WordNet

limit, block, or decrease the action or function of; "inhibit the action of the enzyme"; "inhibit the rate of a chemical reaction"
control and refrain from showing; of emotions, desires, impulses, or behavior (同)bottle up, suppress
limit the range or extent of; "Contact between the young was inhibited by strict social customs"
a substance that retards or stops an activity
the 13th letter of the Roman alphabet (同)m

PrepTutorEJDIC

〈感情・欲望・行動・作用など〉‘を'抑制する / (…しないように)〈人〉‘を'抑制する,妨げる《+『名』+『from』+『名』(do『ing』)》
抑制する人(物) / 化学反応抑制剤
Mach number / mark[s] / Monsieur
Massachusetts / mental age

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/03/29 09:42:54」(JST)

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Monoamine oxidase

Monoamine oxidase inhibitors (MAOIs) are chemicals which inhibit the activity of the monoamine oxidase enzyme family. They have a long history of use as medications prescribed for the treatment of depression. They are particularly effective in treating atypical depression.^[1] They are also used in the treatment of Parkinson's disease and several other disorders.

Because of potentially lethal dietary and drug interactions, monoamine oxidase inhibitors have historically been reserved as a last line of treatment, used only when other classes of antidepressant drugs (for example selective serotonin reuptake inhibitors and tricyclic antidepressants) have failed.^[2] New research into MAOIs indicates that much of the concern over their dangerous dietary side effects stems from misconceptions and misinformation, and that despite proven effectiveness of this class of drugs, it is underutilized and misunderstood in the medical profession.^[3] New research also questions the validity of the perceived severity of dietary reactions, which has historically been based on outdated research.^[4] However this research also notes that many practitioners have a poor understanding of drug interactions, and 'drug interactions can be serious, and concomitant medication use must be stringently overseen' as they 'can cause a dangerous or fatal serotonin syndrome/ toxicity'.^[3]

1 Indications
2 Mechanism of action
- 2.1 Reversibility
- 2.2 Selectivity
3 Dangers
- 3.1 Hypertensive Crisis & Tyramine
- 3.2 Drug Interactions
- 3.3 Withdrawal
- 3.4 Listing of interactions
4 History
5 List of MAO inhibiting drugs
- 5.1 Marketed drugs
- 5.2 Drugs withdrawn from the market
6 See also
7 References

Indications

Newer MAOIs such as selegiline (typically used in the treatment of Parkinson's disease) and the reversible MAOI moclobemide provide a safer alternative^[5] and are now sometimes used as first-line therapy.

MAOIs have been found to be effective in the treatment of panic disorder with agoraphobia,^[6] social phobia,^[7]^[8]^[9] atypical depression^[10]^[11] or mixed anxiety and depression, bulimia,^[12]^[13]^[14]^[15] and post-traumatic stress disorder,^[16] as well as borderline personality disorder.^[17] MAOIs appear to be particularly effective in the management of bipolar depression according to a recent retrospective-analysis.^[18] There are reports of MAOI efficacy in obsessive-compulsive disorder (OCD), trichotillomania, dysmorphophobia, and avoidant personality disorder, but these reports are from uncontrolled case reports.^[5]

MAOIs can also be used in the treatment of Parkinson's disease by targeting MAO-B in particular (therefore affecting dopaminergic neurons), as well as providing an alternative for migraine prophylaxis. Inhibition of both MAO-A and MAO-B is used in the treatment of clinical depression and anxiety.

MAOIs appear to be particularly indicated for outpatients with dysthymia complicated by panic disorder or hysteroid dysphoria, which involves repeated episodes of depressed mood in response to feeling rejected.^[19]

Mechanism of action

MAOIs act by inhibiting the activity of monoamine oxidase, thus preventing the breakdown of monoamine neurotransmitters and thereby increasing their availability. There are two isoforms of monoamine oxidase, MAO-A and MAO-B. MAO-A preferentially deaminates serotonin, melatonin, epinephrine, and norepinephrine. MAO-B preferentially deaminates phenethylamine and certain other trace amines; in contrast, MAO-A preferentially deaminates other trace amines, like tyramine, whereas dopamine is equally deaminated by both types.

