Vitamin E 500unit capsules
Capsule
500unit
Oral
Tocopherol exists in four different forms designated as α, β, δ, and γ.
Active ingredients:
Alpha tocopherol
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British National Formulary
Alpha tocopherol
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
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Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
2.44 to 3.02 hours
Mechanism
Tocopherol acts as a radical scavenger.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
36%
The absorption of tocopherol in the digestive tract requires the presence of fat.
[L2120]…
[L2120]…
Half-life
2.44 to 3.02 hours
The elimination half-life ranged from 2.44 to 3.02 hours for δ-tocopherol, γ-tocopherol, and β-tocopherol.
[A32447]
[A32447]
Protein binding
There has not been described a specific plasma transport protein for tocopherol but it is thought that it is highly bound to lipoproteins such as VLDL, HDL and chylomicrons.
[A32451]…
[A32451]…
Volume of distribution
0.021 mL
The apparent volume of distribution was 0.284 ± 0.021 mL for δ-tocopherol, 0.799…
Metabolism
Excess tocopherol is converted into their corresponding carboxyethylhydroxychroman (CEHC), based on the isomer of tocopherol.
[A32448]…
[A32448]…
Elimination
60%
The pharmacokinetic profile of tocopherol indicates a longer time of excretion for tocopherols when compared to tocotrienols.
[A32447]…
[A32447]…
Clearance
0.081 to 0.190 L/h
Clearance ranged from 0.081 to 0.190 L/h for δ-tocopherol, γ-tocopherol, and β-tocopherol.
[A32447]
[A32447]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Tocopherol exists in four different forms designated as α, β, δ, and γ. They present strong antioxidant activities, and it is determined as the major form of vitamin E. Tocopherol, as a group, is composed of soluble phenolic compounds that consist of a chromanol ring and a 16-carbon phytyl chain. The classification of the tocopherol molecules is designated depending on the number and position of the methyl substituent in the chromanol ring. The different types of tocopherol can be presented trimethylated, dimethylated or methylated in the positions 5-, 7- and 8-. When the carbons at position 5- and 7- are not methylated, they can function as electrophilic centers that can trap reactive oxygen and nitrogen species. Tocopherols can be found in the diet as part of vegetable oil such as corn, soybean, sesame, and cottonseed.[A32436] It is currently under the list of substances generally recognized as safe (GRAS) in the FDA for the use of human consumption.[L2114]
Properties:
liquid
DrugBank indication
Tocopherol can be used as a dietary supplement for patients with a deficit of vitamin E; this is mainly prescribed in the alpha form.
[A32443]
Vitamin E deficiency is rare, and it is primarily found in premature babies of very low birth weight, patients with fat malabsorption or patients with abetalipoproteinemia.
[L2120]
Tocopherol, due to its antioxidant properties, is studied for its use in prevention or treatment in different complex diseases such as cancer,[A32436] atherosclerosis, cardiovascular diseases,[A32442] and age-related macular degeneration.
[A32444]
[A32443]
Vitamin E deficiency is rare, and it is primarily found in premature babies of very low birth weight, patients with fat malabsorption or patients with abetalipoproteinemia.
[L2120]
Tocopherol, due to its antioxidant properties, is studied for its use in prevention or treatment in different complex diseases such as cancer,[A32436] atherosclerosis, cardiovascular diseases,[A32442] and age-related macular degeneration.
[A32444]
Also known as(68)
Methyltocols
tocoferol
tocoferoles
tocopherol
tocophérol
Tocopherols
1.14.14.1
20-HETE synthase
Dosage forms(54)
Liquid (Topical)
Oil (Topical)
Capsule (Oral) — 400 U.I.
Patch (Topical)
Lotion (Topical)
Injection, powder, for solution (Intravenous)
Kit (Topical)
Soap (Topical) — 1.1 g/100g
Drug interactions(809)
Known interactions with other medications. Always consult a healthcare professional.
Orlistat can cause a decrease in the absorption of Tocopherol resulting in a reduced serum concentration and potentially a decrease in efficacy.
Pitolisant
Unknown severity
The serum concentration of Tocopherol can be decreased when it is combined with Pitolisant.
