|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 The most important side effect is an increase in risk for epileptic seizures, which caused the drug to be withdrawn from the market for some time and then caused the recommended dosage to be reduced.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 as a weak norepinephrine-dopamine reuptake inhibitor. However, studies with humans via the oral administration route have demonstrated that it does not significantly affect dopamine levels in the brain at clinically-used doses, casting doubt on the notion that dopamine is involved in its clinical effects. Bupropion is a non-competitive antagonist of neuronal nicotinic acetylcholine receptors (nAChRs), an action which appears to be involved in both its antidepressant benefits and its efficacy in smoking cessation as high and/or altered acetylcholine levels may affect both. 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 Recreational use
- 3 Contraindications
- 4 Side effects
- 5 Overdose
- 6 Interactions
- 7 Pharmacology
- 8 Synthesis
- 9 Regulatory history
- 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 (Prozac) and paroxetine (Paxil), although trends favoring the efficacy of escitalopram (Lexapro), sertraline (Zoloft) and venlafaxine (Effexor) over bupropion have been observed. Mirtazapine (Remeron), 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.
The majority of depressed people suffer from insomnia, but there are some who instead experience constant sleepiness and fatigue. In this subgroup, bupropion has been found to be more effective than selective serotonin reuptake inhibitors (SSRIs) at alleviating the symptoms. There appears to be a modest advantage for the SSRIs compared to 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 and thus as of 2013 it has not been approved in the United States for this use.
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.
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.
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, as well as in pediatric patients, adolescents and young adults due to the increased risk of suicidal ideation.
Very common (>10%) adverse effects include
- Insomnia (which can usually be avoided by avoiding dosing near to bedtime. It is usually transient)
Common (1–10%) adverse effects include
Uncommon (0.1-1%) adverse effects include
- Chest pain
- Tachycardia (high heart rate)
- Increased blood pressure
Rare (0.01–0.1%) adverse effects include
- Orthostatic hypotension
- Abnormal dreams
- Memory impairment
- Paranoid ideation
- Blood glucose disturbances
- Erythema multiforme
- Stevens Johnson syndrome
- Urinary retention
- Urinary frequency
- Elevated liver enzymes
- Angioedema (which is indicative of a hypersensitivity reaction)
- Dyspnoea (also indicative of a hypersensitivity reaction)
- Bronchospasm (also indicative of a hypersensitivity reaction)
- Anaphylactic shock (also indicative of a hypersensitivity reaction)
- A condition similar to serum sickness
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, stopping bupropion abruptly may result in a "discontinuation syndrome" expressed as 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.
Based on animal research and in vitro research with human proteins, bupropion has been characterized as a weak norepinephrine-dopamine reuptake inhibitor (NDRI), and may also act as a releasing agent of dopamine and norepinephrine. 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.
In any case, the above findings suggest that, although weak DAT occupation may occur, oral bupropion at clinically-used doses does not have the actual capacity to elevate dopamine levels in the human brain. In accordance with this finding, based on analogy with serotonin reuptake inhibitors, higher than 50% inhibition of DAT would be needed for the dopamine reuptake mechanism to be a significant mechanism of the drug's action. Moreover, 65%–75% DAT occupancy is necessary for euphoria and abuse potential.
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.
|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.|
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.
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.
Marketed as Aplenzin, Budeprion, Elontril, Wellbutrin, Quomem, Prexaton, Voxra, and Zyban among others.
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