Reversibility

The early MAOIs covalently bound to the monoamine oxidase enzymes, thus inhibiting them irreversibly; the bound enzyme could not function and thus enzyme activity was blocked until the cell made new enzymes. The enzymes turn over approximately every two weeks. A few newer MAOIs, a notable one being moclobemide, are reversible, meaning that they are able to detach from the enzyme to facilitate usual catabolism of the substrate. The level of inhibition in this way is governed by the concentrations of the substrate and the MAOI.^{[medical citation needed]}

Harmaline found in Peganum harmala, Banisteriopsis caapi, and Passiflora incarnata is a reversible inhibitor of monoamine oxidase A (RIMA).^[20]

Selectivity

In addition to reversibility, MAOIs differ by their selectivity of the MAO receptor. Some MAOIs inhibit both MAO-A and MAO-B equally, other MAOIs have been developed to target one over the other.

MAO-A inhibition reduces the breakdown of primarily serotonin, norepinephrine, and dopamine; selective inhibition of MAO-A allows for tyramine to be metabolised via MAO-B.^[21] Agents that act on serotonin if taken with another serotonin-enhancing agent may result in a potentially fatal interaction called serotonin syndrome or with irreversible and unselective inhibitors (such as older MAOIs), of MAO a hypertensive crisis as a result of tyramine food interactions is particularly problematic with older MAOIs. Tyramine is broken down by MAO-A and MAO-B, therefore inhibiting this action may result in its excessive build-up, so diet must be monitored for tyramine intake.

MAO-B inhibition reduces the breakdown mainly of dopamine and phenethylamine so there are no dietary restrictions associated with this. MAO-B would also metabolize tyramine, as the only differences between dopamine, phenethylamine, and tyramine are two phenylhydroxyl groups on carbons 3 and 4. The 4-OH would not be a steric hindrance to MAO-B on tyramine.^[22] Two MAO-Bi drugs, selegiline and rasagiline have been approved by the FDA without dietary restrictions, except in high-dosage treatment, wherein they lose their selectivity.^[23]^[24]

Dangers

Hypertensive Crisis & Tyramine

Patients taking MAOIs generally need to change their diets to limit or avoid foods and beverages containing tyramine. If large amounts of tyramine are consumed, they may suffer hypertensive crisis, which can be fatal.^[3] Examples of foods and beverages with potentially high levels of tyramine include liver and fermented substances, such as alcoholic beverages and aged cheeses.^[25] (See a List of foods containing tyramine).

Tyramine leads to hypertensive crisis by increasing the release of norepinephrine (NE), which causes blood vessels to constrict (through binding to alpha-1 adrenergic receptors).^[26] Ordinarily, MAO-A would destroy the excess NE. When MAO-A is inhibited, though, NE levels get too high, leading to dangerous increases in blood pressure.

Of note, no dietary modifications are needed when taking a reversible inhibitor of MAO-A (i.e., moclobemide) or low doses of selective MAO-B inhibitors (e.g., selegiline 6 mg/24 hours transdermal patch).^[26]^[27]^[28]

Drug Interactions

The most significant risk associated with the use of MAOIs is the potential for interactions with over-the-counter and prescription medicines, illicit drugs or medications, and some supplements (e.g., St. John's wort, tryptophan). It is vital that a doctor supervise such combinations to avoid adverse reactions. For this reason, many users carry an MAOI-card, which lets emergency medical personnel know what drugs to avoid. (E.g., adrenaline dosage should be reduced by 75%, and duration is extended.)^[25]

Tryptophan supplements should not be consumed with MAOIs as the potentially fatal serotonin syndrome may result.^[29]

MAOIs should not be combined with other psychoactive substances (antidepressants, painkillers, stimulants, both legal and illegal etc.) except under expert care. Certain combinations can cause lethal reactions, common examples including SSRIs, tricyclics, MDMA, meperidine,^[30] tramadol, and dextromethorphan.^{[citation needed]} Agents with actions on epinephrine, norepinephrine, or dopamine must be administered at much lower doses due to potentiation and prolonged effect.

