KRP-109
KRP-109 is a neutrophil elastase (NE) inhibitor with activity in reducing lung inflammation. KRP-109 improves survival in mouse models and reduces the number of neutrophils and inflammation in the alveolar walls. KRP-109 significantly reduced cell and neutrophil counts in bronchoalveolar lavage fluid, as well as cytokine levels such as interleukin 1β and macrophage inflammatory protein 2. KRP-109 can be used in the research of severe pneumonia.
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- CAS No.: 1275996-50-3
- 화학식: C26H30N4O7
- 분자량:510.54
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
제품 설명
Chemical Information
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CAS No. 1275996-50-3
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분자량 510.54
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화학식 C26H30N4O7
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SMILES
OC(/C=C\C(O)=O)=O.CCC1=C2C(N=C(C3=C(N4C[C@H](CC4)N(C)C)N=CC=C3)OC2=O)=CC(OC)=C1
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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Phagocytosis Functional Assay
A phagocytosis functional assay measures the ability of phagocytic cells, such as neutrophils, macrophages, monocytes, or microglia/macrophages, to bind and internalize particulate targets including bacteria, yeast particles, beads, or myelin particles. Fluorescent flow-cytometry assays detect target uptake as fluorescence associated with gated phagocytes, while pH-sensitive dyes such as pHrodo increase signal in acidic phagosomal compartments and therefore preferentially report internalized particles rather than particles remaining outside the cell. Microscopy or high-content imaging can be used to confirm intracellular localization and, in some protocols, to follow uptake kinetics.
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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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References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)