55004-75-6

Basic information

• Product Name: 4-HYDROXY-7,8-DIMETHYLCOUMARIN
• Synonyms: 4-HYDROXY-7,8-DIMETHYL-2H-CHROMEN-2-ONE;4-HYDROXY-7,8-DIMETHYLCOUMARIN
• CAS NO: 55004-75-6
• Molecular Formula: C₁₁H₁₀O₃
• Molecular Weight: 190.197
• Mol File: 55004-75-6.mol
• Article Data: 4

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 4-HYDROXY-7,8-DIMETHYLCOUMARIN(CAS DataBase Reference)
• NIST Chemistry Reference: 4-HYDROXY-7,8-DIMETHYLCOUMARIN(55004-75-6)
• EPA Substance Registry System: 4-HYDROXY-7,8-DIMETHYLCOUMARIN(55004-75-6)

Safety Data

• Hazardous Substances Data: 55004-75-6(Hazardous Substances Data)

Upstream product

• 141-82-2 malonic acid 
• 526-75-0 2,3-Dimethylphenol 
• 5384-55-4 1-(2-hydroxy-3,4-dimethylphenyl)ethan-1-one 
• 105-58-8 Diethyl carbonate 

Downstream Products

• 1258700-43-4 C₁₈H₁₅NO₄ 

Relevant articles and documents

Design, synthesis, and mechanism of dihydroartemisinin-coumarin hybrids as potential anti-neuroinflammatory agents

Cancer patients frequently suffer from cancer-related fatigue (CRF), which is a complex syndrome associated with weakness and depressed mood. Neuroinflammation is one of the major inducers of CRF. The aim of this study is to find a potential agent not only on the treatment of cancer, but also for reducing CRF level of cancer patients. In this study, total-thirty new Dihydroartemisinin-Coumarin hybrids (DCH) were designed and synthesized. The in vitro cytotoxicity against cancer cell lines (HT-29, MDA-MB-231, HCT-116, and A549) was evaluated. Simultaneously, we also tested the anti-neuroinflammatory activity of DCH. DCH could inhibit the activated microglia N9 release of NO, TNF-α, and IL-6. The docking analysis was shown that MD-2, the coreceptor of TLR4, might be one of the targets of DCH.

Synthesis and biological evaluation of coumarin-based inhibitors of NAD(P)H: Quinone oxidoreductase-1 (NQO1)

The synthesis is reported here of two novel series of inhibitors of human NAD(P)H quinone oxidoreductase-1 (NQO1), an enzyme overexpressed in several types of tumor cell. The first series comprises substituted symmetric dicoumarol analogues; the second series contains hybrid compounds where one 4-hydroxycoumarin systemis replaced by a different aromatic moiety. Several compounds show equivalent or improved NQO1 inhibition over dicoumarol, both in the presence and in the absence of added protein. Further, correlation is demonstrated between the ability of these agents to inhibit NQO1 and computed binding affinity. We have solved the crystal structure of NQO1 complexed to a hybrid compound and find good agreement with the in silico model. For both MIA PaCa-2 pancreatic tumor cells and HCT116 colon cancer cells, dicoumarol shows the greatest toxicity of all compounds. Thus, we provide a computational, synthetic, and biological platform to generate competitive NQO1 inhibitors with superior pharmacological properties to dicoumarol. This will allow a more definitive study of NQO1 activity in cells, in particular, its drug activating/detoxifying properties and ability to modulate oncoprotein stability. 2009 American Chemical Society.