Benastatin B
Benastatin B is an inhibitor for glutathione S-transferase, that inhibits human pi class GST with an IC50 of 1.10 μg/mL. Benastatin B exhibits board-spectrum antibacterial efficacy, inhibits MRSA with MIC 3.1 μg/mL. Benastatin B exhibits anti-inflammatory efficacy through inhibition of IgE mediated β-hexosaminidase release with an IC50 of 79 μg/mL.
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- CAS. Nr.: 138968-86-2
- Formel: C30H30O7
- Molecular Weight:502.56
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Help & FAQs
Biologische Aktivität
Beschreibung
Chemical Information
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CAS. Nr. 138968-86-2
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Molecular Weight 502.56
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Formel C30H30O7
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SMILES
O=C(C1=C(C2=C(C=C1CCCCC)CCC3=C2C=C4C(C(C5=C(C4(C)C)C=C(O)C=C5O)=O)=C3O)O)O
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Structure Classification
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Initial Source
Streptomyces sp. MI384-DF12
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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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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
Reinheit & Dokumentation
Verweise
[1]. Aoyama T, et al., Benastatins A and B, new inhibitors of glutathione S-transferase, produced by Streptomyces sp. MI384-DF12. II. Structure determination of benastatins A and B. J Antibiot (Tokyo). 1992 Sep;45(9):1391-6. [Content Brief]
[2]. Tsakem B, et al., Structures, biosynthesis and biological activities of benastatins, anthrabenzoxocinones and fredericamycins. Bioorg Chem. 2024 Sep;150:107572. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Benastatin B Related Classifications
HY-N12261 Related Classifications
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