KDO
KDO (3-Deoxy-D-manno-2-octulosonic acid) is a characteristic monosaccharide component of capsular polysaccharides of Gram-negative bacteria and meningococcal lipooligosaccharide (LOS), and can also be present in the polysaccharide components of Nelumbo nucifera. KDO together with lipid A constitutes the LOS inner core and is an essential molecule for CD14/TLR4-mediated proinflammatory signaling. KDO can be used in research related to meningococcal disease and inflammation.
For research use only. We do not sell to patients.
- CAS No.: 10149-14-1
- Formula: C8H14O8
- Molecular Weight:238.19
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
The KDO-positive rfaD mutant Z0401 (expressing truncated LOS containing only lipid A-KDO) shows no significant difference in cell morphology compared to the wild-type LNP14912, whereas the LOS-deficient lpxA mutant Z0204 exhibits outer membrane detachment and structural abnormalities[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 10149-14-1
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Molecular Weight 238.19
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Formula C8H14O8
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SMILES
OC[C@@H](O)[C@@H](O)[C@H](O)[C@H](O)CC(C(O)=O)=O
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Synonyms
3-Deoxy-D-manno-2-octulosonic acid
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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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Gram Staining of Tissue Sections
Gram staining of tissue sections is a histochemical technique used to differentiate Gram-positive and Gram-negative bacteria within histological specimens based on differences in bacterial cell wall structure and dye retention, adapted from classical bacteriological Gram staining into tissue-compatible “histological Gram stain” variants. In tissue applications, modifications of the Brown-Hopps and Brown-Brenn methods are commonly used to improve differentiation of microorganisms embedded within host connective tissue and to reduce overstaining or loss of Gram-negative signal, which are known limitations of earlier approaches. The principle relies on crystal violet-iodine complex retention in Gram-positive organisms and subsequent decolorization and counterstaining steps that allow contrast visualization of Gram-negative organisms against tissue background.
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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)