluoxetine.
In May 1984, Germany’s regulatory agency (BGA) rejected Prozac as "totally unsuitable for treating depression". In May 1985, FDA’s (then) chief safety investigator, Dr. Richard Kapit, wrote: “Unlike traditional tricyclic antidepressants fluoxetine’s profile of adverse side effects more closely resembles that of a stimulant drug than one that causes sedation". He said "It is fluoxetine’s particular profile of adverse side-effects which may perhaps, in the future give rise to the greatest clinical liabilities in the use of this medication to treat depression".
Fluoxetine appeared on the Belgian market in 1986. After over a decade, 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.
A meta-analysis published in February 2008 combined 35 clinical trials of four newer antidepressants (fluoxetine, paroxetine(Paxil), nefazodone (Serzone) and venlafaxine (Effexor)). These antidepressants belonging to three different pharmacological groups were considered together, and the authors did not analyze them separately. The authors concluded that "although the difference [between the placebo and antidepressants] easily attained statistical significance", it did not meet the criterion for clinical significance, as used by the UK's National Institute for Health and Clinical Excellence, "for any but the most severely depressed patients". Some articles in the press using the titles "The creation of the Prozac myth" and "Prozac does not work in majority of depressed patients" presented these general findings about the relative efficacy of antidepressants and placebo as the findings about ineffectiveness of fluoxetine. In a follow-up article, the authors of the meta-analysis noted that "unfortunately, during its initial coverage, the media often portrayed the results as “antidepressants do not work”, which misrepresented our more nuanced pattern of findings".
There has been research on possible effects of fluoxetine on marine life.
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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.
- The 1995 song Country House by Blur sings the lyrics "He's reading Balzac and knocking back Prozac/ It's the helping hand that makes you feel wonderfully bland."
- 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.
- Alison Bechdel's comic book series Dykes to Watch Out For features the character Lois taking Prozac in the 1997 book Hot, Throbbing Dykes to Watch Out for.
- Prozac Diary is a 1998 confessional memoir by Lauren Slater.
- Plato, Not Prozac! is the title of 1999 self help book by Lou Marinoff which proposes classical philosophy as an alternative to conventional pro-pharmaceutical approaches to psychotherapy.
- The Bowling for Soup song 1985 describes a nervous breakdown/midlife crisis of a suburban housewife. It opens with the line "Debbie just hit the wall/she never had it all/One Prozac a day/husband's a CPA..."
- Pets on Prozac was the name of an underground UK house music band which appeared in 2010.
- 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.
- Prozac is often referenced throughout the popular comedic series Ally McBeal where in Season 3 the eponymous character (played by Calista Flockheart) is convinced by her psychiatrist Dr. Shirley Flott (played by Betty White) to take the medication. Flott opines the wondrous benefits of Prozac to almost eucharistic proportions explaining to Ally that she "won't find happiness through love or God: it comes in a pill." Flott also asserts that she herself takes Prozac in suppository form. Though Ally is initially persuaded to take Prozac in order to combat her hallucinations she is later dissuaded by a friend and coworker and ultimately ends up disposing the pills by flushing them down a toilet.
- In the HBO series The Sopranos, mobster Tony Soprano (played by James Gandolfini) is prone to panic attacks. His psychiatrist Dr. Jennifer Melfi (played by Lorraine Bracco) prescribes Prozac as a result.
- Prozac plays an integral role in the plot to the film Love and Other Drugs starring Jake Gyllenhaal who plays a drug salesman for Pfizer who is attempting to promote Zoloft. He discards a large portion of Prozac that is later recovered byhobos and is thereby distributed throughout the country.
- ProzaKc Blues is a song by progressive rock band King Crimson on their 2000 album The ConstruKction of Light.
- Prozac+ is an Italian punk band.
- Including, Symbyax (AR (discontinued), CL, MX, US), 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(all marketed in India)
- The definition of this condition is difficult to come by but it seems to be a form of tardive dyskinesia
- Altamura, AC; Moro, AR; Percudani, M (March 1994). "Clinical Pharmacokinetics of Fluoxetine" (PDF). Clinical Pharmacokinetics 26 (3): 201–214. doi:10.2165/00003088-199426030-00004. PMID 8194283.
