|Systematic (IUPAC) name|
|Trade names||Wellbutrin, Zyban|
|Licence data||US FDA:|
|Protein binding||84% (bupropion), 77% (hydroxybupropion metabolite), 42% (threohydrobupropion metabolite)|
|Metabolism||Hepatic (mostly CYP2B6-mediated hydroxylation, but with some contributions from CYP1A2, CYP2A6, CYP2C9, CYP3A4, CYP2E1 and CYP2C19)|
|Half-life||11 hours (short-term dosing; parent compound) 14–21 hours (chronic dosing; parent compound – depends on formulation), 20 hours (hydroxybupropion), 33 hours (erythrohydrobupropion), 37 hours (threohydrobupropion)|
|Excretion||Renal (87%; 0.5% unchanged), Faecal (10%)|
|(what is this?)|
Bupropion (// bew-PROH-pee-on) (BAN) or bupropion hydrochloride (USAN, BANM), also known as amfebutamone (INN), is a drug of the aminoketone family primarily used as an antidepressant and smoking cessation aid. Marketed as Wellbutrin and other trade names, it is one of the most frequently prescribed antidepressants in the United States, although in many English-speaking countries, including the United Kingdom, Australia and New Zealand, this is an off-label use. It is also widely used, in a formulation marketed as Zyban, to aid people who are trying to quit smoking. It is taken in the form of tablets, and in the United States and most other countries it is available only with a prescription.
Clinically, bupropion serves as an atypical antidepressant fundamentally different from most commonly prescribed antidepressants such as selective serotonin reuptake inhibitors (SSRIs). It is an effective antidepressant on its own, but is also popular as an add-on medication in cases of incomplete response to first-line SSRI antidepressants. In contrast to many other antidepressants, it does not cause weight gain or sexual dysfunction. The most important side effect is an increase in risk for epileptic seizures, which caused the drug to be withdrawn from the market for some time and then caused the recommended dosage to be reduced.
Bupropion is known to affect several different biological targets, and its mechanism of action is only partly understood. It has been widely described in the literature as a weak norepinephrine-dopamine reuptake inhibitor (NDRI). However, this is not entirely accurate. There is evidence that bupropion induces the release of norepinephrine and dopamine in addition to inhibiting their reuptake, similarly to other cathinones like diethylpropion (amfepramone). Moreover, studies with humans via the oral administration route have demonstrated that bupropion does not significantly affect dopamine levels in the brain at clinically-used doses, indicating that its in vitro capacity to inhibit the reuptake and induce the release of dopamine is not involved in its clinical effects. This finding can be reasonably explained by extensive first-pass metabolism of bupropion into metabolites with differing pharmacology. In addition to its monoaminergic actions, bupropion is a non-competitive antagonist of several neuronal nicotinic acetylcholine receptors (nAChRs), a property which appears to be importantly involved in both its antidepressant effects and its efficacy in smoking cessation. Chemically, bupropion belongs to the class of aminoketones and is similar in structure to stimulants such as cathinone and amfepramone, and to phenethylamines in general.
Bupropion was synthesized by Nariman Mehta and patented by Burroughs Wellcome in 1969, which later became part of what is now GlaxoSmithKline. It was first approved for clinical use in the United States in 1989. It was originally called by the generic name amfebutamone, before being renamed in 2000. Its chemical name is 3-chloro-N-tert-butyl-β-ketoamphetamine. It is a substituted cathinone (β-ketoamphetamine), as well as a substituted amphetamine.
- 1 Medical uses
- 2 Contraindications
- 3 Side effects
- 4 Overdose
- 5 Interactions
- 6 Pharmacology
- 7 Physical and chemical properties
- 8 History
- 9 Society and culture
- 10 References
- 11 External links
Bupropion is one of the most widely prescribed antidepressants, and the available evidence indicates that it is effective in clinical depression — as effective as several other widely prescribed drugs, including fluoxetine and paroxetine, although trends favoring the efficacy of escitalopram, sertraline and venlafaxine over bupropion have been observed. Mirtazapine, on the other hand is significantly more effective than bupropion. Bupropion has several features that distinguish it from other antidepressants: for instance, unlike the majority of antidepressants, it does not usually cause sexual dysfunction. Bupropion treatment also is not associated with the somnolence or weight gain that may be produced by other antidepressants.
In depressed people who experience symptoms of sleepiness and fatigue, bupropion has been found to be more effective than selective serotonin reuptake inhibitors (SSRIs) in alleviating these symptoms. There appears to be a modest advantage for the SSRIs over bupropion in the treatment of anxious depression.
According to surveys, the addition to a prescribed SSRI is a common strategy when people do not respond to the SSRI, even though this is not an officially approved indication. The addition of bupropion to an SSRI (most commonly fluoxetine or sertraline) may result in an improvement in some people who have an incomplete response to the first-line antidepressant.
In some countries (including Australia, New Zealand and the UK) this is an off-label use. Bupropion was approved by the U.S. Food and Drug Administration (FDA), in 2006, for the prevention of seasonal affective disorder.
The next most common use is as an aid for smoking cessation where it reduces the severity of nicotine cravings and withdrawal symptoms. A typical bupropion treatment course lasts for seven to twelve weeks, with the patient halting the use of tobacco about ten days into the course. Bupropion approximately doubles the chance of quitting smoking successfully after three months. One year after treatment, the odds of sustaining smoking cessation are still 1.5 times higher in the bupropion group than in the placebo group.
The evidence is clear that bupropion is effective at reducing nicotine cravings. Whether it is more effective than other treatments is not as clear, due to a limited number of studies. The evidence that is available suggests that bupropion is comparable to nicotine replacement therapy, but somewhat less effective than varenicline (Chantix).
Attention deficit hyperactivity disorder
There have been numerous reports of positive results for bupropion as a treatment for attention deficit hyperactivity disorder (ADHD), both in minors and adults. However, in a double-blind study of children, while aggression and hyperactivity as rated by the children's teachers were significantly improved in comparison to placebo, parents and clinicians could not distinguish between the effects of bupropion and placebo. The 2007 guideline on the ADHD treatment from American Academy of Child and Adolescent Psychiatry notes that the evidence for bupropion is "far weaker" than for the FDA-approved treatments. Its effect may also be "considerably less than of the approved agents ... Thus it may be prudent for the clinician to recommend a trial of behavior therapy at this point, before moving to these second-line agents." Similarly, the Texas Department of State Health Services guideline recommends considering bupropion or a tricyclic antidepressant as a fourth-line treatment after trying two different stimulants and atomoxetine.