Nicotine, a substance frequently implicated in tobacco addiction, has been shown to have "relatively weak" addictive properties when administered alone.^[31] The addictive potential increases dramatically after co-administration of an MAOI, which specifically causes sensitization of the locomotor response in rats, a measure of addictive potential.^[32]^[33] This may be reflected in the difficulty of smoking cessation, as tobacco contains naturally-occurring MAOI compounds in addition to the nicotine.^[34]^[35]^[36]

Withdrawal

Antidepressants including MAOIs have some dependence-producing effects, the most notable one being a withdrawal syndrome, which may be severe especially if MAOIs are discontinued abruptly or overly rapidly. However, the dependence-producing potential of MAOIs or antidepressants in general is not as significant as benzodiazepines. Withdrawal symptoms can be managed by a gradual reduction in dosage over a period of weeks, months or years to minimize or prevent withdrawal symptoms.^[37]

MAOIs, as with any antidepressant medications, do not alter the course of the disorder, so it is possible that discontinuation can return the patient to the pre-treatment state.^[38]

This consideration greatly complicates switching a patient between a MAOI and a SSRI, because it is necessary to clear the system completely of one drug before starting another. If one also tapers dosage gradually, the result is that for weeks a depressed patient will have to bear the depression without chemical help during the drug-free interval. This may be preferable to risking the effects of an interaction between the two drugs, but it is often not easy for the patient.^{[citation needed]}

Listing of interactions

The MAOIs are infamous for their numerous drug interactions, including the following kinds of substances:

Substances that are metabolized by monoamine oxidase, as they can be boosted by up to several-fold.
Substances that increase serotonin, norepinephrine, or dopamine activity, as too much of any of these neurochemicals can result in severe acute consequences, including serotonin syndrome, hypertensive crisis, and psychosis, respectively.

Such substances that can react with MAOIs include:

Phenethylamines: 2C-B, Mescaline, Phenethylamine (PEA), etc.
- Amphetamines: Amphetamine,^[39] MDMA, Dextroamphetamine, Methamphetamine, DOM, etc.
Tryptamines: DMT, Psilocin/Psilocybin ("Magic Mushrooms"), etc.
- Lysergamides: Ergolines/LSA, LSD ("Acid"), etc.
Serotonin, Norepinephrine, and/or Dopamine Reuptake Inhibitors:
- Selective Serotonin Reuptake Inhibitors (SSRIs): Citalopram, Dapoxetine, Escitalopram, Fluoxetine, Fluvoxamine, Paroxetine, Sertraline.
- Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): Desvenlafaxine, Duloxetine, Milnacipran, Venlafaxine.
- Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs): Amineptine, Bupropion, Methylphenidate, Nomifensine.
- Norepinephrine Reuptake Inhibitors (NRIs): Atomoxetine, Mazindol, Reboxetine.
- Tricyclic Antidepressants (TCAs): Amitriptyline, Butriptyline, Clomipramine, Desipramine, Dosulepin, Doxepin, Imipramine, Lofepramine, Nortriptyline, Protriptyline, Trimipramine.
- Tetracyclic Antidepressants (TeCAs): Amoxapine, Maprotiline.
- Phenylpiperidine derivative Opioids: Meperidine/Pethidine, Tramadol, Methadone, Fentanyl, Dextropropoxyphene, Propoxyphene.
- Others: Brompheniramine, Chlorpheniramine, Cocaine, Cyclobenzaprine, Dextromethorphan (DXM), Ketamine, MDPV, Nefazodone, Phencyclidine (PCP), Pheniramine, Sibutramine, Trazodone.
Serotonin, Norepinephrine, and/or Dopamine Releasers: 4-Methylaminorex (4-MAR), Amphetamine, Benzphetamine, Cathine, Cathinone, Diethylcathinone, Ephedrine, Levmetamfetamine, Lisdexamfetamine, MDMA ("Ecstasy"), Methamphetamine, Pemoline, Phendimetrazine, Phenethylamine (PEA), Phentermine, Propylhexedrine, Pseudoephedrine, Phenylephrine, Tyramine.
Serotonin, Norepinephrine, and/or Dopamine Supplemental Precursors: 5-HTP, L-DOPA, L-Phenylalanine, L-Tryptophan, L-Tyrosine.
Local and general anesthetic in surgery and dentistry in particular those containing Epinephrine. There is no universally taught or accepted practice regarding dentistry and use of MAOIs such as Phenelzine and it is, therefore, vital to inform all clinicians especially dentists of the potential effect of MAOIs and Local Anesthesia. In preparation for dental work, withdrawal from Phenelzine is specifically advised, however since this takes two weeks it is not always a desirable or practical option. Dentists using Local Anesthesia are advised to use a non-epinephrine anesthetic such as Carbocaine at a level of 3%. Specific attention should be paid to blood pressure during the procedure and the level of the anesthetic should be regularly and appropriately topped up since non-epinephrine anestetics take longer to come into effect and wear off faster. Patients taking Phenelzine are advised to notify their Psychiatrist prior to any dental treatment.
Certain other supplements: Hypericum perforatum ("St John's wort"), Inositol, Rhodiola rosea, S-Adenosyl-L-Methionine (SAMe), L-Theanine.
Other Monoamine Oxidase Inhibitors.