- "PROZAC® Fluoxetine Hydrochloride" (PDF). TGA eBusiness Services. Eli Lilly Australia Pty. Limited. 9 October 2013. Retrieved 23 November 2013.
- "FLUOXETINE HYDROCHLORIDE capsule [Sandoz Inc]". DailyMed. Sandoz Inc. January 2013. Retrieved 23 November 2013.
- "Fluoxetine 20 mg Capsules - Summary of Product Characteristics (SPC)". electronic Medicines Compendium. Accord Healthcare Limited. 21 November 2012. Retrieved 23 November 2013.
- "Prozac, Sarafem (fluoxetine) dosing, indications, interactions, adverse effects, and more". Medscape Reference. WebMD. Retrieved 23 November 2013.
- 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. doi:10.1016/0024-3205(74)90345-2. PMID 4549929.
- "'Generic Prozac' expected to be cleared for sale". CNN. 1 Aug 2001. Retrieved 27 Dec 2012.
- "Prozac Pharmacology, Pharmacokinetics,Studies, Metabolism". RxList.com. 2007. Retrieved April 14, 2007.
- Randi Jenssen Hagerman (16 September 1999). Neurodevelopmental Disorders: Diagnosis and Treatment. Oxford University Press. ISBN 019512314X. "Dech and Budow (1991) were among the first to report the anecdotal use of fluoxetine in a case of PWS to control behavior problems, appetite, and trichotillomania."
- Verispan. "Top 200 Generic Drugs by Units in 2010" (PDF). Drug Topics.
- 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."
- "A Randomized Placebo-Controlled Trial of Fluoxetine in Body Dysmorphic Disorder". JAMA psychiatry.
- Truven Health Analytics, Inc. DrugPoint® System (Internet) [cited 2013 Oct 4]. Greenwood Village, CO: Thomsen Healthcare; 2013.
- Australian Medicines Handbook 2013. The Australian Medicines Handbook Unit Trust; 2013.
- British National Formulary (BNF) 65. Pharmaceutical Pr; 2013.
- Amsterdam JD, Shults J. Efficacy and Safety of Long-Term Fluoxetine Versus Lithium Monotherapy of Bipolar II Disorder: A Randomized, Double-Blind, Placebo-Substitution Study. Am J Psychiatry [Internet]. 2010 Jul [cited 2013 Oct 4];167(7):792–800. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896440/
- "Fluoxetine Hydrochloride". The American Society of Health-System Pharmacists. Retrieved April 3, 2011.
- "NIMH•Eating Disorders". The National Institute of Mental Health. National Institute of Health. 2011. Retrieved 25 November 2013.
- Myers, SM (August 2007). "The status of pharmacotherapy for autism spectrum disorders". Expert Opinion on Pharmacotherapy 8 (11): 1579–1603. doi:10.1517/146565126.96.36.1999. PMID 17685878.
- Doyle, CA; McDougle, CJ (August 2012). "Pharmacotherapy to control behavioral symptoms in children with autism". Expert Opinion on Pharmacotherapy 13 (11): 1615–1629. doi:10.1517/14656566.2012.674110. PMID 22550944.
- Benvenuto, A; Battan, B; Porfirio, MC; Curatolo, P (February 2013). "Pharmacotherapy of autism spectrum disorders". Brain and Development 35 (2): 119–127. doi:10.1016/j.braindev.2012.03.015. PMID 22541665.
- "Prozac prescribing information" (PDF). Eli Lilly. June 21, 2007. Retrieved January 9, 2008.
- 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. doi:10.1371/journal.pmed.0050045. PMC 2253608. PMID 18303940.
- 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. doi:10.1001/jama.2009.1943. PMC 3712503. PMID 20051569. Retrieved 24 March 2013.
- Moncrieff, Joanna (2009). The Myth of the Chemical Cure: A Critique of Psychiatric Drug Treatment (Revised Edition). Basingstoke, UK: Palgrave Macmillan. ISBN 9780230574328.