Bupropion is one of few antidepressants that do not cause sexual dysfunction. A range of studies demonstrate that bupropion not only produces fewer sexual side effects than other antidepressants, but can actually help to alleviate sexual dysfunction. According to a survey of psychiatrists, it is the drug of choice for the treatment of SSRI-induced sexual dysfunction, although this is not an indication approved by the U.S. Food and Drug Administration. There have also been a few studies suggesting that bupropion can improve sexual function in women who are not depressed, if they have hypoactive sexual desire disorder.
Bupropion, when used for treating obesity over a period of 6 to 12 months, may result in weight loss of 2.7 kg over placebo. This is not much different from the weight loss produced by several other medications, such as sibutramine, orlistat and amfepramone.
It has been studied in combination with naltrexone. Concerns from bupropion include an increase in blood pressure and heart rate. In September 2014, a combination was approved by the USFDA for the treatment of obesity.
There has been controversy about whether it is useful to add an antidepressant such as bupropion to a mood stabilizer in patients with bipolar depression, but recent reviews have concluded that bupropion in this situation does no significant harm and may sometimes give significant benefit.
Bupropion has shown no effectiveness in the treatment of cocaine dependence, but there is weak evidence that it may be useful in treating methamphetamine dependence.
Based on studies indicating that bupropion lowers the level of the inflammatory mediator TNF-alpha, there have been suggestions that it might be useful in treating inflammatory bowel disease or other autoimmune conditions, but very little clinical evidence is available.
Bupropion—like other antidepressants, with the exception of duloxetine (Cymbalta)—is not effective in treating chronic low back pain. It does, however, show some promise in the treatment of neuropathic pain.
GlaxoSmithKline advises that bupropion should not be prescribed to individuals with epilepsy or other conditions that lower the seizure threshold, such as anorexia nervosa, bulimia nervosa, active brain tumors, or concurrent alcohol and/or benzodiazepine use and/or withdrawal. It should be avoided in individuals who are also taking monoamine oxidase inhibitors (MAOIs). When switching from MAOIs to bupropion, it is important to include a washout period of about two weeks between the medications. The prescribing information approved by the FDA recommends that caution should be exercised when treating patients with liver damage, severe kidney disease, and severe hypertension, and in pediatric patients, adolescents and young adults due to the increased risk of suicidal ideation.
Epileptic seizures are the most important adverse effect of bupropion. A high incidence of seizures was responsible for the temporary withdrawal of the drug from the market between 1986 and 1989. The risk of seizure is strongly dose-dependent, but also dependent on the preparation. The sustained-release preparation is associated with a seizure incidence of 0.1% at daily dosages of less than 300 mg of bupropion and 0.4% at 300–400 mg. The immediate release preparation is associated with a seizure incidence of 0.4% for dosages below 450 mg; the incidence climbs to 5% for dosages between 450–600 mg per day. For comparison, the incidence of unprovoked seizure in the general population is 0.07 to 0.09%, and the risk of seizure for a variety of other antidepressants is generally between 0 and 0.6% at recommended dosage levels. Given that clinical depression itself has been reported to increase the occurrence of seizures, it has been suggested that low to moderate doses of antidepressants may not actually increase seizure risk at all. However, this same study found that bupropion and clomipramine were unique among antidepressants in that they were associated with increased incidence of seizures.
The prescribing information notes that hypertension, sometimes severe, was observed in some patients, both with and without pre-existing hypertension. The frequency of this adverse effect was under 1% and not significantly higher than found with placebo. A review of the available data carried out in 2008 indicated that bupropion is safe to use in patients with a variety of serious cardiac conditions.
In the UK, more than 7,600 reports of suspected adverse reactions were collected in the first two years after bupropion's approval by the Medicines and Healthcare Products Regulatory Agency as part of the Yellow Card Scheme, which monitored side effects. Approximately 540,000 people were treated with bupropion for smoking cessation during that period. The MHRA received 60 reports of "suspected [emphasis MHRA's] adverse reactions to Zyban which had a fatal outcome". The agency concluded that "in the majority of cases the individual's underlying condition may provide an alternative explanation." This is consistent with a large, 9,300-patient safety study that showed that the mortality of smokers taking bupropion is not higher than the natural mortality of smokers of the same age.
Suicidal thought and behavior are rare in clinical trials, and the FDA requires all antidepressants, including bupropion, to carry a boxed warning stating that antidepressants may increase the risk of suicide in persons younger than 25. This warning is based on a statistical analysis conducted by the FDA which found a 2-fold increase in suicidal thought and behavior in children and adolescents, and 1.5-fold increase in the 18–24 age group. For this analysis the FDA combined the results of 295 trials of 11 antidepressants in order to obtain statistically significant results. Considered in isolation, bupropion was not statistically different from placebo.
Suicidal behavior is less of a concern when bupropion is prescribed for smoking cessation. According to a 2007 Cochrane Database review, there have been four suicides per one million prescriptions and one case of suicidal ideation per ten thousand prescriptions of bupropion for smoking cessation in the UK. The review concludes, "Although some suicides and deaths while taking bupropion have been reported, thus far there is insufficient evidence to suggest they were caused by bupropion."
In 2009 the FDA issued a health advisory warning that the prescription of bupropion for smoking cessation has been associated with reports about unusual behavior changes, agitation and hostility. Some patients, according to the advisory, have become depressed or have had their depression worsen, have had thoughts about suicide or dying, or have attempted suicide. This advisory was based on a review of anti-smoking products that identified 75 reports of "suicidal adverse events" for bupropion over ten years.
Bupropion-induced psychosis may develop in select patient populations, or worsen a pre-existing psychotic syndrome. Symptoms may include delusions, hallucinations, paranoia, and confusion. In most cases these symptoms can be reduced or eliminated by reducing the dose, ceasing treatment or adding antipsychotic medication. However, adding a benzodiazepine to treat psychosis, instead of an antipsychotic, may become a valid alternative according to the model of amphetamine-induced psychosis. Psychotic symptoms are associated with factors such as higher doses of bupropion, a history of bipolar disorder or psychosis, concomitant medications, for example, lithium or benzodiazepines, old age, or substance abuse.
According to several case reports, the use of bupropion at therapeutic doses may induce a mild state of psychological dependence in some users; the associated psychological withdrawal symptoms which have been observed following the abrupt discontinuation of treatment include: dystonia, irritability, anxiety, mania, headache, aches and pains. The prescribing information recommends dose tapering after bupropion has been used for seasonal affective disorder; however it states that dose tapering is not required when discontinuing treatment for smoking cessation.
