BuChE-IN-22
BuChE-IN-22 is a pseudo-irreversible butyrylcholinesterase (BuChE) inhibitor, with IC50 values of 4 nM and 157 nM against hBuChE and hAChE, respectively. It also acts as a prodrug of 7-hydroxysertraline. BuChE-IN-22 releases 7-hydroxysertraline during BuChE inhibition. BuChE-IN-22 completely reverses Aβ25-35-induced short-term and long-term memory impairments in a mouse model of Alzheimer's disease. BuChE-IN-22 can be used in research related to Alzheimer's disease.
For research use only. We do not sell to patients.
- Formula: C23H26Cl2N2O2
- Molecular Weight:433.37
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
hBCHE 4 nM (IC50) |
hAChE 157 nM (IC50) |
In Vitro
BuChE-IN-22 (Compound 8e) (255 μM; 48 h) remains stable in the absence of hBuChE, but is completely metabolized by hBuChE within 48 h, releasing 85% of the serotonin reuptake inhibitor HO-Sert[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Swiss mice (male, 6 weeks old, 30-35 g, intracerebroventricular injection of 9 nmol oligomeric Aβ25-35 peptide)[1]
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Dosage:0.3 mg/kg; 1 mg/kg (long-term non-spatial memory); 3 mg/kg (spatial working memory)
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Administration:i.p.; daily; 7 days (starting 20 minutes post-Aβ25-35 injection)
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Result:Completely prevented Aβ25-35-induced deficits in spontaneous alternation (spatial working memory) at 3 mg/kg.
Completely prevented Aβ25-35-induced deficits in passive avoidance retention latency (long-term non-spatial memory) at 1 mg/kg.
Chemical Information
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Molecular Weight 433.37
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Formula C23H26Cl2N2O2
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SMILES
CN[C@H]1CC[C@@H](C2=CC=C(Cl)C(Cl)=C2)C3=C1C=C(OC(N4CCCCC4)=O)C=C3
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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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How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models
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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)