- Uhr, Manfred; Tontsch, Alina; Namendorf, Christian; Ripke, Stephan; Lucae, Susanne; Ising, Marcus; Dose, Tatjana; Ebinger, Martin; Rosenhagen, Marcus et al. (2008). "Polymorphisms in the Drug Transporter Gene ABCB1 Predict Antidepressant Treatment Response in Depression". Neuron 57 (2): 203–9. doi:10.1016/j.neuron.2007.11.017. PMID 18215618.
- Kato, Masaki; Fukuda, Tsuyoshi; Serretti, Alessandro; Wakeno, Masataka; Okugawa, Gaku; Ikenaga, Yuka; Hosoi, Yuka; Takekita, Yoshiteru; Mandelli, Laura et al. (2008). "ABCB1 (MDR1) gene polymorphisms are associated with the clinical response to paroxetine in patients with major depressive disorder". Progress in Neuro-Psychopharmacology and Biological Psychiatry 32 (2): 398–404. doi:10.1016/j.pnpbp.2007.09.003. PMID 17913323.
- 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. doi:10.3109/15622975.2011.600295. PMID 21905988.
- Wagner, KD (June 2005). "Pharmacotherapy for major depression in children and adolescents". Progress in Neuro-Psychopharmacology and Biological Psychiatry 29 (5): 819–826. doi:10.1016/j.pnpbp.2005.03.005. PMID 15908090.
- Morrison, JL; Riggs, KW; Rurak, DW (March 2005). "Fluoxetine during pregnancy: impact on fetal development". Reproduction, Fertility and Development 17 (6): 641–650. doi:10.1071/RD05030. PMID 16263070.
- Brayfield, A, ed. (13 August 2013). "Fluoxetine Hydrochloride". Martindale: The Complete Drug Reference (London, UK: Pharmaceutical Press). Retrieved 24 November 2013.
- "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.
- 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.
- Lipinski Jr, JF; Mallya, G; Zimmerman, P; Pope Jr, HG (1989). "Fluoxetine-induced akathisia: Clinical and theoretical implications". The Journal of clinical psychiatry 50 (9): 339–42. PMID 2549018.
- Leo, Raphael J. (1996). "Movement Disorders Associated with the Serotonin Selective Reuptake Inhibitors". The Journal of Clinical Psychiatry 57 (10): 449–54. doi:10.4088/JCP.v57n1002. PMID 8909330.
- Hansen, Lars (2001). "A critical review of akathisia, and its possible association with suicidal behaviour". Human Psychopharmacology: Clinical and Experimental 16 (7): 495–505. doi:10.1002/hup.325. PMID 12404546.
- Hansen, L.; Kingdom, D (2006). "Akathisia as a risk factor for suicide". The British Journal of Psychiatry 188 (2): 192. doi:10.1192/bjp.188.2.192. PMID 16449715.
- Gerber, P.; Lynd, LD (1998). "Selective serotonin-reuptake inhibitor-induced movement disorders". Annals of Pharmacotherapy 32 (6): 692–8. doi:10.1345/aph.17302. PMID 9640489.
- Caley, CF (1997). "Extrapyramidal reactions and the selective serotonin-reuptake inhibitors". The Annals of pharmacotherapy 31 (12): 1481–9. PMID 9416386.
- Koda-Kimble, MA; Alldredge, BK (2012). Applied therapeutics: the clinical use of drugs (10th ed.). Baltimore: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-1609137137.
- Brunton, L; Chabner, B; Knollman, B (2010). Goodman and Gilman's The Pharmacological Basis of Therapeutics (in English) (12th ed.). New York: McGraw-Hill Professional. ISBN 978-0071624428.
- Csoka, Antonei; Bahrick, Audrey; Mehtonen, Olli-Pekka (2007). "Persistent Sexual Dysfunction after Discontinuation of Selective Serotonin Reuptake Inhibitors". Journal of Sexual Medicine 5 (1): 227–33. doi:10.1111/j.1743-6109.2007.00630.x. PMID 18173768.
- Blum, Diana; Maldonado, José; Meyer, Everett; Lansberg, Maarten (2008). "Delirium following abrupt discontinuation of fluoxetine". Clinical Neurology and Neurosurgery 110 (1): 69–70. doi:10.1016/j.clineuro.2007.08.016. PMID 17913343.For the earlier case reports see the references cited therein.
