Kadsurenin B
Kadsurenin B is a PAF (platelet-activating factor) antagonist with neuroprotective activity. Kadsurenin B has a wide range of pharmacological research potential, such as antibacterial, anti-inflammatory, neuroprotective, antioxidant, antiplatelet aggregation, cytotoxic, antiparasitic, etc.
For research use only. We do not sell to patients.
- CAS No.: 145701-13-9
- Formula: C20H22O5
- Molecular Weight:342.39
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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CAS No. 145701-13-9
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Molecular Weight 342.39
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Formula C20H22O5
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SMILES
CO[C@@]([C@@H]1O)(C=C2CC=C)[C@@H]([C@@H](C3=CC=C4C(OCO4)=C3)[C@]1([H])C2=O)C
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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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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
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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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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
References
[1]. Ma Y, et al. Studies on PAF antagonistic bicyclo(3,2,1) octanoid neolignans from Piper kadsura. Yao Xue Xue Bao. 1993;28(3):207-11. [Content Brief]
[2]. Fan D, et al. Lignans from the genus Piper L. and their pharmacological activities: An updated review. Fitoterapia. 2023 Mar;165:105403. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)