sEH/AChE-IN-1
sEH/AChE-IN-1 (Compound 12a) is a dual inhibitor of the enzymes soluble epoxide hydrolase (sEH) and acetylcholinesterase (AChE). sEH/AChE-IN-1 provides cumulative effects against neuroinflammation and memory impairment. sEH/AChE-IN-1 has the potential for the research of Alzheimer's disease (AD).
For research use only. We do not sell to patients.
- CAS No.: 2490589-08-5
- Formula: C29H31ClF3N5O3
- Molecular Weight:590.04
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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CAS No. 2490589-08-5
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Molecular Weight 590.04
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Formula C29H31ClF3N5O3
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SMILES
ClC1=CC2=C(C(NCCC(N3CCC(CC3)NC(NC4=CC=C(C=C4)OC(F)(F)F)=O)=O)=C5C(CCCC5)=N2)C=C1
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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
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)