- Rosenbaum, JF; Zajecka, J (1997). "Clinical management of antidepressant discontinuation". The Journal of clinical psychiatry. 58 Suppl 7: 37–40. PMID 9219493.
- 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. PMID 16683860.
- Fava, M (2006). "Prospective studies of adverse events related to antidepressant discontinuation". The Journal of clinical psychiatry. 67 Suppl 4: 14–21. PMID 16683858.
- 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. doi:10.1097/00004714-199806000-00003. PMID 9617977.
- 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). PMID 20704050.
- Levenson M, Holland C. "Antidepressants and Suicidality in Adults: Statistical Evaluation. (Presentation at Psychopharmacologic Drugs Advisory Committee; December 13, 2006)". Retrieved May 13, 2007.
- 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.
- 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.
- 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. doi:10.1038/sj.npp.1300996. PMID 16395296.
- 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.
- Committee on Safety of Medicines Expert Working Group (December 2004). "Report on The Safety of Selective Serotonin Reuptake Inhibitor Antidepressants" (PDF). MHRA. Retrieved September 25, 2007.
- 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.
- Healy, David; Herxheimer, Andrew; Menkes, David B. (2006). "Antidepressants and Violence: Problems at the Interface of Medicine and Law". PLoS Medicine 3 (9): e372. doi:10.1371/journal.pmed.0030372. PMC 1564177. PMID 16968128.
- Breggin, Peter R.; Ginger Ross Breggin (1995). Talking Back to Prozac. Macmillan Publishers. p. 154. ISBN 978-0-312-95606-6.
- "Causation, bias and confounding: a hitchhiker's guide to the epidemiological galaxy".
- 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. doi:10.4088/JCP.09m05256gry. PMC 3026856. PMID 20673556.
- 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. doi:10.4088/JCP.08m04150. PMID 19389333.
- Coccaro EF, Kavoussi RJ (December 1997). "Fluoxetine and impulsive aggressive behavior in personality-disordered subjects". Arch. Gen. Psychiatry 54 (12): 1081–8. doi:10.1001/archpsyc.1997.01830240035005. PMID 9400343.
- 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. doi:10.1007/BF00913794. PMID 2745900.
- 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. doi:10.1111/j.1467-9280.2009.02355.x. PMC 2728471. PMID 19422623.
- 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. doi:10.1111/j.1530-0277.2008.00872.x. PMID 19183141.
- 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. doi:10.1007/s002130100915. PMID 11862359.
- 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.
- 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.
- Sandson, Neil B.; Armstrong, Scott C.; Cozza, Kelly L. (2005). "An Overview of Psychotropic Drug-Drug Interactions". Psychosomatics 46 (5): 464–94. doi:10.1176/appi.psy.46.5.464. PMID 16145193.
- An extensive list of possible interactions is available in Lexi-Comp (September 2008). "Fluoxetine". The Merck Manual Professional. Retrieved on December 28, 2008.
- 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. doi:10.2174/138920006775541561. PMID 16472103.
- Hiemke, Christoph; Härtter, Sebastian (2000). "Pharmacokinetics of selective serotonin reuptake inhibitors". Pharmacology & Therapeutics 85: 11. doi:10.1016/S0163-7258(99)00048-0.
- 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. doi:10.1097/00004714-200008000-00006. PMID 10917403.
- "Drug Treatments in Psychiatry: Antidepressants". Newcastle University School of Neurology, Neurobiology and Psychiatry. 2005. Retrieved April 14, 2007.
- 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. doi:10.1097/00004714-200102000-00008. PMID 11199945.
- 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. doi:10.1016/S0165-0327(00)00333-5. PMID 12063152.
- 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. doi:10.1038/sj.npp.1300749. PMID 15886723.
- 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. doi:10.1016/j.brainres.2004.07.070. PMID 15451388.
- 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. doi:10.1007/BF01285563. PMID 9451727.
- 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. doi:10.1007/s00213-001-0986-x. PMID 11919662.