In the majority of childhood exploratory ingestions involving one or two tablets, children show no apparent symptoms. In teenagers and adults, seizures are more commonly observed, with the seizure rate increasing tenfold with doses of 600 mg daily.
Bupropion overdose rarely results in death, although some cases have been reported. Symptoms include hallucinations and delusions, vomiting, aggressive behavior, and seizures.
Since bupropion is metabolized to hydroxybupropion by the CYP2B6 enzyme, drug interactions with CYP2B6 inhibitors are possible: this includes medications like paroxetine, sertraline, fluoxetine, diazepam, clopidogrel, and orphenadrine. The expected result is the increase of bupropion and decrease of hydroxybupropion blood concentration. The reverse effect (decrease of bupropion and increase of hydroxybupropion) can be expected with CYP2B6 inducers, such as carbamazepine, clotrimazole, rifampicin, ritonavir, St John's wort, phenobarbital, phenytoin and others. Conversely, because bupropion is itself an inhibitor of CYP2D6 (Ki=21 μM), as is its active metabolite, hydroxybupropion (Ki=13.3 μM), it can slow the clearance of other drugs metabolized by this enzyme.
Bupropion lowers the threshold for epileptic seizures, and therefore can potentially interact with other medications that also lower it, such as theophylline, steroids, and some tricyclic antidepressants. The prescribing information recommends minimizing the use of alcohol, since in rare cases bupropion reduces alcohol tolerance, and because the excessive use of alcohol may lower the seizure threshold.
|Exposure (concentration over time; bupropion exposure = 100%) and half-life|
|Half-life||10 h (IR)
17 h (SR)
|21 h||25 h||26 h||26 h|
|Inhibition potency (potency of DA uptake inhibition by bupropion = 100%)|
|DA uptake||100%||No data||No data||No data||No data|
|NE uptake||27%||No data||No data||No data||No data|
|5HT uptake||2%||No data||No data||No data||No data|
|α3β4 nicotinic||53%||15%||10%||No data||No data|
|α4β2 nicotinic||8%||3%||29%||No data||No data|
|α1* nicotinic||12%||13%||13%||No data||No data|
|DA = dopamine; NE = norepinephrine; 5HT = serotonin.|
Based on animal and human proteins research, bupropion has been characterized as a weak norepinephrine-dopamine reuptake inhibitor (NDRI). It has also been found to act as a releasing agent of dopamine and norepinephrine (NDRA). However, in actual humans, bupropion is extensively converted in the body into several active metabolites with differing activity and influence on the effects of bupropion during first-pass metabolism. These metabolites are present in significantly higher levels in the body compared to bupropion itself. The most important example of this is bupropion's most major metabolite, hydroxybupropion, a selective norepinephrine reuptake inhibitor and nACh receptor antagonist that lacks significant dopaminergic actions, which, with oral bupropion treatment, can reach area under the curve (AUC) plasma concentrations that are as much as 16–20 times greater than those of bupropion itself. As such, it may be more accurate to describe bupropion as a prodrug in humans, and for this reason, its effects cannot be understood without reference to its metabolism.
The occupancy of dopamine transporter (DAT) sites by bupropion and its metabolites in the human brain as measured by positron emission tomography was 26% according to GlaxoSmithKline researchers and 14% in an independent study. Despite this weak DAT occupancy however, a subsequent study looked at the actual extracellular concentrations of dopamine in the human brain after an acute oral treatment of bupropion and failed to observe any increase, concluding that the weak DAT occupancy was not sufficient to increase dopamine levels. In contrast, the same study also looked at dopamine levels in the rat brain after administration of bupropion via intraperitoneal injection and did see an increase, which could have been related to species differences. However, an alternative explanation is that the difference had to do with the different routes of administration employed (i.e., oral vs. i.p.) and the associated differences in pharmacokinetics and metabolism that resulted. Although oral bupropion at clinical doses does not appear to have a significant potential for abuse, there are many isolated case reports of bupropion abuse and "cocaine-like" effects in humans who ingested the drug via a non-oral route (e.g., injection, insufflation, etc.), and, notably, awareness of the abuse potential of bupropion via non-conventional routes appears to be especially widespread in correctional facilities.
Bupropion is also known to act as a non-competitive antagonist of the α3β2, α3β4, α4β2, and, very weakly, α7 nACh receptors, and these actions appear to be importantly involved in its beneficial properties not only in smoking cessation, but in depression as well.
Bupropion is metabolized in the liver by the cytochrome P450 isoenzyme CYP2B6. It has several active metabolites: R,R-hydroxybupropion, S,S-hydroxybupropion, threo-hydrobupropion and erythro-hydrobupropion, which are further metabolized to inactive metabolites and eliminated through excretion into the urine. Pharmacological data on bupropion and its metabolites are shown in the table. Bupropion is known to weakly inhibit the α1 adrenergic receptor, with a 14% potency of its dopamine uptake inhibition, and the H1 receptor, with a 9% potency.
The biological activity of bupropion can be attributed to a significant degree to its active metabolites, in particular to S,S-hydroxybupropion. GlaxoSmithKline developed this metabolite as a separate drug called radafaxine, but discontinued development in 2006 due to "an unfavourable risk/benefit assessment".
Bupropion is metabolized to hydroxybupropion by CYP2B6, an isozyme of the cytochrome P450 system. Alcohol causes an increase of CYP2B6 in the liver, and persons with a history of alcohol use metabolize bupropion faster. Bupropion is metabolized to threo-hydrobupropion via cortisone reductase. The metabolic pathway responsible for the creation of erythro-hydrobupropion remains elusive.
The metabolism of bupropion is highly variable: the effective doses of bupropion received by persons who ingest the same amount of the drug may differ by as much as 5.5 times (and the half-life from 3 to 16 hours), and of hydroxybupropion by as much as 7.5 times (and the half-life from 12 to 38 hours). Based on this, some researchers have advocated monitoring of the blood level of bupropion and hydroxybupropion.
Both bupropion and its primary metabolite hydroxybupropion act in the liver as potent inhibitors of the enzyme CYP2D6, which metabolizes not only bupropion itself but also a variety of other drugs and biologically active substances. This mechanism creates the potential for a variety of drug interactions.
