14745-36-9

Basic information

• Product Name: alpha-tocopherol quinol
• Synonyms: alpha-tocopherol quinol;2,3,6-Trimethyl-5-[(3R,7R,11R)-3,7,11,15-tetramethyl-3-hydroxyhexadecyl]hydroquinone;2,3,6-Trimethyl-5-[(3R,7R,11R)-3-hydroxy-3,7,11,15-tetramethylhexadecyl]-1,4-benzenediol;2-[(3R,7R,11R)-3-Hydroxy-3,7,11,15-tetramethylhexadecyl]-3,5,6-trimethyl-1,4-benzenediol;α-Tocopherol hydroquinone
• CAS NO: 14745-36-9
• Molecular Formula: C₂₉H₅₂O₃
• Molecular Weight: 448.72
• Mol File: 14745-36-9.mol
• Article Data: 6

Chemical Properties

• Appearance: /
• CAS DataBase Reference: alpha-tocopherol quinol(CAS DataBase Reference)
• NIST Chemistry Reference: alpha-tocopherol quinol(14745-36-9)
• EPA Substance Registry System: alpha-tocopherol quinol(14745-36-9)

Safety Data

• Hazardous Substances Data: 14745-36-9(Hazardous Substances Data)

Usage

General Description

Alpha-tocopherol quinol, also known as vitamin E quinol, is a potent antioxidant compound that is derived from alpha-tocopherol, the most biologically active form of vitamin E. It is formed through the reduction of alpha-tocopherol by reactive oxygen species and is believed to be a more powerful antioxidant than its parent compound. Alpha-tocopherol quinol has been shown to protect cells and tissues from oxidative damage by neutralizing free radicals and inhibiting lipid peroxidation. It also plays a role in recycling other antioxidants, such as vitamin C, and has been studied for its potential anti-inflammatory and anti-aging effects. Additionally, alpha-tocopherol quinol has been suggested to have therapeutic potential in treating conditions related to oxidative stress, such as cardiovascular disease and neurodegenerative disorders.

InChI:InChI=1/C29H50O2.C6H6O2/c1-20(2)12-9-13-21(3)14-10-15-22(4)16-11-18-29(8)19-17-26-25(7)27(30)23(5)24(6)28(26)31-29;7-5-1-2-6(8)4-3-5/h20-22,30H,9-19H2,1-8H3;1-4,7-8H/t21-,22-,29-;/m1./s1

Upstream product

• 3626-81-1 8a-hydroxy α-tocopherone 
• 197297-77-1 4-(2,5-dimethoxy-3,4,6-trimethylphenyl)butan-2-one 
• 131426-03-4 1-iodo-2,5-bis(methoxy)-3,4,6-trimethylbenzene 
• 16825-16-4 (6R,10R)-6,10,14-trimethylpentadecan-2-one 
• 82299-54-5 2-(2,5-dimethoxy-3,4,6-trimethylphenyl)ethylmagnesium bromide 
• 4537-09-1 1,4-dimethoxy-2,3,5-trimethyl-benzene 
• 91418-95-0 (3R,7R,11R)-1-(2',5'-dimethoxy-3',4',6'-trimethylphenyl)-3,7,11,15-tetramethyl-hexadecan-3-ol 
• 114341-71-8 (4R,8R)-1-Bromo-4,8,12-trimethyltridecane 
• 87247-35-6 (4R,8R)-4,8,12-trimethyltridecan-1-ol 
• 58-95-7 RRR-α-tocopheryl acetate 
• 59-02-9 Tocopherol 
• 150-86-7 phytol 
• 111437-48-0 (2R,3S)-3-Isopropylsulfanylmethyl-2-methyl-2-((4R,8R)-4,8,12-trimethyl-tridecyl)-oxirane 
• 118759-90-3 (3R,7R,11R)-1-Isopropylsulfanyl-3,7,11,15-tetramethyl-hexadecan-3-ol 

Downstream Products

• 59-02-9 Tocopherol 
• 18920-63-3 vitamin E 
• 91418-95-0 (3R,7R,11R)-1-(2',5'-dimethoxy-3',4',6'-trimethylphenyl)-3,7,11,15-tetramethyl-hexadecan-3-ol 

Relevant articles and documents

The reduction of α-tocopherolquinone by human NAD(P)H: Quinone oxidoreductase: The role of α-tocopherolhydroquinone as a cellular antioxidant

α-Tocopherolquinone (TQ), a product of α-tocopherol oxidation, can function as an antioxidant after reduction to α-tocopherolhydroquinone (TQH2). We examined the ability of human NAD(P)H:quinone oxidoreductase (NQO1) to catalyze the reduction o

Vitamin E hydroquinone is an endogenous regulator of ferroptosis via redox control of 15-lipoxygenase

Ferroptosis is a form of programmed cell death associated with inflammation, neurodegeneration, and ischemia. Vitamin E (alpha-tocopherol) has been reported to prevent ferroptosis, but the mechanism by which this occurs is controversial. To elucidate the biochemical mechanism of vitamin E activity, we systematically investigated the effects of its major vitamers and metabolites on lipid oxidation and ferroptosis in a striatal cell model. We found that a specific endogenous metabolite of vitamin E, alpha-tocopherol hydroquinone, was a dramatically more potent inhibitor of ferroptosis than its parent compound, and inhibits 15-lipoxygenase via reduction of the enzyme's non-heme iron from its active Fe3+ state to an inactive Fe2+ state. Furthermore, a non-metabolizable isosteric analog of vitamin E which retains antioxidant activity neither inhibited 15-lipoxygenase nor prevented ferroptosis. These results call into question the prevailing model that vitamin E acts predominantly as a non-specific lipophilic antioxidant. We propose that, similar to the other lipophilic vitamins A, D and K, vitamin E is instead a pro-vitamin, with its quinone/hydroquinone metabolites responsible for its anti-ferroptotic cytoprotective activity.

Improved General Method of Ortho Alkylation of Phenols Using Alkyl Isopropyl Sulfide, Sulfuryl Chloride and Triethylamine. An Expedient Synthesis of Representative Oxygen Heterocycles and (2R,4'R,8'R)-α-Tocopherol

Functionalized alkyl groups have been introduced regioselectively into the ortho position of phenols via sigmatropic rearrangement of isopropylphenoxysulfonium alkylide, providing a quite efficient synthesis of precursors for chromans, chromens, coumarins, and d-α-tocopherol.