MAOB

Official Full Name

monoamine oxidase B

Organism

Homo sapiens

GeneID

4129

Background

The protein encoded by this gene belongs to the flavin monoamine oxidase family. It is a enzyme located in the mitochondrial outer membrane. It catalyzes the oxidative deamination of biogenic and xenobiotic amines and plays an important role in the metabolism of neuroactive and vasoactive amines in the central nervous sysytem and peripheral tissues. This protein preferentially degrades benzylamine and phenylethylamine. [provided by RefSeq, Jul 2008]

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Detailed Information

Monoamine oxidase B (MAO-B) is one of the key enzymes of DA catabolism. It produces some free radicals and other active oxygen species while oxidative catabolism of DA, causing oxidative stress and finally leading to neurons death. MAO-B is covalently linked to cysteine residues in the active central region by a flavine adenine dinucleotide coenzyme, which can catalyze the oxidation of various amines in the organism and eventually produce aldehydes and hydrogen peroxide to participate in cell oxidation. MAO-B is mainly found in peripheral platelets and 5-HT neurons and glial cells in the brain. If the activity of MAO-B is inhibited, the concentration of dopamine (DA) in the central nerve center can be increased to treat Parkinson's disease and Alzheimer's disease. Because MAO-B inhibitors not only improve PD symptoms, but also have neuroprotective effects, they are still hot topics in clinical research.

Figure 1. Monoamine oxidase‐B (MAO‐B) is important for Parkinson's disease progression. (Kang, et al. 2018)

MAOB Inhibitor

Selegiline is the first generation of irreversible and selective propargylamine MAO-B inhibitors. MAO is a protease in cells that decomposes intracellular DA and the lack of DA neurotransmitters in the striatum is a major biochemical feature of PD patients. Therefore, selegiline increases the availability of DA in the brain by inhibiting the activity of MAO-B. In the early treatment of PD, selegiline can be used as a monotherapy, and in the late stage of the disease, PD can be treated with L-dopa. Studies have shown that the clinical trials of 40 patients with chronic schizophrenia indicate the role of selegiline in the adjuvant treatment of cognitive function in patients with schizophrenia. There were 6 randomized, double-blind clinical trials involving selegiline in 500 patients with dementia, with selegiline and vitamin E compared with placebo. The results showed that selegiline and vitamin E were similar in delaying the progression of the disease, both better than placebo.

The new generation of MAO-B inhibitor, dafenamide, selectively inhibits MAO-B to block voltage-dependent sodium channels and N-type calcium channels, thereby inhibiting the release of glutamate. The effect of safflower amide is reversible, high tolerance, small side reaction, and neuroprotective function. Rasagiling is a second-generation propargylamine that is also an irreversible and selective MAO inhibitor with a potency of 5 to 10 times that of selegiline. Unlike selegiline, rasagiline is not metabolized in the body to amphetamine derivatives. Therefore, rasagiline does not produce central excitatory effects and can be taken before bedtime.

By interacting with the mitochondrial outer membrane, selegeran and leishageran can prevent neurotoxin-induced mitochondrial membrane potential imbalance and permeability conversion, and protect mitochondria. Rexagiram can up-regulate the expression of anti-apoptotic bcl-2 protein and down-regulate the expression of pro-apoptotic protein, thus indirectly protecting the nerve. Selegylam can increase the expression level of BDNF protein in the brain and has the activity of anti-starch protein in vitro.

Safinamide is a phenylmethionine derivative and is a highly potent, reversible and specific MAO-B inhibitor. It is currently being used for research on anti-caries, anti-PD and neuroprotection. The selective effect of safinamide on MAO-B was much higher than that of selegeylam and rexagylam. The inhibitory effect of safinamide on mao-b was 5,000 times stronger than that of MAO-A, while selegeylam was 127 times stronger. In addition, the inhibitory effect of safinamide on MAO-B is completely reversible. The inhibitory effect of Safinamide on MAO-B is dose-dependent and does not have time-dependent characteristics. Platelet MAO-B activity was fully restored 8 h after rinsing the platelet membrane or stopping the drug. In contrast, rasagiline is a long-acting MAO-B inhibitor that remains unrecoverable after 24 h of withdrawal and is an irreversible MAO-B inhibitor.

References:

Kang, S. S. , Ahn, E. H. , Zhang, Z. , Liu, X. , Manfredsson, F. P. , & Sandoval, I. M. , et al. (2018). α‐synuclein stimulation of monoamine oxidase‐b and legumain protease mediates the pathology of parkinson\"s disease. The EMBO Journal, e201798878.
2. Riederer, P. , & Thomas Müller. (2016). Use of monoamine oxidase inhibitors in chronic neurodegeneration.

Expert Opinion on Drug Metabolism & Toxicology

, 13(2), 233.
3. Ramsay, R. R. . (2016). Molecular aspects of monoamine oxidase b.

Progress in Neuro-Psychopharmacology and Biological Psychiatry

, 69, 81-89.

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