MAOI

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Monoamine oxidase inhibitor
Drug class
Ribbon diagram of human monoamine oxidase B
Ribbon diagram of human monoamine oxidase B, from PDB: 1GOS​
Class identifiers
SynonymsMAOI, RIMA
UseTreatment of major depressive disorder, treatment-resistant depression, atypical depression, Parkinson's disease, and several other disorders
ATC codeN06AF
Mechanism of actionEnzyme inhibitor
Biological targetMonoamine oxidase enzymes:
MAO-A and/or MAO-B
External links
MeSHD008996
Legal status
In Wikidata

Monoamine oxidase inhibitors (MAOIs) are a class of drugs that inhibit one or both monoamine oxidase enzymes: monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B). These enzymes metabolize monoamine neurotransmitters and related amines, including serotonin, norepinephrine, dopamine, epinephrine, tyramine, and several trace amines.

MAOIs include several pharmacologically distinct groups. The classic antidepressant MAOIs—phenelzine, tranylcypromine, and isocarboxazid—are irreversible, non-selective inhibitors of both MAO-A and MAO-B and are used primarily in major depressive disorder, including treatment-resistant depression.[1] Other MAOIs include reversible inhibitors of MAO-A (RIMAs), such as moclobemide, and selective MAO-B inhibitors, such as selegiline, rasagiline, and safinamide, which are used mainly in Parkinson's disease or, in the case of transdermal selegiline, depression.

MAOI selectivity can vary by dose, route, formulation, and systemic exposure. For example, selegiline is relatively selective for MAO-B at lower doses used in Parkinson's disease, but at higher antidepressant doses also inhibits MAO-A and can function clinically as a non-selective MAOI.[1]

The use of classic MAOIs declined after reports of serious interactions with tyramine-containing foods and some sympathomimetic or serotonergic drugs. Modern reviews and prescribing guides state that classic MAOIs remain effective antidepressants and can be used safely when standard dietary and medication-interaction precautions are followed. The risk of serious tyramine-related blood-pressure reactions is described as limited under modern dietary guidance, partly because food standards, refrigeration, and production methods have reduced tyramine exposure compared with the early decades of MAOI use.[1][2]

Medical uses

Skeletal formula of moclobemide, the prototypical RIMA.

Depression

Classic irreversible MAOIs are used in the treatment of major depressive disorder, especially treatment-resistant depression. Modern guidance recommends considering phenelzine, tranylcypromine, or isocarboxazid after insufficient response to other antidepressant treatments, including selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), mirtazapine, bupropion, tricyclic antidepressants (TCAs), or augmentation strategies.[1] The same guidance states that classic MAOIs are typically considered before electroconvulsive therapy when rapid response is not required, although ECT may be preferred when urgent response is necessary, such as in imminent suicide risk, inanition, or catatonia.[1]

MAOIs have long been associated with efficacy in atypical depression,[3][4] but modern expert guidance also emphasizes their use in severe treatment-resistant depression more broadly, including melancholic or endogenous depression.[1] Phenelzine may be particularly useful when anxiety or panic symptoms predate or accompany depression, while tranylcypromine may be considered when psychomotor retardation or melancholic features are prominent. Isocarboxazid has fewer comparative data, but modern guidance describes it as an effective alternative, including when phenelzine or tranylcypromine are not well tolerated, and as a possible first option where available; its generally favorable tolerability profile may be relevant when sedation, somnolence, weight gain, edema, or other adverse effects limit treatment with another classic MAOI. Expert guidance cautions against treating these distinctions as absolute.[1]

MAOIs may also be effective in some cases of bipolar depression, although antidepressant treatment in bipolar disorder requires specific caution because of the risk of mood switching and the need for mood-stabilizing treatment.[5][1]

MAOIs have been studied or used in several anxiety-related disorders, including panic disorder with agoraphobia,[6] social anxiety disorder,[7][8][9] and mixed anxiety and depressive states. Modern prescribing guidance also notes potential usefulness in treatment-resistant anxiety and panic disorders.[1]

Other studied or reported uses include bulimia nervosa,[10][11][12][13] post-traumatic stress disorder,[14] borderline personality disorder,[15] and obsessive–compulsive disorder (OCD).[16][17] Evidence for some of these indications is limited, and in several cases consists mainly of older trials, small studies, or uncontrolled reports.[18]

Parkinson's disease and other uses

Selective MAO-B inhibitors, including selegiline, rasagiline, and safinamide, are used in the treatment of Parkinson's disease, where inhibition of dopamine metabolism can increase dopaminergic activity.[19] Non-selective MAOIs and MAO-B inhibitors have also been investigated in other neurological contexts, including neuroprotection and migraine prevention, but these uses vary by drug and indication.