History

MAOIs started off due to the serendipitous discovery that iproniazid was a weak MAO inhibitor (MAOI). Originally intended for the treatment of tuberculosis, in 1952, iproniazid antidepressant properties were discovered when researchers noted that the depressed patients given iproniazid experienced a relief of their depression. Subsequent in vitro work led to the discovery that it inhibited MAO and eventually to the monoamine theory of depression. MAOIs became widely used as antidepressants in the early 1950s. The discovery of the 2 isoenzymes of MAO has led to the development of selective MAOIs that may have a more favorable side-effect profile.^[40]

The older MAOIs' heyday was mostly between the years 1957 and 1970.^[21] The initial popularity of the 'classic' non-selective irreversible MAO inhibitors began to wane due to their serious interactions with sympathomimetic drugs and tyramine-containing foods that could lead to dangerous hypertensive emergencies. As a result, the use by medical practitioners of these older MAOIs declined. When scientists discovered that there are two different MAO enzymes (MAO-A and MAO-B), they developed selective compounds for MAO-B, (for example, selegiline, which is used for Parkinson's disease), to reduce the side-effects and serious interactions. Further improvement occurred with the development of compounds (moclobemide and toloxatone) that not only are selective but cause reversible MAO-A inhibition and a reduction in dietary and drug interactions.^[41]^[42] Moclobemide, was the first reversible inhibitor of MAO-A to enter widespread clinical practice.^[43]

A transdermal patch form of the MAOI selegiline, called Emsam, was approved for use in depression by the Food and Drug Administration in the United States on February 28, 2006.^[23]

List of MAO inhibiting drugs

Marketed drugs

Nonselective MAO-A/MAO-B inhibitors
- Hydrazines
  - Isocarboxazid (Marplan)
  - Nialamide (Niamid)
  - Phenelzine (Nardil, Nardelzine)
  - Hydracarbazine
- Non-hydrazines
  - Tranylcypromine (Parnate, Jatrosom)
Selective MAO-A inhibitors
- Bifemelane (Alnert, Celeport) (available in Japan)
- Moclobemide (Aurorix, Manerix)
- Pirlindole (Pirazidol) (available in Russia)
- Toloxatone (Humoryl) (available in France)
Selective MAO-B inhibitors
- Rasagiline (Azilect)
- Selegiline (Deprenyl, Eldepryl, Emsam, Zelapar)

Linezolid is an antibiotic drug with weak MAO-inhibiting activity.^[44]

