alpha-TocopherolquinoneCAS# 7559-04-8 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 7559-04-8 | SDF | Download SDF |
| PubChem ID | 24205 | Appearance | Yellow oil |
| Formula | C29H50O3 | M.Wt | 446.7 |
| Type of Compound | Quinones | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | 2-(3-hydroxy-3,7,11,15-tetramethylhexadecyl)-3,5,6-trimethylcyclohexa-2,5-diene-1,4-dione | ||
| SMILES | CC1=C(C(=O)C(=C(C1=O)C)CCC(C)(CCCC(C)CCCC(C)CCCC(C)C)O)C | ||
| Standard InChIKey | LTVDFSLWFKLJDQ-UHFFFAOYSA-N | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Alpha-Tocopherolquinone has antioxidant effect, can inhibit lipid peroxidation and reduce cell division in both the glioma cell clone and fetal brain cells； it inhibits β-amyloid aggregation and cytotoxicity, disaggregates preformed fibrils and decreases the production of reactive oxygen species, NO and inflammatory cytokines. |
| Targets | ROS | NO | TNF-α | IL Receptor | Beta Amyloid |
| In vivo | Use of an adaptive study design in single ascending-dose pharmacokinetics of A0001 (α-tocopherylquinone) in healthy male subjects.[Pubmed: 21343342]J Clin Pharmacol. 2012 Jan;52(1):65-77.A0001 (alpha-Tocopherolquinone) is a potent antioxidant currently in development for the treatment of symptoms associated with inherited mitochondrial disorders.
Inhibition of lipid peroxidation by alpha-tocopherolquinone and alpha-tocopherolhydroquinone.[Pubmed: 4015671]Biochem Int. 1985 May;10(5):753-61.The antioxidant effect of alpha-Tocopherolquinone and alpha-tocopherolhydroquinone was studied in liposomes and rat liver submitochondrial particles.
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| Cell Research | α-Tocopherolquinone inhibits β-amyloid aggregation and cytotoxicity, disaggregates preformed fibrils and decreases the production of reactive oxygen species, NO and inflammatory cytokines.[Pubmed: 20933033 ]Regulation of cell division in a human glioma cell clone by arachidonic acid and alpha-tocopherolquinone.[Pubmed: 6284351]Cancer Lett. 1982 Feb;15(2):173-8.A human glioma cell clone (12-18 CV), derived from a previously characterized glioblastoma multiforme cell line, was established in culture.
Neurochem Int. 2010 Dec;57(8):914-22.Alzheimer's disease (AD) is a complex, multifactorial neurodegenerative disease. The aggregation of beta-amyloid (Aβ) into extracellular fibrillar deposition is a pathological hallmark of AD. The Aβ aggregate-induced neurotoxicity, inflammatory reactions and oxidative stress are linked strongly to the etiology of AD.
The currently available hitting-one-target drugs are insufficient for the treatment of AD. Therefore, finding multipotent agents able to modulate multiple targets simultaneously is attracting more attention.
Previous studies indicated that vitamin E or its constituent such as α-tocopherol (α-T) was able to attenuate the effects of several pathogenetic factors in AD. However, ineffective or detrimental results were obtained from a number of clinical trials of vitamin E. |
alpha-Tocopherolquinone Dilution Calculator
alpha-Tocopherolquinone Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.2386 mL | 11.1932 mL | 22.3864 mL | 44.7728 mL | 55.966 mL |
| 5 mM | 0.4477 mL | 2.2386 mL | 4.4773 mL | 8.9546 mL | 11.1932 mL |
| 10 mM | 0.2239 mL | 1.1193 mL | 2.2386 mL | 4.4773 mL | 5.5966 mL |
| 50 mM | 0.0448 mL | 0.2239 mL | 0.4477 mL | 0.8955 mL | 1.1193 mL |
| 100 mM | 0.0224 mL | 0.1119 mL | 0.2239 mL | 0.4477 mL | 0.5597 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Use of an adaptive study design in single ascending-dose pharmacokinetics of A0001 (alpha-tocopherylquinone) in healthy male subjects.[Pubmed:21343342]
J Clin Pharmacol. 2012 Jan;52(1):65-77.
