NMDA receptor antagonist 9
NMDA receptor antagonist 9 is a selective GluN2B subunit-containing NMDA receptor antagonist with a Ki of 5.2 nM. NMDA receptor antagonist 9 exhibits 9-fold selectivity over σ1 receptors, shows poor selectivity towards σ2 receptors. NMDA receptor antagonist 9 inhibits ion flux through GluN2B subunit-containing NMDA receptors. NMDA receptor antagonist 9 can be used for the research of neurological disease, such as alzheimer’s disease and parkinson’s disease.
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- 화학식: C21H25NO2
- 분자량:323.43
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
IC50 & Target
[1]|
GluN2B 5.2 nM (Ki) |
σ2 4.2 nM (Ki) |
σ1 49 nM (Ki) |
In Vitro
NMDA receptor antagonist 9 (Compound cis-15a) binds to GluN2B subunit-containing NMDA receptors in recombinant L(tk-) cells with a Ki of 5.2 ± 1.9 nM[1].
NMDA receptor antagonist 9 (1 μM) inhibits ion flux at GluN2B subunit-containing NMDA receptors expressed in Xenopus laevis oocytes by 76 ± 2%[1].
NMDA receptor antagonist 9 binds to σ1 and σ2 receptors in guinea pig brain membranes with a Ki of 49 ± 7 and 4.2 ± 0.6 nM[1].
NMDA receptor antagonist 9 (90 min at 37 °C) exhibits high phase I metabolic stability in mouse liver microsomes, with 89 ± 6% intact after incubation[1].
NMDA receptor antagonist 9 (90 min at 37 °C) retains high metabolic stability in mouse liver microsomes with NADPH and UDP-GA, with 88% intact after incubation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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분자량 323.43
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화학식 C21H25NO2
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SMILES
OC1=CC=C2C(C[C@@H]([C@@H]2O)N3CCC(CC3)CC4=CC=CC=C4)=C1
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- NMDA receptor antagonist 9
- NMDA receptor antagonist9
- NMDA receptor antagonist-9
- iGluR
- Sigma Receptor
- ischemic stroke
- parkinson’s disease
- GluN2B subunit-containing NMDA receptor
- ifenprodil binding site
- huntington’s disease
- depression
- neuropathic pain
- σ2 receptors
- σ1 receptors
- alzheimer’s disease
- Inhibitor
- inhibitor
- inhibit