AChE/BChE-IN-30
AChE/BChE-IN-30 (Compound 3g) is a Cholinesterase dual-target competitive inhibitor. AChE/BChE-IN-30 can inhibit AChE and BChE with IC50 values of 0.338 and 2.087 μM and Ki values of 0.045 and 0.789 μM. AChE/BChE-IN-30 can be used for the research of neurological disease, such as Alzheimer's disease.
For research use only. We do not sell to patients.
- Formula: C26H22N4O2S2
- Molecular Weight:486.61
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
AChE 0.338 μM (IC50) |
BChE 2.087 μM (IC50) |
AChE 0.045 μM (Ki) |
BChE 0.789 μM (Ki) |
In Vitro
Chemical Information
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Molecular Weight 486.61
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Formula C26H22N4O2S2
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SMILES
N#CC1=CC=C(C2=CSC(N3N=C(C4=CC=C(OC)C(OC)=C4)CC3C5=CC=C(C)S5)=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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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
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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)