1. Neuronal Signaling Apoptosis Stem Cell/Wnt PI3K/Akt/mTOR Immunology/Inflammation
  2. Cholinesterase (ChE) Bcl-2 Family GSK-3 Wnt β-catenin Amyloid-β Apoptosis Interleukin Related TNF Receptor
  3. BChE-IN-49

BChE-IN-49 is an orally active BChE inhibitor with IC50 values of 0.73 μM and 6.43 μM against BChE and AChE, respectively. BChE-IN-49 reduces AChE levels to inhibit the degradation of acetylcholine. By inhibiting GSK-3β, BChE-IN-49 potently activates the Wnt/β-catenin signaling pathway, exerting potent anti-, antioxidant, anti-neuroinflammatory and anti-apoptotic effects. BChE-IN-49 can be used in research related to Alzheimer's disease.

For research use only. We do not sell to patients.

BChE-IN-49

BChE-IN-49 Chemical Structure

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Description

BChE-IN-49 is an orally active BChE inhibitor with IC50 values of 0.73 μM and 6.43 μM against BChE and AChE, respectively. BChE-IN-49 reduces AChE levels to inhibit the degradation of acetylcholine. By inhibiting GSK-3β, BChE-IN-49 potently activates the Wnt/β-catenin signaling pathway, exerting potent anti-, antioxidant, anti-neuroinflammatory and anti-apoptotic effects. BChE-IN-49 can be used in research related to Alzheimer's disease[1].

IC50 & Target[1]

BChE

0.73 μM ()

AChE

6.43 μM ()

Bax

 

Bcl-2

 

IL-1β

 

GSK-3β

 

In Vivo

BChE-IN-49 (Compound 10) (30 mg/kg; p.o.; once daily for 5 weeks) significantly improves cognitive function in AlCl3-induced AD rats, reduces Alzheimer's disease pathophysiological markers, regulates neuroinflammation, apoptosis and the Wnt/β-catenin pathway, and enhances oxidative stress defense capacity[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague Dawley (adult male, 300-320 g, AlCl3-induced AD model)[1]
Dosage: 30 mg/kg
Administration: p.o.; daily; 5 weeks (concurrent with AlCl3 i.p. dosing)
Result: Effectively reversed the cognitive dysfunction induced by AlCl3 in rats.
Inhibited the key enzyme (BACE1) that generates Aβ to reduce Aβ deposition.
Significantly increased the level of BDNF, which had neuroprotective and repair effects.
Reduced levels of pro-inflammatory cytokines IL-1β and TNF-α.
Effectively inhibited neuronal apoptosis.
Strongly activated the Wnt/β-catenin neuroprotective pathway, while inhibiting its negative regulatory factor GSK-3β.
Significantly reversed the decline in DA, NE and 5-HT levels caused by AlCl3, restoring them by 4.5 times, 2.6 times and 5.6 times respectively.



Molecular Weight

395.90

Formula

C22H18ClNO2S

SMILES

O=C1N(C2=CC=C(Cl)C=C2)C(C3=CC=CC=C3)OC4=C1C5=C(CCCC5)S4

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
References
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BChE-IN-49
Cat. No.:
HY-181248
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