Physical and chemical properties
Bupropion is a substituted cathinone. It is synthesized in two chemical steps starting from 3'-chloro-propiophenone. The alpha position adjacent to the ketone is first brominated followed by nucleophilic displacement of the resulting alpha-bromoketone with t-butylamine and treated with hydrochloric acid to give bupropion as the hydrochloride salt in 75–85% overall yield.
Bupropion was invented by Nariman Mehta of Burroughs Wellcome (now GlaxoSmithKline) in 1969, and the US patent for it was granted in 1974. It was approved by the United States Food and Drug Administration (FDA) as an antidepressant on 30 December 1985, and marketed under the name Wellbutrin. However, a significant incidence of epileptic seizures at the originally recommended dosage caused the withdrawal of the drug in 1986. Subsequently, the risk of seizures was found to be highly dose-dependent, and bupropion was re-introduced to the market in 1989 with a lower maximum recommended daily dose.
In 1996, the FDA approved a sustained-release formulation of bupropion called Wellbutrin SR, intended to be taken twice a day (as compared with three times a day for immediate-release Wellbutrin). In 2003, the FDA approved another sustained-release formulation called Wellbutrin XL, intended for once-daily dosing. Wellbutrin SR and XL are available in generic form in the United States and Canada. In Canada, generic XR bupropion is distributed by Mylan. In 1997, bupropion was approved by the FDA for use as a smoking cessation aid under the name Zyban. In 2006, Wellbutrin XL was similarly approved as a treatment for seasonal affective disorder.
Issue with generic bioequivalence
On 11 October 2007, two providers of consumer information on nutritional products and supplements, ConsumerLab.com and The People's Pharmacy, released the results of comparative tests of different brands of bupropion. The People's Pharmacy received multiple reports of increased side effects and decreased efficacy of generic bupropion, which prompted it to ask ConsumerLab.com to test the products in question. The tests showed that "one of a few generic versions of Wellbutrin XL 300 mg, sold as Budeprion XL 300 mg, didn't perform the same as the brand-name pill in the lab." The FDA investigated these complaints and concluded that Budeprion XL is equivalent to Wellbutrin XL in regard to bioavailability of bupropion and its main active metabolite hydroxybupropion. The FDA also said that coincidental natural mood variation is the most likely explanation for the apparent worsening of depression after the switch from Wellbutrin XL to Budeprion XL. On 3 October 2012, however, the FDA reversed this opinion, announcing that "Budeprion XL 300 mg fails to demonstrate therapeutic equivalence to Wellbutrin XL 300 mg." The FDA did not test the bioequivalence of any of the other generic versions of Wellbutrin XL 300 mg, but requested that the four manufacturers submit data on this question to the FDA by March 2013. As of October 2013 the FDA has made determinations on the formulations from some manufacturers not being bioequivalent. FDA Update from Oct 2013
In 2012, the U.S. Justice Department announced that GlaxoSmithKline had agreed to plead guilty and pay a $3-billion fine, in part for promoting the unapproved use of Wellbutrin for weight loss and sexual dysfunction.
In France, marketing authorization was granted for Zyban on 3 August 2001, with a maximum daily dose of 300 mg; only sustained-release bupropion is available, and only as a smoking cessation aid. Bupropion was granted a licence for use in adults with major depression in the Netherlands in early 2007, with GlaxoSmithKline expecting subsequent approval in other European countries.
Society and culture
Bupropion is marketed under many brand names including Aplenzin, Budeprion, Elontril, Wellbutrin, Quomem, Prexaton, Voxra, and Zyban among others.
According to the US government classification of psychiatric medications, bupropion is "non-abusable". However, in animal studies, squirrel monkeys and rats could be induced to self-administer bupropion via the injection route, which is often taken as a sign of addiction potential; however, there are significant interspecies differences in bupropion metabolism. There have been a number of anecdotal and case-study reports of bupropion abuse, but the bulk of evidence indicates that the subjective effects of bupropion via the oral route are markedly different from those of addictive stimulants such as cocaine or amphetamine. In any case, bupropion, via non-conventional routes of administration (e.g., injection, insufflation), is reported to be abused in Canada, and in recent years in United States prisons.
- "Zyban 150 mg prolonged release film-coated tablets – Summary of Product Characteristics (SPC)". electronic Medicines Compendium. GlaxoSmithKline UK. 1 August 2013. Retrieved 22 October 2013.
- "Prexaton Bupropion hydrochloride PRODUCT INFORMATION". TGA eBusiness Services. Ascent Pharma Pty Ltd. 2 October 2012. Retrieved 22 October 2013.
- "BUPROPION HYDROCHLORIDE tablet, film coated [Sandoz Inc]". DailyMed. Sandoz, Inc. April 2013. Retrieved 22 October 2013.
- Zhu, A. Z. X.; Zhou, Q.; Cox, L. S.; Ahluwalia, J. S.; Benowitz, N. L.; Tyndale, R. F. (3 September 2014). "Gene Variants in CYP2C19 Are Associated with Altered In Vivo Bupropion Pharmacokinetics but Not Bupropion-Assisted Smoking Cessation Outcomes". Drug Metabolism and Disposition 42 (11): 1971–1977. doi:10.1124/dmd.114.060285. PMID 25187485.
- Brunton, L; Chabner, B; Knollman, B (2010). Goodman and Gilman's The Pharmacological Basis of Therapeutics (12th ed.). New York: McGraw-Hill Professional. ISBN 978-0-07-162442-8.
- "PRODUCT INFORMATION ZYBAN® SUSTAINED RELEASE TABLETS". TGA eBusiness Services. Aspen Pharmacare Australia Pty Ltd. 19 April 2013. Retrieved 22 October 2013.
- "WELLBUTRIN (bupropion hydrochloride) tablet, film coated [GlaxoSmithKline LLC]". DailyMed. GlaxoSmithKline LLC. March 2013. Retrieved 22 October 2013.
- Dr. Ian Morton, I.K. Morton, Judith M. Hall (31 October 1999). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 57–. ISBN 978-0-7514-0499-9.
- Dictionary of Organic Compounds. CRC Press. pp. 104–. ISBN 978-0-412-54090-5.
- Index Nominum 2000: International Drug Directory. Taylor & Francis. January 2000. pp. 38–. ISBN 978-3-88763-075-1.
- "Bupropion (By mouth)". PubMed Health. Bethesda, USA: National Institute of Health. 1 June 2014. Retrieved 18 July 2014.
