MAO-B-IN-47
MAO-B-IN-47 is a selective monoamine oxidase B (MAO-B) inhibitor with a Ki of 875 nM. MAO-B-IN-47 shows an IC50 >100 μM for SH-SY5Y cells. MAO-B-IN-47 shows neuroprotective effect in 6-OHDA-treated SH-SY5Y cells. MAO-B-IN-47 can be used for the research of neurological disease, such as Parkinson’s disease (PD).
For research use only. We do not sell to patients.
- CAS No.: 67082-01-3
- Formula: C16H13F3O
- Molecular Weight:278.27
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
MAO-B 875 nM (Ki) |
In Vitro
MAO-B-IN-47 (Compound 5a) (0-40 μM) shows no significant inhibitory effects on the proliferation of either normal (hSDFs, AT -MSCs) or cancer (A-375, U87-MG, SH-SY5Y) cells[1].
MAO-B-IN-47 (12.5-100 μM, 2 h) shows neuroprotective effect in 6-OHDA-treated SH-SY5Y cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:SH-SY5Y cells
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Concentration:12.5 μM, 25 μM, 50 μM and 100μM
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Incubation Time:2 h followed by 6-OHDA for 24 h
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Result:Resulted in higher cell viability.
Significantly increased the IC50 of 6-OHDA at 12.5 μM and 25 μM.
Chemical Information
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CAS No. 67082-01-3
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Molecular Weight 278.27
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Formula C16H13F3O
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SMILES
O=C(C1=CC(C(F)(F)F)=CC=C1)CCC2=CC=CC=C2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)