PeptideDB

Selegiline

CAS: 14611-51-9 F: C13H17N W: 187.28

Selegiline (Deprenyl) is a potent, selective and irreversible inhibitor of MAO-B, with an IC50 of 51 nM. Selegiline exhi
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Bioactivity Selegiline (Deprenyl) is a potent, selective and irreversible inhibitor of MAO-B, with an IC50 of 51 nM. Selegiline exhibits 450-flod selectivity for MAO-B over MAO-A (IC50=23 μM). Selegiline can be used for the research of Parkinson's disease, Alzheimer's disease and major depressive disorder[1][2][3].
Invitro Selegiline (1 nM-1 μM) inhibits recombinant human MAO-B in a concentration-dependent manner[1].Selegiline (10 mM) increases the efflux of norepinephrine (NE), dopamine (DA) and serotonin (5-HT) from the rat hypothalamus in vitro. Selegiline inhibits the efflux of dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA) in a dose-dependent manner[3].
In Vivo Selegiline (1 mg/kg; i.p. daily for 24 days) reduces Cocaine self-administration of mice and does not affect Cocaine-caused body weight loss. Selegiline reduces 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations in frontal cortex[4]. Animal Model:
Name Selegiline
CAS 14611-51-9
Formula C13H17N
Molar Mass 187.28
Transport Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Reference [1]. Chaurasiya ND, et, al. Selective Inhibition of Human Monoamine Oxidase B by Acacetin 7-Methyl Ether Isolated from Turnera diffusa (Damiana). Molecules. 2019 Feb 23;24(4):810. [2]. Tatton WG, et, al. Modulation of gene expression rather than monoamine oxidase inhibition: (-)-deprenyl-related compounds in controlling neurodegeneration. Neurology. 1996 Dec;47(6 Suppl 3):S171-83. [3]. MohanKumar PS, et, al. Deprenyl stimulates the efflux of monoamines from the rat hypothalamus in vitro. Brain Res Bull. 2001 Apr;54(6):675-80. [4]. Ho MC, et, al. Chronic treatment with monoamine oxidase-B inhibitors decreases cocaine reward in mice. Psychopharmacology (Berl). 2009 Jul;205(1):141-9.