7537-06-6

Upstream product

• 5417-19-6 1-(chloromethyl)-3,4-dimethoxy-2-methylbenzene 
• 143-33-9 sodium cyanide 
• 151-50-8 potassium cyanide 
• 4463-33-6 1,2-dimethoxy-3-methylbenzene 

Downstream Products

• 7537-14-6 1-(3,4-Dimethoxy-2-methyl-phenyl)-propan-2-one 
• 899442-84-3 methyl (4E)-2-(3,4-dimethoxy-2-methylphenyl)-5,9-dimethyldeca-4,8-dienoate 
• 899442-93-4 2-(3,4-dimethoxy-2-methyl-phenyl)-5,9-dimethyl-deca-4,8-dienoic acid 
• 6834-56-6 3,4-dimethoxy-2-methylphenylacetic acid 
• 7537-10-2 2-(3,4-Dimethoxy-2-methyl-phenyl)-3-oxo-butyronitrile 

Relevant academic research and scientific papers

DNA oxidative damage by terpene catechols as analogues of natural terpene quinone methide precursors in the presence of Cu(II) and/or NADH

Natural terpene quinone methides (QM) and their derivatives have been investigated as therapeutics due to their broad antifungal, antibacterial, and antitumor activities. Recently, we reported that a terpene QM was formed from the catechol precursor through the disproportionation of Cu(II)/(I) redox cycle, and extensive DNA damage was observed throughout the oxidation process. In this paper, we investigate DNA damage with a series of terpene catechols as analogues of natural QM precursors and suggest that reactive oxygen species (ROS) are responsible for the observed DNA damage in the Cu2+-induced oxidation despite the stereo- and structural difference of these catechol or subsequent oxidation products. In addition, the presence of NADH significantly enhanced the extent of DNA damage by oxidation of these catechols. Especially with alkene catechols 6-7, the extent of DNA damage was independent of the concentration of catechols, implying that NADH enables the continuous production of ROS through the redox cycle of catechols/quinones.