- Brayfield, A, ed. (22 October 2013). "Bupropion". Martindale: The Complete Drug Reference. London, UK: Pharmaceutical Press. Retrieved 18 July 2014.
- Fava M, Rush AJ, Thase ME et al. (2005). "15 years of clinical experience with bupropion HCl: from bupropion to bupropion SR to bupropion XL". Prim Care Companion J Clin Psychiatry 7 (3): 106–13. doi:10.4088/pcc.v07n0305. PMC 1163271. PMID 16027765.
- Linda P. Dwoskin (29 January 2014). Emerging Targets & Therapeutics in the Treatment of Psychostimulant Abuse. Elsevier Science. pp. 177–216. ISBN 978-0-12-420177-4.
- Allan Tasman, Jerald Kay, Jeffrey A. Lieberman, Michael B. First, Mario Maj (11 October 2011). Psychiatry. John Wiley & Sons. ISBN 978-1-119-96540-4.
- Arias HR, Santamaría A, Ali SF (2009). "Pharmacological and neurotoxicological actions mediated by bupropion and diethylpropion". Int. Rev. Neurobiol. 88: 223–55. doi:10.1016/S0074-7742(09)88009-4. PMID 19897080.
- Arias HR (2009). "Is the inhibition of nicotinic acetylcholine receptors by bupropion involved in its clinical actions?". Int. J. Biochem. Cell Biol. 41 (11): 2098–108. doi:10.1016/j.biocel.2009.05.015. PMID 19497387.
- Dell’Osso, Bernardo; Palazzo, M. Carlotta; Oldani, Lucio; Altamura, A. Carlo (2011). "The Noradrenergic Action in Antidepressant Treatments: Pharmacological and Clinical Aspects". CNS Neuroscience & Therapeutics 17 (6): 723–732. doi:10.1111/j.1755-5949.2010.00217.x. ISSN 1755-5930.
- The INN originally assigned in 1974 by the World Health Organization was "amfebutamone". In 2000, the INN was reassigned as bupropion. See World Health Organization (2000). "International Nonproprietary Names for Pharmaceutical Substances (INN). Proposed INN: List 83" (PDF). WHO Drug Information 14 (2). Archived from the original (PDF) on 31 May 2011. Retrieved 22 June 2009.
- Moreira R (October 2011). "The efficacy and tolerability of bupropion in the treatment of major depressive disorder". Clin Drug Investig. 31 Suppl 1: 5–17. doi:10.2165/1159616-S0-000000000-00000. PMID 22015858.
- Cipriani A, Furukawa TA, Salanti G, Geddes JR, Higgins JP, Churchill R, Watanabe N, Nakagawa A, Omori IM, McGuire H, Tansella M, Barbui C (February 2009). "Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis" (PDF). Lancet 373 (9665): 746–758. doi:10.1016/S0140-6736(09)60046-5. PMID 19185342.
- Clayton AH (2003). "Antidepressant-Associated Sexual Dysfunction: A Potentially Avoidable Therapeutic Challenge". Primary Psychiatry 10 (1): 55–61.
- Dhillon S, Yang LP, Curran MP (2008). "Bupropion: a review of its use in the management of major depressive disorder". Drugs 68 (5): 653–89. doi:10.2165/00003495-200868050-00011. PMID 18370448.
- Baldwin DS, Papakostas GI (2006). "Symptoms of fatigue and sleepiness in major depressive disorder". J Clin Psychiatry. 67 Suppl 6 (Suppl 6): 9–15. PMID 16848671.
- Papakostas GI, Stahl SM, Krishen A, Seifert CA, Tucker VL, Goodale EP, Fava M (August 2008). "Efficacy of bupropion and the selective serotonin reuptake inhibitors in the treatment of major depressive disorder with high levels of anxiety (anxious depression): a pooled analysis of 10 studies". J Clin Psychiatry 69 (8): 1287–92. doi:10.4088/JCP.v69n0812. PMID 18605812.
- Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB (February 2006). "Use of bupropion in combination with serotonin reuptake inhibitors". Biol. Psychiatry 59 (3): 203–10. doi:10.1016/j.biopsych.2005.06.027. PMID 16165100.
- Rossi, S, ed. (2013). Australian Medicines Handbook (2013 ed.). Adelaide: The Australian Medicines Handbook Unit Trust. ISBN 978-0-9805790-9-3.
- Joint Formulary Committee (2013). British National Formulary (BNF) (65 ed.). London, UK: Pharmaceutical Press. ISBN 978-0-85711-084-8.
- "First drug for seasonal depression". FDA Consum 40 (5): 7. 2006. PMID 17328102.
- Wu P, Wilson K, Dimoulas P, Mills EJ (2006). "Effectiveness of smoking cessation therapies: a systematic review and meta-analysis". BMC Public Health 6: 300. doi:10.1186/1471-2458-6-300. PMC 1764891. PMID 17156479.
- Kornfield R, Watson S, Higashi A, Dusetzina S, Conti R, Garfield R, Dorsey ER, Huskamp HA, Alexander GC (April 2013). "Impact of FDA Advisories on Pharmacologic Treatment of Attention Deficit Hyperactivity Disorder". Psychiatric Services 64 (4): 339–46. doi:10.1176/appi.ps.201200147. PMC 4023684. PMID 23318985.
- Cantwell DP (1998). "ADHD through the life span: the role of bupropion in treatment". J Clin Psychiatry. 59 Suppl 4: 92–4. PMID 9554326.
- Pliszka S (July 2007). "Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder". J Am Acad Child Adolesc Psychiatry 46 (7): 894–921. doi:10.1097/chi.0b013e318054e724. PMID 17581453.
- Pliszka SR, Crismon ML, Hughes CW, Corners CK, Emslie GJ, Jensen PS, McCracken JT, Swanson JM, Lopez M (June 2006). "The Texas Children's Medication Algorithm Project: revision of the algorithm for pharmacotherapy of attention-deficit/hyperactivity disorder". J Am Acad Child Adolesc Psychiatry 45 (6): 642–57. doi:10.1097/01.chi.0000215326.51175.eb. PMID 16721314.
- Serretti A, Chiesa A (June 2009). "Treatment-emergent sexual dysfunction related to antidepressants: a meta-analysis". J Clin Psychopharmacol 29 (3): 259–66. doi:10.1097/JCP.0b013e3181a5233f. PMID 19440080.