Methylene blue, the antidote indicated for drug-induced methemoglobinemia, among a plethora of other off-label uses, is a highly potent, reversible MAO inhibitor.^[45]

Drugs withdrawn from the market

Nonselective MAO-A/MAO-B inhibitors
- Hydrazines
  - Benmoxin (Nerusil, Neuralex)
  - Iproclozide (Sursum)
  - Iproniazid (Marsilid, Iprozid, Ipronid, Rivivol, Propilniazida) (discontinued worldwide except for France)
  - Mebanazine (Actomol)
  - Octamoxin (Ximaol, Nimaol)
  - Pheniprazine (Catron)
  - Phenoxypropazine (Drazine)
  - Pivalylbenzhydrazine (Tersavid)
  - Safrazine (Safra) (discontinued worldwide except for Japan)
- Non-hydrazines
  - Caroxazone (Surodil, Timostenil)
Selective MAO-A inhibitors
- Minaprine (Cantor)

References

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UpToDate Contents

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1. 成人におけるうつ病治療としてのモノアミン酸化酵素阻害剤（MAOI） monoamine oxidase inhibitors maois for treating depressed adults
2. パーキンソン病に対する神経保護療法 neuroprotective therapy for parkinson disease
3. Fire safety in the operating room
4. Overview of gastrointestinal tract perforation
5. 成人における抗うつ剤：薬剤の変更および投与中止 antidepressant medication in adults switching and discontinuing medication

English Journal

Development of fluorinated methoxylated chalcones as selective monoamine oxidase-B inhibitors: Synthesis, biochemistry and molecular docking studies.

Mathew B1, Mathew GE2, Uçar G3, Baysal I3, Suresh J4, Vilapurathu JK5, Prakasan A2, Suresh JK2, Thomas A2.
Bioorganic chemistry.Bioorg Chem.2015 Oct;62:22-9. doi: 10.1016/j.bioorg.2015.07.001. Epub 2015 Jul 9.
A series of methoxylated chalcones with fluoro and trifluoromethyl derivatives were synthesized and investigated for their ability to inhibit human monoamine oxidase A and B. The chemical structures of the compounds have been characterized by means of their (1)H NMR, (13)C NMR, Mass spectroscopic da
PMID 26189013

Rasagiline for the treatment of Parkinson's disease: an update.

Stocchi F1, Fossati C1, Torti M1.
Expert opinion on pharmacotherapy.Expert Opin Pharmacother.2015 Oct;16(14):2231-41. doi: 10.1517/14656566.2015.1086748.
INTRODUCTION: Rasagiline is a potent, selective, irreversible Monoamine Oxidase-B (MAO-B) inhibitor, developed to prolong the action of dopamine in the brain. It has been demonstrated that rasagiline can improve motor and some non-motor symptoms (NMS) in both early and advanced Parkinson's disease (
PMID 26364897

Acute and sub-chronic toxicity study of diaveridine in Wistar rats.

Wang X1, Su S1, Ihsan A2, Huang Q3, Chen D3, Cheng G3, Liu Z4, Wang Y5, Yuan Z6.
Regulatory toxicology and pharmacology : RTP.Regul Toxicol Pharmacol.2015 Oct;73(1):232-40. doi: 10.1016/j.yrtph.2015.07.010. Epub 2015 Jul 21.
Diaveridine, a developed dihydrofolate reductase inhibitor, has been widely used as anticoccidial drug and antibacterial synergist. However, few studies have been performed to investigate its toxicity. To provide detailed toxicity with a wide spectrum of doses for diaveridine, acute and sub-chronic
PMID 26209270

Japanese Journal

Role of the ubiquitin-proteasome system and autophagy in regulation of insulin sensitivity in serum-starved 3T3-L1 adipocytes

Zhang Yemin,Ye Mao,Chen Leyuan Jack,Li Mingxin,Tang Zhao,Wang Changhua
Endocrine Journal 62(8), 673-686, 2015
… Inhibition of the UPS with bortezomib (BZM), a highly selective, reversible 26S proteasome inhibitor induced compensatory activation of autophagy but did not affect significantly insulin action. …
NAID 130005094618

