76322-07-1

Upstream product

• 672-13-9 2-hydroxy-5-methoxybenzaldehyde 
• 105-36-2 ethyl bromoacetate 
• 105-39-5 chloroacetic acid ethyl ester 
• 150-76-5 4-methoxy-phenol 

Downstream Products

• 50551-56-9 ethyl 5-methoxybenzofuran-2-carboxylate 
• 76322-12-8 (2-ethoxycarbonylmethoxy-5-methoxyphenyl)hydroxyacetonitrile 
• 24589-93-3 2-(2-formyl-4-methoxyphenoxy)acetic acid 
• 860744-04-3 (2',4'-dihydroxy-5-methoxy-α'-oxo-bibenzyl-2-yloxy)-acetic acid 
• 10242-08-7 5-methoxybenzofuran-2-carboxylic acid 
• 76322-20-8 ethyl(2-ethoxycarbonylmethoxy-5-methoxyphenyl)acetate 
• 858847-30-0 (2-Carboxymethoxy-5-methoxy-phenyl)-acetic acid 
• 76322-25-3 6-methoxychroman-3-one 
• 260784-18-7 5-(2-carboxymethoxy-5-methoxybenzylidene)-4-oxo-2-thioxothiazolidine 

Relevant academic research and scientific papers

Synthesis and biological evaluation of novel shikonin-benzo[b]furan derivatives as tubulin polymerization inhibitors targeting the colchicine binding site

A novel series of shikonin-benzo[b]furan derivatives were designed and synthesized as tubulin polymerization inhibitors, and their biological activities were evaluated. Most compounds revealed the comparable anti-proliferation activities against the cancer cell lines to that of shikonin and simultaneously low cytotoxicity to non-cancer cells. Among them, compound 6c displayed powerful anti-cancer activity with the IC50 value of 0.18 μM against HT29 cells, which was significantly better than that of the reference drugs shikonin and CA-4. What's more, 6c could inhibit tubulin polymerization and compete with [3H] colchicine in binding to tubulin. Further biological studies depicted that 6c can induce cell apoptosis and cell mitochondria depolarize, regulate the expression of apoptosis related proteins in HT29 cells. Besides, 6c actuated the HT29 cell cycle arrest at G2/M phase, and influenced the expression of the cell-cycle related protein. Moreover, 6c displayed potent inhibition on cell migration and tube formation that contributes to the antiangiogenesis. These results prompt us to consider 6c as a potential tubulin polymerization inhibitor and is worthy for further study.

INHIBITORS OF ALPHA-AMINO-BETA-CARBOXYMUCONIC ACID SEMIALDEHYDE DECARBOXYLASE

The present disclosure discloses compounds capable of modulating the activity of α- amino-β-carboxymuconic acid semialdehyde decarboxylase (ACMSD), which are useful for the prevention and/or the treatment of diseases and disorders associated with defects in NAD+ biosynthesis, e.g., metabolic disorders, neurodegenerative diseases, chronic inflammatory diseases, kidney diseases, and diseases associated with ageing. The present application also discloses pharmaceutical compositions comprising said compounds and the use of such compounds as a medicament.

BENZOFURAN AND BENZOTHIOPHENE-2-CARBOXYLIC ACID AMIDE DERIVATIVES

The present invention relates to compounds of formula I wherein X, A and R1 to R4 are as defined in the description and claims, and pharmaceutically acceptable salts thereof. The compounds are useful for the treatment and/or prevention of diseases which are associated with the modulation of H3 receptors.

Synthesis and aldose reductase inhibitory activity of a new series of 5- [[2-(ω-carboxyalkoxy)aryl]methylene]-4-oxo-2-thioxothiazolidine derivatives

A new series of 5-[[2-(ω-carboxyalkoxy)aryl]methylene]-4-oxo-2- thioxothiazolidine derivatives was synthesized and evaluated for their potency as aldose reductase inhibitors (ARIs). Their activities were examined in terms of their inhibitory effect on rat lens aldose reductase in vitro and in terms of the preventive effect on sorbitol accumulation in the sciatic nerve of streptozotocin (STZ)-induced diabetic rats in vivo. Of these compounds, some of the naphthylmethylene thiazolidine derivatives were comparable to Zenarestat in the inhibitory potency in vitro and in vivo. In particular, compound 30 was 1.5 times more potent than Zenarestat in the in vivo activity, and had an adequate potency for clinical development.