Pargyline is a non-selective MAOI that was previously used as an antihypertensive agent to treat hypertension.[19][20]

Adverse effects and safety

Common adverse effects

The adverse-effect profile of MAOIs varies by drug, dose, and selectivity. Common adverse effects of classic irreversible MAOIs can include orthostatic hypotension, sleep disturbance, sedation or somnolence, insomnia, dry mouth, sexual dysfunction, urinary retention, constipation, edema, weight change, agitation, and paresthesias.[1]

Orthostatic hypotension is a predictable dose-related effect of classic MAOIs. It often appears after dose increases, may peak after about 10 to 14 days, and often improves over the following weeks. Blood-pressure measurements while sitting or lying and standing can help distinguish this effect from baseline variation or transient post-dose increases.[1]

The pattern differs among classic MAOIs. Phenelzine is more often associated with weight gain, edema, somnolence, sexual dysfunction, pyridoxine deficiency, and rare hepatotoxicity, while tranylcypromine is less associated with weight gain and hepatotoxicity but may produce more insomnia and transient post-dose blood-pressure increases.[1] Isocarboxazid is generally described as better tolerated than phenelzine, although higher doses can produce anticholinergic-type adverse effects, insomnia, subjective weakness, edema, carbohydrate cravings, and rare hepatotoxicity.[1]

Tyramine and hypertensive reactions

People taking classic irreversible, non-selective MAOIs generally need to limit foods and beverages containing substantial amounts of tyramine. Tyramine is formed by microbial decarboxylation of tyrosine and may be present in high amounts in some foods that are fermented, matured, aged, or spoiled. Because inhibition of MAO reduces the breakdown of dietary tyramine in the gastrointestinal tract and liver, excessive tyramine intake can raise blood pressure through peripheral norepinephrine release; this blood-pressure-raising effect is often called a pressor response. In serious cases, it can cause hypertensive urgency or emergency.[1][2]

Higher-risk foods include some aged cheeses, some artisan beers using natural yeasts, some fermented meats, and fermented products such as soy sauce, miso, tempeh, sauerkraut, Marmite, and kimchi.[1] Modern food standards, refrigeration, and starter-culture methods have substantially reduced tyramine levels in many foods compared with the 1950s and 1960s. Modern guidance describes the risk of a serious blood-pressure increase as limited when dietary and medication precautions are followed, although it cannot be fully ruled out.[1][2]

Historical estimates from the early decades of MAOI use reported hypertensive reactions in a small minority of treated patients. One review cited early tranylcypromine-era estimates of hypertensive crisis around 0.5% and death around 0.001%, before modern tyramine-restricted diets and before the lower tyramine levels associated with contemporary food production. Later safety reviews describe fatal tyramine-related reactions as extremely rare, with no deaths from MAOI-induced hypertension reported in the medical literature for several decades.[21][2]

Blood-pressure elevation after excessive tyramine intake is usually self-limiting and typically reaches its maximum within about 2 hours.[1] Modern guidance discourages rapid blood-pressure reduction outside appropriate medical supervision, because overtreatment can cause hypotensive overshoot; sublingual nifedipine is specifically discouraged.[1]

Dietary risk differs among MAOI subclasses. RIMAs such as moclobemide are reversible MAO-A inhibitors and generally have lower tyramine-related dietary risk than classic irreversible non-selective MAOIs.[22] Low-dose selective MAO-B inhibitors also have lower tyramine-related dietary risk. However, these distinctions depend on the specific drug, dose, route, and formulation, and higher doses or formulations that also inhibit MAO-A may require dietary precautions.[1]

Withdrawal and discontinuation

Abrupt or rapid discontinuation of MAOIs can cause discontinuation symptoms, which may include anxiety, agitation, insomnia or drowsiness, hallucinations, delirium, paranoid symptoms, and mania or hypomania.[1] As with many antidepressants, gradual dose reduction is generally used to reduce the risk and severity of discontinuation symptoms.[23]

After stopping an irreversible MAOI, MAO activity returns only as new enzyme is synthesized or repaired, so dietary and medication precautions generally continue for a period after discontinuation. Washout periods are especially important when switching between an MAOI and drugs with significant serotonin reuptake inhibition or serotonin-releasing activity.[1]