- Stahl SM, Pradko JF, Haight BR, Modell JG, Rockett CB, Learned-Coughlin S (2004). "A review of the neuropharmacology of bupropion, a dual norepinephrine and dopamine reuptake inhibitor". Prim Care Companion J Clin Psychiatry 6 (4): 159–166. doi:10.4088/PCC.v06n0403. PMC 514842. PMID 15361919.
- Foley KF, DeSanty KP, Kast RE (September 2006). "Bupropion: pharmacology and therapeutic applications". Expert Rev Neurother 6 (9): 1249–65. doi:10.1586/1473718.104.22.1689. PMID 17009913.
- Li Z, Maglione M, Tu W, Mojica W, Arterburn D, Shugarman LR, Hilton L, Suttorp M, Solomon V, Shekelle PG, Morton SC (April 2005). "Meta-analysis: pharmacologic treatment of obesity". Ann. Intern. Med. 142 (7): 532–46. doi:10.7326/0003-4819-142-7-200504050-00012. PMID 15809465.
- Ryan DH, Bray GA (June 2013). "Pharmacologic treatment options for obesity: what is old is new again.". Current hypertension reports 15 (3): 182–9. doi:10.1007/s11906-013-0343-6. PMID 23625271.
- "Contrave prescribing information" (PDF). United States Food and Drug Administration. Takeda Pharmaceuticals America, Inc. 10 September 2014. p. 1. Retrieved 6 April 2015.
- Gijsman HJ, Geddes JR, Rendell JM, Nolen WA, Goodwin GM (September 2004). "Antidepressants for bipolar depression: a systematic review of randomized, controlled trials". Am J Psychiatry 161 (9): 1537–47. doi:10.1176/appi.ajp.161.9.1537. PMID 15337640.
- Yatham LN, Kennedy SH, O'Donovan C, Parikh SV, MacQueen G, McIntyre RS, Sharma V, Beaulieu S; Guidelines Group (December 2006). "Canadian Network for Mood and Anxiety Treatments (CANMAT) guidelines for the management of patients with bipolar disorder: update 2007". Bipolar Disord 8 (6): 721–39. doi:10.1111/j.1399-5618.2006.00432.x. PMID 17156158.
- Kampman KM (June 2008). "The search for medications to treat stimulant dependence". Addict Sci Clin Pract 4 (2): 28–35. doi:10.1151/ascp084228. PMC 2797110. PMID 18497715.
- Mikocka-Walus AA, Turnbull DA, Moulding NT, Wilson IG, Andrews JM, Holtmann GJ (2006). "Antidepressants and inflammatory bowel disease: a systematic review". Clin Pract Epidemiol Ment Health 2: 24. doi:10.1186/1745-0179-2-24. PMC 1599716. PMID 16984660.
- "FDA clears Cymbalta to treat chronic musculoskeletal pain". FDA Press Announcements. Food and Drug Administration. 4 November 2010. Retrieved 19 August 2013.
The U.S. Food and Drug Administration ... approved Cymbalta (duloxetine hydrochloride) to treat chronic musculoskeletal pain, including discomfort from osteoarthritis and chronic lower back pain.
- Urquhart DM, Hoving JL, Assendelft WW, Roland M, van Tulder MW (2008). Urquhart DM, ed. "Antidepressants for non-specific low back pain". Cochrane Database Syst Rev (1): CD001703. doi:10.1002/14651858.CD001703.pub3. PMID 18253994.
- Shah TH, Moradimehr A (August 2010). "Bupropion for the treatment of neuropathic pain". Am J Hosp Palliat Care 27 (5): 333–6. doi:10.1177/1049909110361229. PMID 20185402.
- "Wellbutrin XL Prescribing Information" (PDF). GlaxoSmithKline. December 2008. Retrieved 16 January 2010.
- Hales E, Yudofsky JA, ed. (2003). The American Psychiatric Press Textbook of Psychiatry. Washington, DC: American Psychiatric Publishing, Inc.
- Pisani F, Oteri G, Costa C, Di Raimondo G, Di Perri R (2002). "Effects of psychotropic drugs on seizure threshold". Drug Saf 25 (2): 91–110. doi:10.2165/00002018-200225020-00004. PMID 11888352.
- Alper K, Schwartz KA, Kolts RL, Khan A (August 2007). "Seizure incidence in psychopharmacological clinical trials: an analysis of Food and Drug Administration (FDA) summary basis of approval reports". Biol. Psychiatry 62 (4): 345–54. doi:10.1016/j.biopsych.2006.09.023. PMID 17223086.
- Taylor D (December 2008). "Antidepressant drugs and cardiovascular pathology: a clinical overview of effectiveness and safety". Acta Psychiatr Scand 118 (6): 434–42. doi:10.1111/j.1600-0447.2008.01260.x. PMID 18785947.
- "Zyban (bupropion hydrochloride) – safety update". Medicines and Healthcare products Regulatory Agency. 24 July 2002. Archived from the original on 28 September 2007. Retrieved 7 October 2006.
- Hubbard R, Lewis S, West J, Smith C, Godfrey C, Smeeth L, Farrington P, Britton J (October 2005). "Bupropion and the risk of sudden death: a self-controlled case-series analysis using The Health Improvement Network". Thorax 60 (10): 848–50. doi:10.1136/thx.2005.041798. PMC 1747199. PMID 16055620.
- Levenson M, Holland C. "Antidepressants and suicidality in adults: statistical evaluation. (Presentation at Psychopharmacologic Drugs Advisory Committee; December 13, 2006)". U.S. Food and Drug Administration. Retrieved 13 May 2007.
- Hughes JR, Stead LF, Lancaster T (2007). Hughes JR, ed. "Antidepressants for smoking cessation". Cochrane Database Syst Rev (1): CD000031. doi:10.1002/14651858.CD000031.pub3. PMID 17253443.
- "Public Health Advisory: FDA requires new boxed warnings for the smoking cessation drugs Chantix and Zyban". U.S. Food and Drug Administration (FDA). 1 July 2009. Retrieved 3 July 2009.
- "The smoking cessation aids varenicline (marketed as Chantix) and bupropion (marketed as Zyban and generics) suicidal ideation and behavior" (PDF). Drug Safety Newsletter (U.S. Food and Drug Administration (FDA)) 2 (1): 1–4. 2009.
- Kumar S, Kodela S, Detweiler JG, Kim KY, Detweiler MB (November–December 2011). "Bupropion-induced psychosis: folklore or fact? A Systematic Review of the Literature". Gen Hosp Psychiatry 156 (12): 612–7. doi:10.1016/j.genhosppsych.2011.07.001. PMID 21872337.
