78933-14-9

Upstream product

• 138206-45-8 2'-Hydroxy-2-methoxyacetophenone 
• 794-94-5 p-Methoxybenzoic anhydride 
• 6889-78-7 4'-(methoxy)-3-hydroxyflavone 
• 74-88-4 methyl iodide 
• 3327-24-0 1-(2-hydroxyphenyl)-3-(4-methoxyphenyl)-2-propen-1-one 
• 118-93-4 o-hydroxyacetophenone 
• 123-11-5 4-methoxy-benzaldehyde 
• 34000-29-8 [E]-3-(p-methoxyphenyl)-1-(2-hydroxyphenyl)prop-2-en-1-one 
• 5538-51-2 O-acetylsalicyloyl chloride 
• 3034-08-0 2-(4-methoxyphenyl)-2,3-dihydro-4H-chromen-4-one 
• 77-78-1 dimethyl sulfate 
• 186581-53-3 diazomethane 

Downstream Products

• 344578-81-0 3-acetoxy-2,3,4'-trimethoxyflavan-4-one 
• 88187-15-9 3-ethoxy-2,3,4'-trimethoxyflavan-4-one 
• 88187-14-8 2,3,3,4'-tetramethoxyflavan-4-one 
• 88187-16-0 2,3,3,4'-tetramethoxyflavan-4-ol 
• 88187-11-5 3-bromo-2-ethoxy-3,4'-dimethoxyflavan-4-one 
• 88187-12-6 3-bromo-2,3,4'-trimethoxyflavan-4-one 

Relevant academic research and scientific papers

Synthesis and effects on cell viability of flavonols and 3-methyl ether derivatives on human leukemia cells

Flavonoids are polyphenolic compounds which display an array of biological activities and are considered potential antitumor agents. Here we evaluated the antiproliferative activity of selected synthetic flavonoids against human leukemia cell lines. We found that 4′-bromoflavonol (flavonol 3) was the most potent. This compound inhibited proliferation in a concentration-dependent manner, induced apoptosis and blocked cell cycle progression at the S phase. Cell death was found to be associated with the cleavage and activation of multiple caspases, the activation of the mitogen-activated protein kinase pathway and the up-regulation of two death receptors (death receptor 4 and death receptor 5) for tumor necrosis factor-related apoptosis-inducing ligand. Moreover, combined treatments using 4′-bromoflavonol and TRAIL led to an increased cytotoxicity compared to single treatments. These results provide a basis for further exploring the potential applications of this combination for the treatment of cancer.

Synthesis and biological evaluation of flavones and benzoflavones as inhibitors of BCRP/ABCG2

Multidrug resistance (MDR) often leads to a failure of cancer chemotherapy. Breast Cancer Resistance Protein (BCRP/ABCG2), a member of the superfamily of ATP binding cassette proteins has been found to confer MDR in cancer cells by transporting molecules with amphiphilic character out of the cells using energy from ATP hydrolysis. Inhibiting BCRP can be a solution to overcome MDR.We synthesized a series of flavones, 7,8-benzofl avones and 5,6-benzo flavones with varying substituents at positions 3, 3′ and 4′ of the (benzo)fl avone structure. All synthesized compounds were tested for BCRP inhibition in Hoechst 33342 and pheophorbide A accumulation assays using MDCK cells expressing BCRP. All the compounds were further screened for their P-glycoprotein (P-gp) and Multidrug resistance-associated protein 1 (MRP1) inhibitory activity by calcein AM accumulation assay to check the selectivity towards BCRP. In addition most active compounds were investigated for their cytotoxicity. It was observed that in most cases 7,8-benzoflavones are more potent in comparison to the 5,6-benzoflavones. In general it was found that presence of a 3-OCH3 substituent leads to increase in activity in comparison to presence of OH or no substitution at position 3. Also, it was found that presence of 3′,4′-OCH3 on phenyl ring lead to increase in activity as compared to other substituents. Compound 24, a 7,8-benzoflavone derivative was found to be most potent being 50 times selective for BCRP and showing very low cytotoxicity at higher concentrations.

Synthesis of Some 3-Methoxyflavones and Chromones

3-Methoxy-3',4'-methylenedioxyflavone (I), 3,4'-dimethoxyflavone (II), 3,3',4'-trimethoxyflavone (III), 3-methoxy-4'-chloroflavone (IV), 3-methoxy-2-(2-furyl)chromone (V) and 3-methoxy-2-styrylchromone (VI) have been synthesised by methylation of the corresponding 3-hydroxy compounds.