BuChE-IN-23
BuChE-IN-23 is an orally active, blood-brain barrier permeable butyrylcholinesterase (eqBuChE) inhibitor with an IC50 of 15.59 μM and a Ki of 29.33 μM. BuChE-IN-23 exhibits an IC50 of 38.65 μM against hBuChE and shows selectivity for butyrylcholinesterase over acetylcholinesterase. BuChE-IN-23 inhibits LPS (HY-D1056)-induced nitric oxide production, attenuates hippocampal glial cell activation and neuroinflammation, suppresses the TLR4/p38 MAPK signaling pathway, and regulates the IL-1β/C3-mediated microglia-astrocyte inflammatory axis. BuChE-IN-23 can be used for the research of Alzheimer's disease.
For research use only. We do not sell to patients.
- CAS No.: 3067571-93-8
- Formula: C25H25NO6
- Molecular Weight:435.47
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
eqBCHE 15.59 μM (IC50) |
BuChE 38.65 μM (IC50) |
IL-1β |
In Vitro
BuChE-IN-23 (Compound E14) (20 μM; 24 h) exhibits extremely low cytotoxicity in BV2 microglial cells[1].
BuChE-IN-23 (15 μM; 25 h) potently inhibits lipopolysaccharide-induced nitric oxide production in BV2 microglia, with an IC50 of 9.76 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:mouse microglial BV2 cells
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Concentration:20 μM
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Incubation Time:24 h
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Result:Maintained cell viability above 90% at 20 μM, indicating acceptable cytocompatibility.
In Vivo
BuChE-IN-23 (500 mg/kg; p.o.; single dose) exhibits good acute tolerability in mice, with no observable organ toxicity following a single oral dose of 500 mg/kg[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 J (male, 3 months old, intracerebroventricular injection of oligomeric Aβ1-42 on Day 1 and Day 7)[1]
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Dosage:3 mg/kg; 10 mg/kg
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Administration:p.o.; daily; 14 days
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Result:Significantly increased the discrimination ratio relative to the oAβ group, comparable to Rivastigmine.
Markedly increased the number of platform crossings relative to the oAβ group, comparable to Rivastigmine.
Significantly reduced hippocampal IBA1 and 6E10 fluorescence intensity, attenuating microglial activation and Aβ deposition.
Significantly downregulated hippocampal protein levels of IBA1, GFAP, TLR4, and IL-1β, and reduced the p-p38/p38 ratio relative to the oAβ group.
Significantly reduced hippocampal GFAP and TNF-α fluorescence intensity, suppressing astrocytic activation and pro-inflammatory cytokine expression.
Significantly decreased hippocampal IL-1β and C3 fluorescence intensity, attenuating microglial IL-1β production and astrocytic C3 activation.
Chemical Information
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CAS No. 3067571-93-8
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Molecular Weight 435.47
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Formula C25H25NO6
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SMILES
O=C1C(OCC2=CC=CC=C2)=C(/C=C/C3=CC=C(O)C=C3)OC(COC(N(CC)C)=O)=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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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
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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)
Keywords
- BuChE-IN-23
- 3067571-93-8
- Cholinesterase (ChE)
- Toll-like Receptor (TLR)
- p38 MAPK
- Interleukin Related
- Complement System
- nitric oxide
- IL-1β/C3-mediated microglia-astrocyte inflammatory axis
- lipopolysaccharide
- alzheimer's disease
- acetylcholinesterase
- hippocampal glial activation
- neuroinflammation
- TLR4/p38 MAPK signaling
- BV2 microglial cells
- butyrylcholinesterase
- Inhibitor
- inhibitor
- inhibit