BuChE-IN-20
BuChE-IN-20 is a selective butyrylcholinesterase (hBuChE) inhibitor (IC50 = 0.13 μM) with BBB permeability. BuChE-IN-20 is a L-Tryptophan derivative. BuChE-IN-20 possesses neuroprotective properties by inhibiting the production of nitric oxide (NO) and lowering the levels of ROS. BuChE-IN-20 is proficient in inhibiting the self-aggregation of amyloid-beta (Aβ) peptides. BuChE-IN-20 can be used in research for Alzheimer’s disease.
For research use only. We do not sell to patients.
- Formula: C29H29FN4O2
- Molecular Weight:484.56
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
BChE 0.13 nM (IC50) |
In Vitro
BuChE-IN-20 (Compound 4d-13) (5 μM, 10 min) shows selectivity for BuChE through enzymatic activity assays of hAChE and hBuChE[1].
BuChE-IN-20 (20 μM, 48 h) prevents the aggregation and deposition of Aβ1-42, thereby exerting neuroprotective effects by inhibiting the formation of toxic amyloid plaques, and mitigate the neurotoxicity induced by Aβ1-42 through ROS generation[1].
BuChE-IN-20 (1 mM, 30 min) exerts scavenging capacities for hydroxyl radicals 775 times that of vitamin C[1].
BuChE-IN-20 (5-10 μM, 4 h pretreatment and 8 h cotreatment with LPS) decreases intracellular reactive oxygen species (ROS) concentration-dependently in LPS (1.5 μg/mL) (HY-D1056)-induced RAW264.7 cells[1].
BuChE-IN-20 (6.25-12.5 μM, 4 h pretreatment and 24 h cotreatment with LPS) demonstrates potent inhibitory activity on LPS (2 μg/mL)-induced NO production in RAW264.7 cells[1].
BuChE-IN-20 (1-100 μM, 24 h) exerts inhibitory effects and free radical scavenging at sub-micromolar concentrations in mouse BV-2 cell line, with a safety margin of nearly 150-fold regarding cytotoxicity[1].
BuChE-IN-20 (1-10 μM, 24 h pretreatment and 24 h cotreatment with LPS) decreases IL-1β levels in LPS (100 ng/mL)-induced BV-2 cells[1].
BuChE-IN-20 (1-20 μM, 6 h pretreatment and 24 h cotreatment with NMDA/Sodium L-Glutamate) mitigates the cytotoxic effects dose-dependently in NMDA (20 mM)/Sodium L-Glutamate(Glu) (HY-N0455B)-induced SH-SY5Y cell injury model[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:LPS (100 ng/mL)-induced BV-2 cells
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Concentration:1, 5, 10 μM
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Incubation Time:24 h pretreatment and 24 h cotreatment with LPS
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Result:Exhibited a dose-dependent reduction in IL-1β expression, while having a lesser effect on IL-6 and TNF-α.
Inhibited the production, release, and NLRP3-mediated maturation of IL-1β directly.
Inhibited the NF-κB and MAPK signaling pathways to reduce IL-1β indirectly.
In Vivo
BuChE-IN-20 (10-40 mg/kg, p.o., one single dose) shows notable positive effect on improving learning and memory function in (-)-Scopolamine hydrobromide (HY-W010892) (3 mg/kg, i.p.)-induced ICR mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:(-)-Scopolamine hydrobromide (HY-W010892) (3 mg/kg, i.p.)-induced ICR mice [1]
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Dosage:10-40 mg/kg
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Administration:Oral gavage (p.o.)
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Result:Recovered the impairment of hippocampus-dependent memory and spatial learning functions induced by (-)-Scopolamine hydrobromide.
Mitigated the cognitive impairment induced by (-)-Scopolamine hydrobromide at the dosage of 40 mg/kg via gavage, evidenced by a reduction in escape latency and a decrease in the traversed distance to the escape platform.
Chemical Information
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Molecular Weight 484.56
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Formula C29H29FN4O2
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SMILES
OC1=C(F)C=C(CN[C@@H](CC2=CNC3=CC=CC=C32)C(N(C)CCC4=CNC5=C4C=CC=C5)=O)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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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Transepithelial/transendothelial electrical resistance assay
TEER measures electrical resistance across epithelial or endothelial monolayers cultured on permeable supports, and the readout reflects ionic conductance through the cell barrier, especially the paracellular pathway regulated by junctional integrity. TEER can be measured without destroying the monolayer and is commonly used before or during transport, permeability, barrier-disruption, and barrier-maturation experiments. TEER values are influenced by biological maturation and technical conditions; reported factors include temperature, medium formulation, passage number, electrode geometry, membrane properties, and junctional length during early monolayer maturation. Therefore, TEER should be interpreted with blank-insert subtraction, area normalization, repeated readings, and, when possible, orthogonal barrier readouts such as FITC-dextran flux or tight-junction staining.
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Amyloid: Congo Red Amyloid Staining
Congo red amyloid staining is a histochemical method used to detect extracellular amyloid deposits in tissue sections based on the affinity of Congo red dye for β-pleated sheet-rich protein aggregates. When bound to amyloid, Congo red produces characteristic apple-green birefringence under polarized light microscopy, which is widely regarded as a diagnostic feature of amyloid deposition in histopathology. The diagnostic principle relies on the combination of dye binding (congophilia) and optical anisotropy under polarized illumination, which distinguishes amyloid from most non-amyloid eosinophilic extracellular deposits in routine histological evaluation. Amyloid identification by Congo red staining remains a cornerstone in diagnostic pathology despite the availability of adjunct methods such as immunohistochemistry and mass spectrometry, particularly because of its ability to localize deposits directly within tissue architecture. The specificity of Congo red-positive deposits is incre
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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)