L-703717
L-703717 is a NMDA receptor antagonist. L-703717 preferentially binds to cerebellar-specific NMDA receptors consisting of a GluRepsilon3 subunit and eventually accumulates in rodent cerebellum. L-703717 can be used for the research of neurological disease.
For research use only. We do not sell to patients.
- CAS No.: 142326-92-9
- Formula: C23H18ClNO3
- Molecular Weight:391.85
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All iGluR Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
NMDA Receptor |
Chemical Information
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CAS No. 142326-92-9
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Molecular Weight 391.85
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Formula C23H18ClNO3
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SMILES
OC1=C(C2=CC(CC3=CC=C(OC)C=C3)=CC=C2)C(NC4=CC(Cl)=CC=C14)=O
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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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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)