- 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. doi:10.1016/S0893-133X(02)00377-9. PMID 12464452.
- 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. doi:10.1007/s00213-001-0986-x. PMID 11919662.only injections of 10 and 20 mg/kg fluoxetine resulted in the increase of all three neurotransmitters. 3 mg/kg increased only serotonin and did not increase dopamine and norepinephrine. The injection with 0.7 mg/kg fluoxetine corresponds to the standard therapeutic dose of luoxetine, see Wyneken, Ursula; Sandoval, Mauricio; Sandoval, Soledad; Jorquera, Franscisco; González, Ignacio; Vargas, Francisco; Falcon, Romina; Monari, Milena; Orrego, Fernando (2006). "Clinically Relevant Doses of Fluoxetine and Reboxetine Induce Changes in the TrkB Content of Central Excitatory Synapses". Neuropsychopharmacology 31 (11): 2415–23. doi:10.1038/sj.npp.1301052. PMID 16554746.
- 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. doi:10.1016/j.neuropharm.2009.03.004. PMID 19298831.
- De-Spinning In Vitro Data.
- 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. doi:10.1016/S0006-8993(98)01256-6. PMID 9889376.
- 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. PMID 3871765.
- 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. doi:10.1097/00004714-199106000-00024. PMID 1741813.
- R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 645–648.
- 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. doi:10.1016/S0024-3205(74)80012-3. PMID 4550008.
- 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. doi:10.1016/S0014-2999(97)01393-9. PMID 9537821.
- 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. doi:10.1007/BF02246453. PMID 8876023.
- 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. doi:10.1016/0014-2999(96)00254-3. PMID 8831113.
- 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. doi:10.2174/1871524910909030197. PMID 20021354.
- Roth, BL; Driscol, J (12 January 2011). "PDSP Ki Database". 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.
- 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. doi:10.1016/0024-3205(95)00209-O. PMID 7623609.
- Breggin, Peter R.; Ginger Ross Breggin (1995). Talking Back to Prozac. Macmillan Publishers. pp. 1–2. ISBN 978-0-312-95606-6.
- Fax from the BGA to Eli Lilly, 25 May 1984
- Kapit R. FDA Safety Review NDA 18-963, March 23, 1985.
- Swiatek, Jeff (August 2, 2001). "Prozac's profitable run coming to an end for Lilly". The Indianapolis Star.
- "Electronic Orange Book". Food and Drug Administration. April 2007. Retrieved May 24, 2007.
- Carlsson, Arvid; Wong, David T. (1997). "A note on the discovery of selective serotonin reuptake inhibitors". Life Sciences 61 (12): 1203. doi:10.1016/S0024-3205(97)00662-0. PMID 9315511.
- "Patent Expiration Dates for Common Brand-Name Drugs". Retrieved July 20, 2007.
- Class, Selena (December 2, 2002). "Pharma Overview". Retrieved June 15, 2009.
- Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT (February 2008). "Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration". PLoS Medicine. Retrieved February 26, 2008.
- "The creation of the Prozac myth". The Guardian (London). February 27, 2008. Retrieved March 1, 2008.
- Day, Michael (February 26, 2008). "Prozac does not work in majority of depressed patients". New Scientist. Retrieved March 1, 2008.
- Blue, Laura (February 26, 2008). "Antidepressants Hardly Help". Time. Retrieved March 1, 2008.
- Johnson, Blair T.; Kirsch, Irving (2008). "Do antidepressants work? Statistical significance versus clinical benefits". Significance 5 (2): 54. doi:10.1111/j.1740-9713.2008.00286.x.
- "Press Release – FAA Proposes New Policy on Antidepressants for Pilots". Faa.gov. April 2, 2010. Retrieved February 10, 2012.
- Ravilious, K (July 16, 2010). "Prozac Pollution Making Shrimp Reckless". National Geographic. Retrieved 25 November 2013.
- "Fluoxetine". Drugs.com. 2013. Retrieved 25 November 2013.
- Trouble in Prozac, from Fortune magazine
- Fluoxetine, from the United States National Library of Medicine's Drug Information Portal
- Biographies of inventors: