6711-33-7

Usage

Uses

Used in Plastic and Rubber Industry:
N-Acetyl-N-hydroxyacetamide is used as an antioxidant for [application reason] to prevent the degradation of plastic and rubber materials, thereby enhancing their durability and performance.
Used in Pharmaceutical Industry:
N-Acetyl-N-hydroxyacetamide is used as a pharmaceutical intermediate for [application reason] in the synthesis of certain drugs, such as antiviral medication and blood thinners, contributing to the development of effective treatments for various medical conditions.
Used in Cancer Treatment Research:
N-Acetyl-N-hydroxyacetamide is used as a potential cancer treatment agent for [application reason] its ability to inhibit the growth of tumor cells, offering a promising avenue for further research and development in oncology.

InChI:InChI=1/C4H7NO3/c1-3(6)5(8)4(2)7/h8H,1-2H3

Upstream product

• 19479-87-9 (O-carboxymethyl)hydroxylamine 
• 7732-18-5 water 
• 3710-84-7 N-ethyl-N-hydroxy-ethanamine 
• 4797-93-7 N-acetyl-N-(benzyloxy)acetamide 

Relevant academic research and scientific papers

Cellular protection of SNAP-25 against botulinum neurotoxin/A: Inhibition of thioredoxin reductase through a suicide substrate mechanism

Botulium neurotoxins (BoNTs) are among the most lethal toxins known to man. They are comprised of seven serotypes with BoNT/A being the most deadly; yet, there is no approved therapeutic for their intoxication or one that has even advanced to clinical trials. Botulinum neurotoxicity is ultimately governed through light chain (LC) protease SNARE protein cleavage leading to a loss of neurotransmitter release. Pharmacological attempts to ablate BoNT/A intoxication have sought to either nullify cellular toxin entry or critical biochemical junctions found within its intricate mechanism of action. In these regards, reports have surfaced of nonpeptidic small molecule inhibitors, but few have demonstrated efficacy in neutralizing cellular toxicity, a key prerequisite before rodent lethality studies can be initiated. On the basis of a lead discovered in our BoNT/A cellular assay campaign, we investigated a family of N-hydroxysuccinimide inhibitors grounded upon structure activity relationship (SAR) fundamentals. Molecules stemming from this SAR exercise were theorized to be protease inhibitors. However, this proposition was overturned on the basis of extensive kinetic analysis. Unexpectedly, inhibitor data pointed to thioredoxin reductase (TrxR), an essential component required for BoNT protease translocation. Also unforeseen was the inhibitors' mechanism of action against TrxR, which was found to be brokered through a suicide-mechanism utilizing quinone methide as the inactivating element. This new series of TrxR inhibitors provides an alternative means to negate the etiological agent responsible for BoNT intoxication, the LC protease.

RADICAL PRODUCTS OF HYDROXYLAMINES, NITRONES AND SPIN ADDUCTS IN THE PROCESS OF GRADUAL OXIDATION WITH COORDINATED PEROXY-RADICALS

Hydroperoxides and cobalt-coordinated peroxy-radicals oxidize hydroxylamines as e.g.Et2NOH, (PhCH2)2NOH, PhCH2PhNOH to the respective nitrones, and the spin adducts - nitrone and peroxy-radical - are formed.In contrast to hydroperoxides the coordinated peroxy radicals can oxidize the formed spin adducts, the methylene or methine groups next to nitrogen being converted into carbonyl groups.The radical intermediates corresponding to individual steps of the gradual oxidation have been identified by means of EPR spectra.