223409
Copper
shot, −3-+14 mesh, 99%
Sinónimos:
Cu
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About This Item
Fórmula empírica (notación de Hill):
Cu
Número de CAS:
Peso molecular:
63.55
EC Number:
MDL number:
UNSPSC Code:
12161600
PubChem Substance ID:
NACRES:
NA.22
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Quality Level
assay
99%
form
shot
reaction suitability
core: copper
reagent type: catalyst
resistivity
1.673 μΩ-cm, 20°C
particle size
−3-+14 mesh
bp
2567 °C (lit.)
mp
1083.4 °C (lit.)
density
8.94 g/mL at 25 °C (lit.)
SMILES string
[Cu]
InChI
1S/Cu
InChI key
RYGMFSIKBFXOCR-UHFFFAOYSA-N
Categorías relacionadas
Storage Class
13 - Non Combustible Solids
wgk_germany
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
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Science (New York, N.Y.), 343(6167), 167-170 (2013-12-18)
Carbon monoxide (CO) produced in many large-scale industrial oxidation processes is difficult to separate from nitrogen (N2), and afterward, CO is further oxidized to carbon dioxide. Here, we report a soft nanoporous crystalline material that selectively adsorbs CO with adaptable
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Proceedings of the National Academy of Sciences of the United States of America, 111(1), 149-154 (2013-12-18)
Lytic polysaccharide monooxygenases (LPMOs) exhibit a mononuclear copper-containing active site and use dioxygen and a reducing agent to oxidatively cleave glycosidic linkages in polysaccharides. LPMOs represent a unique paradigm in carbohydrate turnover and exhibit synergy with hydrolytic enzymes in biomass
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A method has been developed for the preparation of N-alkynylated sulfoximines involving the copper-catalyzed decarboxylative coupling of sulfoximines with aryl propiolic acids. A range of substituents on both the sulfoximidoyl moiety and the aryl group of the propiolic acid were
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Heavy metals in cells are typically regulated by PIB-type ATPases. The first structure of the class, a Cu(+)-ATPase from Legionella pneumophila (LpCopA), outlined a copper transport pathway across the membrane, which was inferred to be occluded. Here we show by
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Hepatic abnormalities in Long-Evans Cinnamon (LEC) rats, an animal model of Wilson disease (WD), were restored by the expression of the human ATP7B cDNA under the control of CAG promoter. Expression of ATP7B transcript and protein in the liver of
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