Drug interactions

Mechanism-based interactions

MAOI interactions are best assessed by mechanism rather than by broad drug class. The highest-risk interactions include drugs that substantially increase serotonin, especially those with significant serotonin reuptake inhibition or serotonin-releasing activity. Examples generally avoided for this reason include SSRIs, SNRIs, clomipramine, imipramine, chlorpheniramine, brompheniramine, MDMA, meperidine, tramadol, methadone, tapentadol, dextromethorphan, dextropropoxyphene, pentazocine, and levorphanol.[1] The main risk is serotonin toxicity, a dose-related condition that can include tremor, hyperreflexia, clonus, agitation, autonomic instability, and, in severe cases, life-threatening toxicity.[24][25]

Other combinations are avoided because of different mechanisms or limited safety data. Modern MAOI prescribing guidance lists pancuronium, cocaine, methyldopa, reserpine, St John's wort, ayahuasca, and drugs that also have clinically relevant MAOI activity, such as methylene blue and linezolid, as combinations to avoid with classic MAOIs. Methylene blue and linezolid are not serotonin reuptake inhibitors; they are usually avoided with classic MAOIs because they also have MAOI activity, safety data are limited, and there is usually little clinical reason to combine multiple MAOIs. The main serotonin-toxicity concern is when their MAOI activity overlaps with drugs that substantially increase serotonin, such as serotonin reuptake inhibitors or serotonin-releasing agents.[1]

Some drugs can markedly increase catecholamine signaling or blood pressure. Medium- or high-dose amphetamines and fenfluramine are avoided because of serotonin-releasing activity. Low-dose amphetamines, ephedrine, and pseudoephedrine are treated as strong relative contraindications rather than absolute contraindications; if used by experienced clinicians, reduced dosing, slow titration, and blood-pressure monitoring are required.[1] Direct adrenergic agents such as epinephrine, norepinephrine, phenylephrine, isoproterenol, and dobutamine are not absolute contraindications, but their blood-pressure-raising effects may be potentiated, so reduced initial dosing and careful titration are advised.[1]

Several drug classes contain both higher- and lower-risk agents. Tricyclic antidepressants are not pharmacologically uniform: clomipramine and imipramine are avoided because of significant serotonin reuptake inhibition, whereas other TCAs are considered compatible with MAOIs when selected appropriately, started at low doses, titrated gradually, and monitored.[1] Ziprasidone and lumateperone are distinguished from most other antipsychotics because they have clinically significant serotonin reuptake inhibition; other antipsychotics are generally considered compatible with MAOIs when otherwise appropriate.[1]

Serotonin precursors are also relevant to MAOI interaction risk. 5-HTP and other serotonin precursors may increase serotonin-toxicity risk. L-tryptophan is not categorically contraindicated with MAOIs and has been used by experienced clinicians as an augmenting agent, but serotonin-mediated adverse effects such as hyperreflexia or clonus may occur, particularly at higher doses.[1]

Interactions with psychoactive substances vary by mechanism, and the evidence base is limited. A 2026 narrative review reported suspected serotonin toxicity with MAOIs in combination with amphetamine, dextromethorphan, MDMA, meperidine, methadone, and tramadol. Hypertensive urgency or emergency was reported with MAOIs in combination with some tyramine-containing alcohol, amphetamine, cocaine, dextroamphetamine, khat, methamphetamine, and psilocybin mushrooms.[26] Because MAOIs can reduce metabolism of some psychoactive substances and alter monoamine signaling, interaction risk should not be generalized across broad categories such as "psychedelics" or "stimulants".[26]

Switching from or to MAOIs

When switching from an SSRI, SNRI, clomipramine, imipramine, or another drug with significant serotonin reuptake inhibition or serotonin-releasing activity, a washout period is required before MAOI initiation. The usual washout principle is five half-lives of the previous drug, with longer intervals for drugs such as fluoxetine and vortioxetine.[1]

Switching from one classic MAOI to another is usually handled more cautiously than switching within many other antidepressant classes. Many guidelines advise a washout period, especially after an irreversible MAOI. However, this general rule is distinct from planned specialist-supervised MAOI-to-MAOI switching. Modified washouts, cautious cross-tapers, and rapid switches have been reported in selected patients. Published reports are limited, but have not clearly shown serotonin toxicity from MAOI-to-MAOI switching itself; one 2018 report described outpatient cross-taper and inpatient rapid-switch strategies without adverse events. These approaches remain specialist-level strategies requiring close monitoring and further study.[1][27]

Combination and augmentation strategies

Some agents historically listed as incompatible with MAOIs are described in modern specialist guidance as possible combination, bridging, augmentation, or side-effect-management options in monitored clinical settings.[1]