Angiogenesis Inhibitor, Endostar, Prevents Vasa Vasorum Neovascularization in a Swine Atherosclerosis Model

Xu Xiaoming,Mao Wei,Chai Yueyang,Dai Jin,Chen Qian,Wang Lihui,Zhuang Qin,Pan Yongming,Chen Minli,Ni Guibao,Huang Zhaoquan
Journal of Atherosclerosis and Thrombosis advpub(0), 2015
Aim: Vasa vasorum neovascularization is a key feature of atherosclerosis (AS) and is strongly associated with inflammatory infiltration, lipid deposition, intraplaque hemorrhage, and hemosiderin depos …
NAID 130005072455

Role of the ubiquitin-proteasome system and autophagy in regulation of insulin sensitivity in serum-starved 3T3-L1 adipocytes

Zhang Yemin,Ye Mao,Chen Leyuan Jack,Li Mingxin,Tang Zhao,Wang Changhua
Endocrine Journal advpub(0), 2015
… Inhibition of the UPS with bortezomib (BZM), a highly selective, reversible 26S proteasome inhibitor induced compensatory activation of autophagy but did not affect significantly insulin action. …
NAID 130005066952

Related Pictures

★リンクテーブル★

リンク元	「チラミン」「モノアミン酸化酵素阻害薬」
関連記事	「inhibit」「inhibitor」「MA」「MAO」「M」

「チラミン」

　　[★]

英: tyramine
同: p-ヒドロキシフェニルエチルアミン p-hydroxyphenylethylamine
関: MAO inhibitor

特徴

ノルアドレナリンの放出を促進する→レセルピンで処理されると作用が消失
チーズ、赤ワイン、ビール、にしん、鶏肝、チョコレートに多く含まれる

薬理作用

間接的にアドレナリン受容体を刺激する。

シナプス前膜からノルアドレナリンの分泌を促すことによる

適応

気管支喘息

→β受容体作動薬に取って代わられる

鼻づまり

→α受容体作動薬に取って代わられる

※　鼻粘膜にはα受容体しかない

脊髄・硬膜外麻酔の低血圧に対する対処
ナルコプシー
夜尿症

注意

タキヒラキシス tachyphylaxisを起こしやすい
コカイン、三環系抗うつ薬(imipramine, desipramine)がuptake1を抑制
MAO阻害薬を使用している場合、チラミンが投与されると神経終末中のノルアドレナリンの分解が押さえられてシナプス小胞内の貯蔵量がまし、チラミンにより大量のノルアドレナリンが放出される→高血圧発作(クリーゼ)を起こす。

「モノアミン酸化酵素阻害薬」

　　[★]

英: monoamine oxidase inhibitor, MAOI
同: MAO阻害薬 MAO inhibitor、モノアミンオキシダーゼ阻害薬

副作用

起立性低血圧(once the body adapts to higher basal level of catecholamines, it is nolonger able to further vasoconstrict in response to stress), hepatotoxicity, and hypomania.
MAO(特にA型)阻害薬使用時に、チラミン含有量の高い食物(ワイン、チーズ、チョコレートなど)を摂取すると、チラミンが分解されずに高血圧発作を起こす

「inhibit」

　　[★]

v.

抑制する、阻害する、阻止する

関: abrogate、block、depress、depression、deter、inhibition、interdict、prevent、prevention、repress、repression、restrain、restraint、suppress、suppression

「inhibitor」

　　[★]

n.

阻害剤、阻害薬、抑制薬、抑制剤、(内在性物質について)インヒビター、抑制物質

関: blocker、depressant、suppressant

「MA」

　　[★]

「MAO」

　　[★] モノアミンオキシダーゼ monoamine oxidase

「M」

　　[★] メチオニン methionine 　　

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匿名

検索

案内

MAO inhibitor