Rapid synthesis of flavone-based monoamine oxidase (MAO) inhibitors targeting two active sites using click chemistry

2016 ◽  
Vol 89 (1) ◽  
pp. 141-151 ◽  
Author(s):  
Wei Zhen Jia ◽  
Feng Cheng ◽  
Yin Jun Zhang ◽  
Jin Yan Ge ◽  
Shao Q. Yao ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Click Chemistry ◽  
Active Sites ◽  
Mao Inhibitors ◽  
Rapid Synthesis

A “Click Chemistry Platform” for the Rapid Synthesis of Bispecific Molecules for Inducing Protein Degradation

2017 ◽  
Vol 61 (2) ◽  
pp. 453-461 ◽  
Author(s):  
Ryan P. Wurz ◽  
Ken Dellamaggiore ◽  
Hannah Dou ◽  
Noelle Javier ◽  
Mei-Chu Lo ◽  
...  
Keyword(s):  
Protein Degradation ◽  
Click Chemistry ◽  
Rapid Synthesis

Rapid Synthesis of Triazole-Modified Resveratrol Analogues via Click Chemistry

2006 ◽  
Vol 49 (2) ◽  
pp. 467-470 ◽  
Author(s):  
Francesca Pagliai ◽  
Tracey Pirali ◽  
Erika Del Grosso ◽  
Riccardo Di Brisco ◽  
Gian Cesare Tron ◽  
...  
Keyword(s):  
Click Chemistry ◽  
Rapid Synthesis ◽  
Resveratrol Analogues

A Clinical and Biochemical Study of Monoamine Oxidase Inhibition in Depressed Patients

1961 ◽  
Vol 107 (447) ◽  
pp. 239-243 ◽  
Author(s):  
W. G. Dewhurst ◽  
C. M. B. Pare
Keyword(s):  
Monoamine Oxidase ◽  
Clinical Application ◽  
Biochemical Study ◽  
Toxic Effects ◽  
Mao Inhibitors ◽  
Monoamine Oxidase Inhibition ◽  
Depressed Patients ◽  
Depressant Action ◽  
Oxidase Inhibition ◽  
Enzyme Monoamine Oxidase

The discovery that iproniazid benefits certain subjects with depression, linked with the demonstration that it inhibits the enzyme monoamine oxidase (MAO), led to the hypothesis that inhibition of MAO was the essential mechanism by which iproniazid caused relief of symptoms (Pletscher, 1959). Iproniazid, unfortunately, can produce serious toxic effects, particularly on the liver (Pare and Sandler, 1959), and this has limited its clinical application. For this reason a search has been made for MAO inhibitors with an effective anti-depressant action yet without the serious toxic effects of iproniazid. Among the newer compounds for which such claims have been made is N-isonicotinoyl (-N-N-benzylcarboxamidoethyl) hydrazine or Nialamide.

Effects of Two Substituted Hydrazine Monoamine Oxidase (MAO) Inhibitors on Neurotransmitter Amines, γ-Aminobutyric Acid, and Alanine in Rat Brain

1993 ◽  
Vol 82 (9) ◽  
pp. 934-937 ◽  
Author(s):  
Naoto Yamada ◽  
Saburo Takahashi ◽  
Kathryn G. Todd ◽  
Glen B. Baker ◽  
Paul R. Paetsch
Keyword(s):  
Monoamine Oxidase ◽  
Rat Brain ◽  
Aminobutyric Acid ◽  
Mao Inhibitors

scholarly journals Psychotropic Drugs (2) Interaction between Monoamine Oxidase (MAO) Inhibitors and other Substances

1965 ◽  
Vol 58 (11P2) ◽  
pp. 967-978 ◽  
Author(s):  
Folke Sjöqvist
Keyword(s):  
Monoamine Oxidase ◽  
Animal Experiments ◽  
Pharmacological Action ◽  
Mao Inhibitors ◽  
Pharmacological Interaction ◽  
Biochemical Effects ◽  
Impaired Metabolism ◽  
Other Substances ◽  
Indirectly Acting Sympathomimetic Amines ◽  
Noradrenaline And Adrenaline