- Howard WT, Warnock JK (December 1999). "Bupropion-induced psychosis". Am J Psychiatry 156 (12): 2017–8. PMID 10588428.
- Javelot T, Javelot H, Baratta A, Weiner L, Messaoudi M, Lemoine P (December 2010). "Acute psychotic disorders related to bupropion: review of the literature". Encephale 36 (6): 461–71. doi:10.1016/j.encep.2010.01.005. PMID 21130229.
- Nemeroff CB, Schatzberg AF (2006). Essentials of clinical psychopharmacology. Washington, D.C: American Psychiatric Publishing. p. 146. ISBN 1-58562-243-5.
- Berigan TR (April 2002). "Bupropion-associated withdrawal symptoms revisited: a case report". Prim Care Companion J Clin Psychiatry 4 (2): 78. doi:10.4088/PCC.v04n0208a. PMC 181231. PMID 15014751.
- "Prescribing information – Zyban (bupropion hydrochloride) sustained-release tablets" (PDF). Glaxo Smith-Kline. Retrieved 6 January 2010.
- Taylor D, Carol P, Shitij K (2012). The Maudsley prescribing guidelines in psychiatry. West Sussex: Wiley-Blackwell. ISBN 978-0-470-97969-3.
- White N, Litovitz T, Clancy C (December 2008). "Suicidal antidepressant overdoses: a comparative analysis by antidepressant type". Journal of Medical Toxicology 4 (4): 238–250. doi:10.1007/BF03161207. PMC 3550116. PMID 19031375.
- Beuhler MC, Spiller HA, Sasser HC (March 2010). "The outcome of unintentional pediatric bupropion ingestions: a NPDS database review". J Med Toxicol 6 (1): 4–8. doi:10.1007/s13181-010-0027-4. PMC 3550434. PMID 20213217.
- Johnston JA, Lineberry CG, Ascher JA, Davidson J, Khayrallah MA, Feighner JP, Stark P (November 1991). "A 102-center prospective study of seizure in association with bupropion". J Clin Psychiatry 52 (11): 450–6. PMID 1744061.
- Spiller HA, Bottei E, Kalin L (2008). "Fatal bupropion overdose with post mortem blood concentrations". Forensic Sci Med Pathol 4 (1): 47–50. doi:10.1007/s12024-007-0030-5. PMID 19291469.
- Jefferson JW, Pradko JF, Muir KT (November 2005). "Bupropion for major depressive disorder: Pharmacokinetic and formulation considerations". Clin Ther 27 (11): 1685–95. doi:10.1016/j.clinthera.2005.11.011. PMID 16368442.
- Dwoskin LP, Rauhut AS, King-Pospisil KA, Bardo MT (2006). "Review of the pharmacology and clinical profile of bupropion, an antidepressant and tobacco use cessation agent". CNS Drug Rev 12 (3–4): 178–207. doi:10.1111/j.1527-3458.2006.00178.x. PMID 17227286.
- Horst WD, Preskorn SH (December 1998). "Mechanisms of action and clinical characteristics of three atypical antidepressants: venlafaxine, nefazodone, bupropion". J Affect Disord 51 (3): 237–54. doi:10.1016/S0165-0327(98)00222-5. PMID 10333980.
- Johnston AJ, Ascher J, Leadbetter R, Schmith VD, Patel DK, Durcan M, Bentley B (2002). "Pharmacokinetic optimisation of sustained-release bupropion for smoking cessation". Drugs. 62 Suppl 2: 11–24. doi:10.2165/00003495-200262002-00002. PMID 12109932.
- Xu H, Loboz KK, Gross AS, McLachlan AJ (March 2007). "Stereoselective analysis of hydroxybupropion and application to drug interaction studies". Chirality 19 (3): 163–70. doi:10.1002/chir.20356. PMID 17167747.
- Bondarev ML, Bondareva TS, Young R, Glennon RA (August 2003). "Behavioral and biochemical investigations of bupropion metabolites". Eur. J. Pharmacol. 474 (1): 85–93. doi:10.1016/S0014-2999(03)02010-7. PMID 12909199.
- Damaj MI, Carroll FI, Eaton JB, Navarro HA, Blough BE, Mirza S, Lukas RJ, Martin BR (September 2004). "Enantioselective effects of hydroxy metabolites of bupropion on behavior and on function of monoamine transporters and nicotinic receptors". Mol. Pharmacol. 66 (3): 675–82. doi:10.1124/mol.104.001313. PMID 15322260.
- Thomas L. Lemke, David A. Williams (24 January 2012). Foye's Principles of Medicinal Chemistry. Lippincott Williams & Wilkins. pp. 611–613. ISBN 978-1-60913-345-0.
- Lawrence A. Labbate, Maurizio Fava, Jerrold F. Rosenbaum, George W. Arana (28 March 2012). Handbook of Psychiatric Drug Therapy. Lippincott Williams & Wilkins. pp. 64–. ISBN 978-1-4511-5307-1.
- Warner C, Shoaib M (September 2005). "How does bupropion work as a smoking cessation aid?". Addict Biol 10 (3): 219–31. doi:10.1080/13556210500222670. PMID 16109583.
- Stephen M. Stahl (2008). Depression and Bipolar Disorder: Stahl's Essential Psychopharmacology. Cambridge University Press. pp. 102–. ISBN 978-0-521-88663-5.
- Ascher JA, Cole JO, Colin JN et al. (September 1995). "Bupropion: a review of its mechanism of antidepressant activity". J Clin Psychiatry 56 (9): 395–401. PMID 7665537.
- Learned-Coughlin SM, Bergström M, Savitcheva I, Ascher J, Schmith VD, Långstrom B (October 2003). "In vivo activity of bupropion at the human dopamine transporter as measured by positron emission tomography". Biol. Psychiatry 54 (8): 800–5. doi:10.1016/S0006-3223(02)01834-6. PMID 14550679.
- Meyer JH, Goulding VS, Wilson AA, Hussey D, Christensen BK, Houle S (August 2002). "Bupropion occupancy of the dopamine transporter is low during clinical treatment". Psychopharmacology (Berl.) 163 (1): 102–5. doi:10.1007/s00213-002-1166-3. PMID 12185406.
- Oppek K, Koller G, Zwergal A, Pogarell O (June 2014). "Intravenous Administration and Abuse of Bupropion: A Case Report and a Review of the Literature". J Addict Med 8 (4): 290–3. doi:10.1097/ADM.0000000000000044. PMID 24950138.