During switches from serotonin-reuptake-inhibiting antidepressants to classic MAOIs, nortriptyline, lithium, and low-dose mirtazapine are described as possible bridging agents during the washout period and later MAOI initiation.[1]

As examples of augmentation strategies, modern guidance discusses lithium, methylphenidate, modafinil, bupropion, reboxetine, triiodothyronine (T3), pramipexole, agomelatine, and TCAs other than imipramine and clomipramine. Imipramine and clomipramine are excluded because of significant serotonin reuptake inhibition. Among the remaining TCAs, amitriptyline is described as having the most pronounced serotonergic activity, but the cited guidance states that the combination of amitriptyline and an MAOI does not result in serotonin toxicity. TCA selection and dosing still require caution because TCAs differ in other pharmacological effects. For insomnia associated with MAOI treatment, trazodone, mirtazapine, or doxepin are described as options at low doses; the cited guidance notes that these agents do not have significant serotonin reuptake inhibition at the doses discussed. The same guidance also describes successful comedication in some MAOI partial responders with full-dose trazodone or mirtazapine, reflecting a distinction between serotonin-reuptake-inhibiting antidepressants and agents with little or no clinically significant serotonin reuptake inhibition.[1]

Potent norepinephrine reuptake inhibitors, including nortriptyline, desipramine, protriptyline, and reboxetine, may also attenuate tyramine-related blood-pressure increases because tyramine enters sympathetic neurons through the norepinephrine transporter. This may offer some protection against excessive tyramine exposure, although it is not a substitute for dietary precautions or clinical monitoring.[1][28]

Perioperative and anesthesia considerations

Historically, patients were often advised to discontinue irreversible MAOIs before surgery or general anesthesia. More recent MAOI prescribing guidance does not support routine discontinuation before surgery. Instead, it recommends planning anesthesia around the MAOI by avoiding specific interacting drugs, selecting non-serotonergic analgesics when possible, and adjusting vasopressor dosing when needed. The MAOI should not be discontinued without consultation with the prescribing clinician.[1]

Important perioperative interaction risks include serotonergic opioid analgesics such as meperidine and tramadol, as well as other opioids or analgesics with serotonergic or uncertain-risk properties, including methadone, tapentadol, dextromethorphan, dextropropoxyphene, pentazocine, and levorphanol.[1][29] Opioids without significant serotonergic activity are considered generally compatible with MAOIs, although usual clinical monitoring remains necessary.[1]

Pancuronium, a muscle relaxant sometimes used with general anesthetics, is separately listed in modern MAOI prescribing guidance as a combination that should be avoided.[1] Perioperative methylene blue and linezolid should generally be avoided with classic MAOIs because they have clinically relevant MAOI activity. They are not serotonin reuptake inhibitors themselves, but can increase serotonin-toxicity risk when other drugs with significant serotonin reuptake inhibition or serotonin-releasing activity are also involved.[1]

In dental and local-anesthetic contexts, cocaine-containing local anesthetics are avoided. Epinephrine-containing local anesthetics may require lower doses or shorter treatment duration, and alternatives such as felypressin may be considered in patients with cardiovascular or cerebrovascular conditions.[1]

Pharmacology

Ribbon diagram of a monomer of human MAO-A, with FAD and clorgiline bound, oriented as if attached to the outer membrane of a mitochondrion. From PDB: 2BXS​.

Mechanism of action

MAOIs act by inhibiting monoamine oxidase, a mitochondrial enzyme involved in the oxidative deamination and breakdown of monoamine neurotransmitters and related amines. MAO-A preferentially metabolizes serotonin, norepinephrine, epinephrine, and tyramine, while MAO-B preferentially metabolizes phenethylamine and certain other trace amines. Dopamine is metabolized by both MAO-A and MAO-B.[19]

These isoenzyme differences are clinically relevant. Inhibition of MAO-A is especially important for antidepressant effects involving serotonin and norepinephrine and for tyramine-related dietary risk, while MAO-B inhibition is important in Parkinson's disease because of its role in dopamine metabolism. Classic antidepressant MAOIs inhibit both isoenzymes, whereas several Parkinson's disease MAOIs are relatively MAO-B-selective at recommended doses.[19][1]

Inhibition of MAO reduces monoamine breakdown and thereby increases the availability of monoamines. Classic antidepressant MAOIs increase monoamine neurotransmitters within as well as outside neurons, which distinguishes them from reuptake inhibitors, whose primary action is to block transporter-mediated reuptake and produce relative extracellular increases.[1]

Reversibility

Early antidepressant MAOIs, including phenelzine, tranylcypromine, and isocarboxazid, irreversibly inhibit MAO. The inhibited enzyme remains inactive until new enzyme is synthesized or functional enzyme is otherwise restored. This explains why the pharmacodynamic effects of irreversible MAOIs outlast their plasma half-lives and why medication and dietary interaction precautions continue after discontinuation.

