Monardic acid A
Monardic acid A is a selective inhibitor of AChE, with an IC50 of 53.1 μM against AChE from electric eel. Monardic acid A shows weak inhibitory activity against human erythrocyte AChE (IC50 >100 μM) and has no significant inhibitory effect on BChE. Monardic acid A reduces acetylcholine breakdown by inhibiting AChE activity, and also exhibits inhibitory activity against histamine release and hyaluronidase, thus exerting anti-inflammatory and neurotransmitter regulatory effects. Monardic acid A can be isolated from lungwort (Pulmonaria officinalis) and thyme (Thymus gobicus), and is mainly used in the development of anti-inflammatory drugs and drugs related to neurodegenerative diseases.
For research use only. We do not sell to patients.
- CAS No.: 1607436-76-9
- Formula: C27H22O12
- Molecular Weight:538.46
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
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AChE |
Chemical Information
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CAS No. 1607436-76-9
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Molecular Weight 538.46
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Formula C27H22O12
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SMILES
OC([C@@H]1C2=C(/C=C/C(O[C@@H](C(O)=O)CC3=CC(O)=C(C=C3)O)=O)C=CC(O)=C2O[C@H]1C4=CC(O)=C(C=C4)O)=O
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Structure Classification
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Initial Source
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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 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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Monardic acid A Related Classifications
HY-N16715 Related Classifications
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