Monoamine oxidase inhibitors (MAOI) in clinical use have an irreversible action on MAO, and this persists until the enzyme has been resynthesized. The effects of small daily doses of MAOI are therefore cumulative. The biochemical effects of these drugs will involve several substrates of MAO, e.g. dopamine, tyramine, serotonin and, to a lesser extent, noradrenaline and adrenaline. MAO probably regulates the metabolism of catecholamines and serotonin in tissues, while catechol-O-methyltransferase is responsible for the metabolism of circulating noradrenaline and adrenaline. Certain pharmacological effects of MAOI are related to the accumulation of monoamines in various tissues that follows the decrease of intraneuronal deamination. Among these effects are reversal of the reserpine syndrome in animals and augmentation of the pharmacological action of monoamines. Other effects are unrelated to the inhibition of MAO, e.g. immediate desynchronization of EEG and initial pressor effects. MAOI may potentiate or change the action of several other drugs and even certain foods. The mechanisms involved are usually reasonably predictable from animal experiments. Substrates of MAO, e.g. dopamine and tyramine, evoke augmented and prolonged effects in patients treated with MAOI. This is partly due to an impaired metabolism of the circulating amines. In addition, inhibition of intestinal and hepatic MAO largely increases the absorption of tryamine from cheeses and other foods. Usually innocuous amounts of tyramine may therefore cause hypertensive reactions in patients treated with MAOI. Indirectly acting sympathomimetic amines, such as amphetamines, ephedrine and MAOI with amphetamine-like properties, can be potentiated, because they may release increased amounts of nor-adrenaline from sympathetic nerve endings after MAO inhibition. The effects of any amine, whether a substrate of MAO or not, may be enhanced by MAO inhibitors producing postganglionic block. This is due to ‘denervation’ supersensitivity of adrenergic receptors. Harmful pharmacological interaction is also possible between MAO inhibitors and agents which release (reserpine) or replete (amine precursors, e.g. L-DOPA in broad beans) monoamines centrally and peripherally. Drugs that sensitize adrenergic and tryptaminergic receptors to the action of monoamines, e.g. imipramine-like compounds, may be greatly potentiated by MAO inhibitors. The anti-hypertensive effects of thiazides and ganglion-blocking agents may be enhanced by MAOI. A few drugs are known to exert prolonged effects in occasional patients treated with MAOI, e.g. pethidine, phenothiazines and pentobarbital. MAOI may possibly decelerate the metabolism of these compounds by a nonspecific inhibition of liver microsomal enzymes. Finally, a great number of agents have been found empirically to evoke augmented effects after inhibition of MAO, e.g. insulin and anti-Parkinson drugs.

Anesthesia for a Patient on Monoamine Oxidase Inhibitors

2016 ◽  
Vol 1 (2) ◽  
pp. 81-83 ◽  
Author(s):  
Ram P Singh ◽  
Richa Agrawal
Keyword(s):  
Monoamine Oxidase ◽  
Drug Interactions ◽  
Spinal Anesthesia ◽  
Preoperative Evaluation ◽  
Multidrug Resistant ◽  
Monoamine Oxidase Inhibitors ◽  
Bipolar Hemiarthroplasty ◽  
Mao Inhibitors ◽  
Anesthetic Drugs ◽  
Increased Risk

ABSTRACT Monoamine oxidase (MAO) inhibitors are frequently used for multidrug-resistant major depression, which is emerging as an epidemic in the modern era. Anesthesia during chronic use of MAO inhibitors is a matter of debate because of increased risk of drug interactions with various anesthetic drugs. Cardiac disorders contribute to perioperative and postoperative complications. Recent studies illustrate the safety of anesthesia without discontinuation of MAO inhibitors if sympathetic homeostasis is maintained and known drug interactions are avoided. In this case study, a 72-year-old male psychiatric patient on permanent treatment with tranylcypromine (30 mg/day) was admitted for bipolar hemiarthroplasty. After complete aseptic precautions, spinal anesthesia was achieved by 12.5 mg 0.5% heavy bupivacaine and 30 μg clonidine intrathecally. The anesthetic effect was adequate, but surgery was not completed timely and the effect of spinal anesthesia was weaned off, so general anesthesia was given and surgery was completed. There was no perioperative or postoperative complication. In conclusion, general or regional anesthesia for noncardiac surgery without discontinuation of MAO inhibitors may be safe after careful preoperative evaluation of the patient. How to cite this article Krishan G, Singh RP, Agrawal M, Agrawal R. Anesthesia for a Patient on Monoamine Oxidase Inhibitors. Int J Adv Integ Med Sci 2016;1(2):81-83.

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