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Assay
98%
mp
88-90 °C (lit.)
SMILES string
CC(NO)=O
InChI
1S/C2H5NO2/c1-2(4)3-5/h5H,1H3,(H,3,4)
InChI key
RRUDCFGSUDOHDG-UHFFFAOYSA-N
Gene Information
human ... CA2(760) , MMP3(4314)
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General description
Acetohydroxamic acid is a potent inhibitor of bacterial urease activity and reduces urinary ammonia levels. 2-Acetohydroxamic acid loaded floating microspheres forms an efficient drug delivery system for the treatment of Helicobacter pylori.
Application
Acetohydroxamic acid was used:
- to study the mechanism of complexation of iron (III) with acetohydroxamic acid
- to study the inhibitory mechanism of lansoprazole and omeprazole on Helicobacter pyloni
- in urease inhibition studies
- for in situ generation of nitrosocarbonylmethane as a Diels-Alder dienophile
Used in urease inhibition studies and for in situ generation of nitrosocarbonylmethane as a Diels-Alder dienophile.
Signal Word
Danger
Hazard Statements
Precautionary Statements
Hazard Classifications
Repr. 1B
Storage Class Code
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
WGK
WGK 3
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Chem. Abstr., 116, 124530f-124530f (1992)
Mechanism of iron (III) complex formation. Activation volumes for the complexation of the iron (III) ion with thiocyanate ion and acetohydroxamic acid.
Inorganic Chemistry, 22(14), 2070-2073 (1983)
The Journal of pharmacy and pharmacology, 55(12), 1607-1613 (2004-01-24)
This investigation is part of our ongoing effort to develop effective drug delivery systems for the treatment of Helicobacter pylori infection using polycarbonate (PC) floating microspheres as drug carriers. In an effort to augment the anti-H. pylori effect of acetohydroxamic
Antimicrobial agents and chemotherapy, 37(4), 769-774 (1993-04-01)
The gastric proton pump inhibitor lansoprazole, its active analog AG-2000, and omeprazole dose dependently inhibited urease activity extracted with distilled water from Helicobacter pylori cells; the 50% inhibitory concentrations were between 3.6 and 9.5 microM, which were more potent than
Journal of the Chemical Society. Perkin Transactions 1, 1001-1001 (1991)
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