5657-19-2

Usage

Uses

Used in Pharmaceutical Industry:
N-(2-FUROYL)GLYCINE is used as an intermediate in the synthesis of non-nucleoside inhibitors of HCV NS5b RNA polymerase for the treatment of Hepatitis C virus infection. Its incorporation into these inhibitors aids in the development of antiviral drugs that can effectively target and suppress the replication of the virus.
Additionally, N-(2-FUROYL)GLYCINE is used as a building block in the synthesis of benzimidazolylazabicyclooctylethylpiperidines, which are CCR5 antagonists. These antagonists play a crucial role in the treatment of HIV infection by blocking the CCR5 co-receptor, thus preventing the virus from entering and infecting host cells. This application highlights the versatility of N-(2-FUROYL)GLYCINE in contributing to the development of therapeutic agents for the management of viral diseases.

InChI:InChI=1/C15H12N2OS/c1-10-6-2-4-8-12(10)16-17-15-14(18)11-7-3-5-9-13(11)19-15/h2-9,16H,1H3/b17-15-

Upstream product

• 527-69-5 2-furancarbonyl chloride 
• 56-40-6 glycine 
• 88-14-2 2-furanoic acid 

Downstream Products

• 80589-23-7 4-ethoxymethylene-2-[2]furyl-4H-oxazol-5-one 
• 69763-44-6 4-(E)-benzylidene-2-furan-2-yl-4H-oxazol-5-one 
• 88-14-2 2-furanoic acid 
• 56-40-6 glycine 
• 1160366-89-1 (S)-N-[[3-[3-fluoro-4-[4-[2-(furan-2-carboxamido)acetyl]piperazin-1-yl]phenyl]-2-oxo-5-oxazolidinyl]methyl]acetamide 
• 1245631-23-5 C₂₈H₃₀N₆O₄ 
• 1421066-85-4 C₃₁H₃₇N₃O₄ 
• 1262839-68-8 C₂₈H₂₈F₃N₃O₄ 

Relevant academic research and scientific papers

4-Sulfamoylphenylalkylamides as Inhibitors of Carbonic Anhydrases Expressed in Vibrio cholerae

A current issue of antimicrobial therapy is the resistance to treatment with worldwide consequences. Thus, the identification of innovative targets is an intriguing challenge in the drug and development process aimed at newer antimicrobial agents. The state-of-art of anticholera therapy might comprise the reduction of the expression of cholera toxin, which could be reached through the inhibition of carbonic anhydrases expressed in Vibrio cholerae (VchCAα, VchCAβ, and VchCAγ). Therefore, we focused our interest on the exploitation of sulfonamides as VchCA inhibitors. We planned to design and synthesize new benzenesulfonamides based on our knowledge of the VchCA catalytic site. The synthesized compounds were tested thus collecting useful SAR information. From our investigation, we identified new potent VchCA inhibitors, some of them displayed high affinity toward VchCAγ class, for which few inhibitors are currently reported in literature. The best interesting VchCAγ inhibitor (S)-N-(1-oxo-1-((4-sulfamoylbenzyl)amino)propan-2-yl)furan-2-carboxamide (40) resulted more active and selective inhibitor when compared with acetazolamide (AAZ) as well as previously reported VchCA inhibitors.

METABOLISM AND EXCRETION OF FURFURAL IN THE RAT AND MOUSE

The fate of furfural (2-furancarboxaldehyde) was investigated in male and female Fischer 344 (F344) rats given single oral doses of 1, 10 and 60 mg/kg and male and female CD1 mice given 1, 20 and 200 mg/kg furfural. There was a very high recovery (more than 90 percent of dose) of radioactivity in all dose groups in 72 hr. The major route of elimination was by the urine, with much smaller amounts present in the faeces and exhaled as 14CO2. The residue in the carcass after 72 hr was less than 1 percent of the administered dose. Furoylglycine and furanacryloylglycine were identified as the major urinary metabolites by high-performance thin-layer chromatography, radio-HPLC, gas chromatography-mass spectrometry and 1H-nuclear magnetic resonance spectroscopy, by comparison with synthetic reference compounds. There were only subtle differences in the metabolic profile as a function of dose size, sex and species. An additional minor polar metabolite was excreted by male rats and mice, and the parent acids of the glycine conjugates were excreted at the higher doses. The results are discussed in terms of the participation of xenobiotics in the chain elongation reactions of fatty acid biosynthesis.