Epoxyquinomicin C
Epoxyquinomicin C is an antibiotic that can be isolated from Amycolatopsis sp. Epoxyquinomicin C exhibits anti-inflammatory effects against collagen-induced arthritis. Epoxyquinomicin C can be designed for synthesis of the NF-κB Inhibitor DHMEQ.
For research use only. We do not sell to patients.
- CAS No.: 200496-85-1
- Formula: C14H13NO6
- Molecular Weight:291.26
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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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Biological Activity
Description
Chemical Information
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CAS No. 200496-85-1
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Molecular Weight 291.26
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Formula C14H13NO6
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SMILES
OC[C@]12[C@]([C@H](C(NC(C3=C(C=CC=C3)O)=O)=CC2=O)O)([H])O1
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Structure Classification
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Initial Source
Amycolatopsis sp. MK299-95F4
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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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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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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
[1]. Matsumoto N, et al., Epoxyquinomicins A, B, C and D, new antibiotics from Amycolatopsis. I. Taxonomy, fermentation, isolation and antimicrobial activities. J Antibiot (Tokyo). 1997 Nov;50(11):900-5. [Content Brief]
[2]. Lin Y, et al., Inhibition of Late and Early Phases of Cancer Metastasis by the NF-κB Inhibitor DHMEQ Derived from Microbial Bioactive Metabolite Epoxyquinomicin: A Review. Int J Mol Sci. 2018 Mar 3;19(3):729. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Epoxyquinomicin C Related Classifications
HY-N14977 Related Classifications
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