- Hilliard WT, Barloon L, Farley P, Penn JV, Koranek A (July 2013). "Bupropion diversion and misuse in the correctional facility". J Correct Health Care 19 (3): 211–7. doi:10.1177/1078345813486448. PMID 23788587.
- Carroll FI, Blough BE, Mascarella SW, Navarro HA, Lukas RJ, Damaj MI (2014). "Bupropion and bupropion analogs as treatments for CNS disorders". Adv. Pharmacol. 69: 177–216. doi:10.1016/B978-0-12-420118-7.00005-6. PMID 24484978.
- "GlaxoSmithKline (GSK) Reviews Novel Therapeutics For CNS Disorders And Confirms Strong Pipeline Momentum" (Press release). PRNewswire. 23 November 2004. Retrieved 18 August 2007.
- GlaxoSmithKline (26 July 2006) PDF (136 KB). Press release. Retrieved on 18 August 2007.
- Meyer A, Vuorinen A, Zielinska AE, Strajhar P, Lavery GG, Schuster D, Odermatt A (September 2013). "Formation of threohydrobupropion from bupropion is dependent on 11β-hydroxysteroid dehydrogenase 1.". Drug metabolism and disposition: the biological fate of chemicals 41 (9): 1671–8. doi:10.1124/dmd.113.052936. PMID 23804523.
- Hesse LM, He P, Krishnaswamy S, Hao Q, Hogan K, von Moltke LL, Greenblatt DJ, Court MH (April 2004). "Pharmacogenetic determinants of inter-individual variability in bupropion hydroxylation by cytochrome P450 2B6 in human liver microsomes". Pharmacogenetics 14 (4): 225–38. doi:10.1097/00008571-200404000-00002. PMID 15083067.
- Preskorn SH (1991). "Should bupropion dosage be adjusted based upon therapeutic drug monitoring?". Psychopharmacol Bull 27 (4): 637–43. PMID 1813908.
- Suckow RF, Smith TM, Perumal AS, Cooper TB (1986). "Pharmacokinetics of bupropion and metabolites in plasma and brain of rats, mice, and guinea pigs". Drug Metab. Dispos. 14 (6): 692–7. PMID 2877828.
- Weintraub D, Linder MW (2000). "Amphetamine positive toxicology screen secondary to bupropion". Depress Anxiety 12 (1): 53–4. doi:10.1002/1520-6394(2000)12:1<53::AID-DA8>3.0.CO;2-4. PMID 10999247.
- Nixon AL, Long WH, Puopolo PR, Flood JG (June 1995). "Bupropion metabolites produce false-positive urine amphetamine results". Clin. Chem. 41 (6 Pt 1): 955–6. PMID 7768026.
- Mehta NB (25 June 1974). "United States Patent 3,819,706: Meta-chloro substituted α-butylamino-propiophenones". USPTO. Retrieved 2 June 2008.
- Perrine DM, Ross JT, Nervi SJ, Zimmerman RH (2000). "A Short, One-Pot Synthesis of Bupropion (Zyban, Wellbutrin)". Journal of Chemical Education 77 (11): 1479. Bibcode:2000JChEd..77.1479P. doi:10.1021/ed077p1479.
- "Wellbutrin label and approval history.". U.S. Food and Drug Administration Center for Drug Evaluation and Research. Retrieved 18 August 2007.
- "Bupropion (Wellbutrin)". eMedExpert.com. 31 March 2008. Retrieved 20 August 2013.
- Whitten L (April 2006). "Bupropion helps people with schizophrenia quit smoking". National Institute on Drug Abuse Research Findings 20 (5). Retrieved 27 May 2013.
- "Seasonal affective disorder drug Wellbutrin XL wins approval". CNN. 14 June 2006. Retrieved 19 August 2007.
- Waknine, Yael (8 May 2008). "FDA Approvals: Advair, Relistor, Aplenzin". Medscape. Retrieved 9 May 2008.
- "Generic drug equality questioned". Retrieved 13 October 2007.
- Jacqueline Stenson (12 October 2007). "Report questions generic antidepressant". msnbc.com. Retrieved 13 October 2007.
- "Review of therapeutic equivalence: generic bupropion XL 300 mg and Wellbutrin XL 300 mg". Archived from the original on 6 June 2011. Retrieved 19 April 2008.
- "Budeprion XL 300 mg not therapeutically equivalent to Wellbutrin XL 300 mg" (Press release). FDA. 3 October 2012. Retrieved 23 March 2013.
- Thomas K, Schmidt MS (2 July 2012). "Glaxo agrees to pay $3 billion in fraud settlement". The New York Times.
- "Zyban : sevrage tabagique et sécurité d'emploi" [Zyban: smoking cessation and job security] (Press release) (in French). Agence française de sécurité sanitaire des produits de santé. 18 January 2002. Retrieved 25 January 2011.
- GlaxoSmithKline (16 January 2007). "GlaxoSmithKline receives first European approval for Wellbutrin XR" (Press release). GlaxoSmithKline. Retrieved 25 January 2011.
- "Abuse potential of common psychiatric medications". Substance abuse treatment for persons with HIV/AIDS. Treatment Improvement Protocol. Rockville: Substance Abuse and Mental Health Services Administration. pp. 83–4.
- Lile JA, Nader MA (2003). "The abuse liability and therapeutic potential of drugs evaluated for cocaine addiction as predicted by animal models". Current Neuropharmacology 1: 21–46. doi:10.2174/1570159033360566.
- Antidepressant Wellbutrin becomes 'poor man's cocaine' on Toronto streets Global News 18 September 2013.
- Philipps, DeAnne (February 2012). "Wellbutrin®: Misuse and Abuse by Incarcerated Individuals". Journal of Addictions Nursing 23 (1): 65–69. doi:10.3109/10884602.2011.647838.
- Baribeau, Danielle; Araki, Keyghobad Farid (May–June 2013). "Intravenous Bupropion: A Previously Undocumented Method of Abuse of a Commonly Prescribed Antidepressant Agent". Journal of Addiction Medicine 7 (3): 216–217. doi:10.1097/ADM.0b013e3182824863.
- Official Wellbutrin website
- List of international brand names for bupropion
- Bupropion at DMOZ
- Wellbutrin Pharmacology, Pharmacokinetics, Studies, Metabolism – Bupropion – RxList Monographs
- NAMI Wellbutrin
- Bupropion article from mentalhealth.com