A0001 (alpha-tocopherylquinone) is a potent antioxidant currently in development for the treatment of symptoms associated with inherited mitochondrial disorders. A0001 pharmacokinetics were studied in a single-blind, adaptive design study following a single daily oral dose of placebo (n = 2) or ascending doses of A0001 (n = 8) at 0.25 and 0.5 g under a fasted state or a 0.5- to 6-g dose with a high-fat meal. Dose escalation was based on safety assessment, and proceeding dose levels were selected based on interim pharmacokinetic analyses. A0001 plasma concentration-time profiles were similar across doses, reaching peak concentration within 4 to 6 hours, with concentrations returning to baseline within 24 hours. Exposure was highly dependent on food and dosing frequency. Exposure was nearly 60-fold higher with food but increased subproportionally above 1-g dose; however, the nonproportionality was offset by administering A0001 in divided doses (0.735 g, 3 times per day). The potential for an A0001:vitamin E interaction was also explored, as vitamin E use is prevalent in this patient population, and suggested that a clinically significant pharmacokinetic interaction is not likely. A0001 was well tolerated with no serious adverse events or dose-limiting toxicities. These findings suggest that A0001 has a favorable pharmacokinetic profile when administered orally with food.
alpha-Tocopherol quinone inhibits beta-amyloid aggregation and cytotoxicity, disaggregates preformed fibrils and decreases the production of reactive oxygen species, NO and inflammatory cytokines.[Pubmed:20933033]
Neurochem Int. 2010 Dec;57(8):914-22.
Alzheimer's disease (AD) is a complex, multifactorial neurodegenerative disease. The aggregation of beta-amyloid (Abeta) into extracellular fibrillar deposition is a pathological hallmark of AD. The Abeta aggregate-induced neurotoxicity, inflammatory reactions and oxidative stress are linked strongly to the etiology of AD. The currently available hitting-one-target drugs are insufficient for the treatment of AD. Therefore, finding multipotent agents able to modulate multiple targets simultaneously is attracting more attention. Previous studies indicated that vitamin E or its constituent such as alpha-tocopherol (alpha-T) was able to attenuate the effects of several pathogenetic factors in AD. However, ineffective or detrimental results were obtained from a number of clinical trials of vitamin E. Here, we showed that naturally synthesized RRR-alpha-tocopherol quinone (alpha-TQ), a main derivative of alpha-T, could inhibit Abeta42 fibril formation dose-dependently. Further investigations indicated that alpha-TQ could attenuate Abeta42-induced neurotoxicity toward SH-SY5Y neuroblastoma cells, disaggregate preformed fibrils and interfere with natural intracellular Abeta oligomer formation. Moreover, alpha-TQ could decrease the formation of reactive oxygen species (ROS) and NO, and modulate the production of cytokines by decreasing TNF-alpha and IL-1beta and increasing IL-4 formation in microglia. Taken together, alpha-TQ targeting multiple pathogenetic factors deserves further investigation for prevention and treatment of AD.
Regulation of cell division in a human glioma cell clone by arachidonic acid and alpha-tocopherolquinone.[Pubmed:6284351]
Cancer Lett. 1982 Feb;15(2):173-8.
A human glioma cell clone (12-18 CV), derived from a previously characterized glioblastoma multiforme cell line, was established in culture. Lipid peroxidation (thiobarbituric acid test) occurred when either 8,11,14-eicosatrienoic acid or 5,8,11-eicosatetraenoic acid (arachidonic acid) was added to the cells in culture. The extent of lipid peroxidation was similar in fetal brain cells (CH II) treated with these polyunsaturated fatty acids. The antioxidant, alpha-Tocopherolquinone, inhibited lipid peroxidation in both the glioma cell clone and fetal brain cells. Arachidonic acid significantly reduced cell division in both the glioma cell clone and fetal brain cells. alpha-Tocopherolquinone restored cell division to control levels in both cultures. These data show that cells from a tumor clone retain the capacity for lipid peroxidation. Furthermore, cell division in a tumor clone is correlated with lipid peroxidation in the same way that cell division in other cell lines is correlated with lipid peroxidation.
Inhibition of lipid peroxidation by alpha-tocopherolquinone and alpha-tocopherolhydroquinone.[Pubmed:4015671]
Biochem Int. 1985 May;10(5):753-61.
The antioxidant effect of alpha-Tocopherolquinone and alpha-tocopherolhydroquinone was studied in liposomes and rat liver submitochondrial particles. Both alpha-Tocopherolquinone and alpha-tocopherolhydroquinone inhibit lipid peroxidation induced by ascorbate/Fe2+ in liposomes and by cumene hydroperoxide in submitochondrial particles. Alpha-tocopherolhydroquinone is much more effective than alpha-Tocopherolquinone in inhibiting lipid peroxidation. Submitochondrial particles, depleted of ubiquinones and reincorporated with alpha-Tocopherolquinone, are protected from lipid peroxidation only in the presence of succinate. alpha-Tocopherolquinone cannot replace endogenous ubiquinones in the respiratory chain function, nevertheless it can be reduced by the mitochondrial respiratory chain substrates, presumably through the reduced ubiquinones.
