Neuroprotective agent 18
Neuroprotective agent 18 is a potent neuroprotective agent. Neuroprotective agent 18 inhibits the activity of NF-κB thereby significantly downregulating the expression of downstream pro-inflammatory mediators (TNF-α, IL-6) and inflammatory enzymes (COX-2) in the hippocampus. Neuroprotective agent 18 binds to AChE thereby partially inhibiting it and modulating cholinergic neurotransmission. Neuroprotective agent 18 can be used in research on Alzheimer's disease.
For research use only. We do not sell to patients.
- Formula: C21H22N2O5
- Molecular Weight:382.41
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
NF-κB |
COX-2 |
IL-6 |
TNF-α |
AChE |
In Vitro
Neuroprotective agent 18 (compound M5) is capable of binding favorably to multiple proteins involved in neuroinflammation. Neuroprotective agent 18 exhibits moderate to strong docking score (-7.9 kcal/mol, -7.7 kcal/mol, -7.3 kcal/mol and -7.1 kcal/mol) for COX-2, TNF-α, IL-6 complex and NF-κB. Neuroprotective agent 18 produces a comparatively stronger docking score (-9.0 kcal/mol) for AChE[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 albino mice (Male, 8-10 weeks, 25-30 g) received daily intraperitoneal injections of Scopolamine (1 mg/kg) for 6 days[1].
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Dosage:1 mg/kg, 5 mg/kg, 10 mg/kg
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Administration:i.p.; once daily; for 6 days
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Result:Restored spatial learning and memory consolidation capabilities in a dose-dependent manner in the Morris Water Maze (MWM) test.
Effectively improved hippocampus-dependent short-term working memory in the Y-Maze Test.
Significantly reduced the concentrations of the pro-inflammatory cytokines TNF-α and IL-6 in the hippocampus in a dose-dependent manner, while simultaneously downregulating the expression levels of the inflammation-related enzyme COX-2 and the upstream inflammatory transcription factor NF-κB.
Chemical Information
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Molecular Weight 382.41
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Formula C21H22N2O5
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SMILES
O=C(ON=C/1CNCC2=CC=CC=C2)C1=C\C3=CC(OC)=C(OC)C(OC)=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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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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)