3357-55-9

Upstream product

• 6829-40-9 aminomalonic acid diethyl ester 
• 91469-69-1 ethylesters of amino malonic acid 
• 1068-90-2 2-acetylaminomalonic acid diethyl ester 
• 5256-74-6 1,3-diethyl 2-diazopropanedioate 
• 75-05-8 acetonitrile 

Downstream Products

• 3357-56-0 2-methyl-5-ethoxyoxazole-4-carboxylic acid 
• 3357-62-8 2-methyl-4-(chlorocarbonyl)-5-ethoxyoxazole 
• 3356-83-0 2-methyl-4-(methylaminocarbonyl)-5-ethoxyoxazole 
• 128269-81-8 2-methyl-4-<(N-methylamino)thiocarbonyl>-5-ethoxyoxazole 
• 128242-88-6 2-methyl-4-<(N-methylamino)carbonyl>-5-ethoxyoxazole 
• 128242-99-9 2-methyl-4-(ethoxycarbonyl)-5-(N-methylamino)thiazole 
• 121031-28-5 3-Methyl-5,7-dioxo-6-phenyl-6,7-dihydro-5H-[1,2,4]triazolo[1,2-a][1,2,4]triazole-1,1-dicarboxylic acid diethyl ester 

Relevant academic research and scientific papers

Peroxisome proliferator-activated receptor-γ mediates the anti-inflammatory effect of 3-hydroxy-4-pyridinecarboxylic acid derivatives: Synthesis and biological evaluation

Seven 3-hydroxy-4-pyridinecarboxylic acid derivatives (HPs), aza-analogues of salicylic acid and structurally close to other potent inflammatory pyridine compounds such as aminopyridinylmethanols and aminopyridinamines, were synthesized, and their anti-inflammatory activity was evaluated. The synthesis was performed by adopting a general procedure involving an intramolecular Diels-Alder cycloaddition of oxazoles with acrylic acid to form various substituted pyridinic acids. The newly synthesized HPs did not exhibit cytotoxic activity on human monocytes-derived macrophages at concentrations up to 10 2 μM. Anti-inflammatory activity of the compounds was screened in vitro by evaluating the capability to inhibit cytokines release from lipopolysaccharide (LPS) stimulated human macrophages. 3-Hydroxy-1-methyl-4- pyridinecarboxylic acid (24) was found to be the most active HP. At 10 μM concentration, HP 24 reduced LPS-induced and nuclear factor-κB activation and cyclooxygenase-2 expression, while increased intracellular reactive oxygen species generation and peroxisome proliferator-activated receptor (PPAR-γ) mRNA transcript level. Indeed, pre-treatment of LPS-exposed human macrophages with PPAR-γ specific antagonist completely prevented HP 24-induced TNF-α and IL8 down regulation, demonstrating that the PPARγ pathway is mandatory for the HP 24 anti-inflammatory effect. Finally, daily treatment with HP 24 ameliorated the outcome of DSS-induced colitis in mice, significantly reducing colonic MPO activity and IL-1β tissue levels.

HCV INHIBITING BI-CYCLIC PYRIMIDINES

The present invention relates to the use of bi-cyclic pyrimidines as inhibitors of HCV replication as well as their use in pharmaceutical compositions aimed to treat or combat HCV infections. In addition, the present invention relates to processes for pre