Reversible inhibitors of monoamine oxidase A (RIMAs), such as moclobemide, bind reversibly to MAO-A. Their inhibition can be displaced more readily than that of irreversible MAOIs, contributing to lower tyramine-related dietary risk. RIMAs are also generally safer than older irreversible MAOIs in single-drug overdose.[30] However, RIMAs can still interact with drugs that substantially increase serotonergic activity because MAO-A metabolizes serotonin.[1]

Harmaline, found in Peganum harmala, Banisteriopsis caapi, and Passiflora incarnata, is a reversible inhibitor of monoamine oxidase A.[31]

Selectivity

In addition to reversibility, MAOIs differ in their relative selectivity for MAO-A and MAO-B. Selectivity is not always a fixed property of a drug and may depend on dose, formulation, route of administration, and systemic exposure. Some drugs are non-selective at usual clinical doses, while others are relatively selective for MAO-A or MAO-B only within particular dosing ranges.

The classic antidepressant MAOIs phenelzine, tranylcypromine, and isocarboxazid are generally described as irreversible, non-selective inhibitors of both MAO-A and MAO-B at therapeutic antidepressant doses.[1] By contrast, selegiline, rasagiline, and safinamide are used mainly as MAO-B-selective agents in Parkinson's disease. This selectivity is dose-dependent. At higher doses, selegiline also inhibits MAO-A and can function clinically as a non-selective MAOI antidepressant; dietary restrictions for transdermal selegiline vary by dose.[1]

Selective MAO-B inhibition at recommended Parkinson's disease doses is generally associated with much lower tyramine-related dietary risk than non-selective MAO-A/MAO-B inhibition. However, this distinction is dose-dependent, and higher doses or formulations that also inhibit MAO-A may require dietary precautions.[1]

For this reason, selectivity, dietary restrictions, and interaction risk vary by drug, dose, formulation, and clinical use.

History

The history of MAOIs began with the serendipitous discovery that iproniazid, originally developed for tuberculosis, had antidepressant properties and inhibited monoamine oxidase.[32] Iproniazid and related early MAOIs became important early antidepressants and contributed to the development of the monoamine theory of depression.

The older MAOIs were used most widely between the late 1950s and around 1970.[33] Some MAOIs also had non-psychiatric uses; for example, pargyline was used as an antihypertensive agent.[19][20] Their use declined after serious interactions with sympathomimetic drugs and tyramine-containing foods were recognized. The later discovery of MAO-A and MAO-B isoenzymes led to the development of selective MAO-B inhibitors for Parkinson's disease and reversible MAO-A inhibitors with lower dietary tyramine risk.[34][35][36]

Moclobemide was the first reversible inhibitor of MAO-A to enter widespread clinical practice.[37] A transdermal patch form of selegiline, marketed as Emsam, was approved by the Food and Drug Administration in the United States for major depressive disorder on 28 February 2006.[38]

List of MAO-inhibiting drugs

Classic irreversible antidepressant MAOIs

Classic antidepressant MAOIs are irreversible, non-selective inhibitors of MAO-A and MAO-B at therapeutic antidepressant doses.[1]

MAOIs used for depression in the United States include:[39]

  • Isocarboxazid
  • Phenelzine
  • Tranylcypromine
  • Transdermal selegiline

Reversible MAO-A inhibitors

Other RIMAs or RIMA-like agents include:

Selective MAO-B inhibitors

Selective MAO-B inhibitors are used mainly in Parkinson's disease. Their selectivity is dose-dependent and should not be assumed to apply at all doses or routes.

Other drugs with MAOI activity

Some drugs not primarily used as antidepressant MAOIs have clinically relevant MAO-inhibiting activity.

  • Linezolid, an antibiotic with weak reversible MAO-inhibiting activity[41]
  • Methylene blue, which has clinically relevant MAO-A-inhibiting activity and can precipitate serotonin toxicity when combined with drugs that have clinically significant serotonin reuptake inhibition or serotonin-releasing activity[1][42]
  • Furazolidone, an antibiotic with MAO-inhibiting activity[43]

Naturally occurring reversible MAOIs

Several naturally occurring reversible MAOIs have been characterized.[44]

Withdrawn or discontinued MAOIs

Research compounds

See also

References

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