Cefotiam may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Mesalazine
Moderate
Mesalazine may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cefmenoxime
Moderate
Cefmenoxime may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cefmetazole
Moderate
Cefmetazole may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Pamidronic acid
Moderate
Pamidronic acid may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Tenofovir disoproxil
Moderate
Tenofovir disoproxil may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Indomethacin
Moderate
Indomethacin may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cidofovir may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cefpiramide
Moderate
Cefpiramide may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Ceftazidime
Moderate
Ceftazidime may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Loracarbef
Moderate
Loracarbef may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cefalotin may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Nabumetone
Moderate
Nabumetone may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Ketorolac may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Tenoxicam may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Celecoxib may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cefotaxime
Moderate
Cefotaxime may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Tolmetin may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Foscarnet may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Rofecoxib may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Piroxicam may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Methotrexate
Moderate
Methotrexate may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cephalexin
Moderate
Cephalexin may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Fenoprofen
Moderate
Fenoprofen may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Valaciclovir
Moderate
Valaciclovir may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Valdecoxib
Moderate
Valdecoxib may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Diclofenac
Moderate
Diclofenac may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Sulindac may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Bacitracin
Moderate
Bacitracin may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Amphotericin B
Moderate
Amphotericin B may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cephaloglycin
Moderate
Cephaloglycin may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Flurbiprofen
Moderate
Flurbiprofen may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Adefovir dipivoxil
Moderate
Adefovir dipivoxil may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Pentamidine
Moderate
Pentamidine may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Etodolac may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Mefenamic acid
Moderate
Mefenamic acid may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Acyclovir may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Naproxen may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Sulfasalazine
Moderate
Sulfasalazine may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Phenylbutazone
Moderate
Phenylbutazone may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Meloxicam may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Carprofen may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Cefaclor may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Diflunisal
Moderate
Diflunisal may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Ceforanide
Moderate
Ceforanide may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Salicylic acid
Moderate
Salicylic acid may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Meclofenamic acid
Moderate
Meclofenamic acid may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Acetylsalicylic acid
Moderate
Acetylsalicylic acid may decrease the excretion rate of Tocopherol which could result in a higher serum level.
Showing 50 of 809 interactions
Toxicity & overdose
Tocopherols are considered as non-toxic but if very high doses are administered, there are reports of hemorrhagic activity. Reproductive and developmental toxicity tests are negative. These negative results were also observed in the analysis of mutagenicity and carcinogenicity.
[A32461]
[A32461]
How it works
Mechanism of action
Tocopherol acts as a radical scavenger. It mainly acts as an antioxidant for lipid bilayers. Tocopherol's functions depend on the H-atom donating ability, location, and movement within the membrane, as well as the efficiency in the radical recycling by some cytosolic reductants such as ascorbate.[A32445] Tocopherol actions are related to the trap of radicals, and it has been shown that even in the absence of substituents in the ortho-positions, tocopherol can trap more than two radicals. The type of radicals available for tocopherol are alkyl and peroxy.[L2123]
Pharmacodynamics
The antioxidant effects of tocopherol can be translated into different changes at the pharmacodynamic level. In vitro studies have shown that this antioxidant activity can produce modification in protein kinase C (PKC) which will later be translated into an inhibition of cell death. Some other derivate effects are the anti-inflammatory properties of tocopherol which can be related to the modulation of cytokines or prostaglandins, prostanoids and thromboxanes.[A32445]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
The absorption of tocopherol in the digestive tract requires the presence of fat.
[L2120]
The bioavailability of tocopherols is highly dependent on the type of isomer that is administered where the alpha-tocopherol can present a bioavailability of 36%. This isomer specificity also determines the intestinal permeability in which the gamma-tocopherol presents a very low permeability. After oral administration, the Cmax was 1353.79 ng/ml for δ-tocopherol, 547.45 ng/ml for γ-tocopherol, 704.16 ng/ml for β-tocopherol, and 2754.36 ng/ml for α-tocopherol.
The Tmax is three to four hours for δ-tocopherol, γ-tocopherol, and β-tocopherol and about six hours for α-tocopherol.
[A32447]
[L2120]
The bioavailability of tocopherols is highly dependent on the type of isomer that is administered where the alpha-tocopherol can present a bioavailability of 36%. This isomer specificity also determines the intestinal permeability in which the gamma-tocopherol presents a very low permeability. After oral administration, the Cmax was 1353.79 ng/ml for δ-tocopherol, 547.45 ng/ml for γ-tocopherol, 704.16 ng/ml for β-tocopherol, and 2754.36 ng/ml for α-tocopherol.
The Tmax is three to four hours for δ-tocopherol, γ-tocopherol, and β-tocopherol and about six hours for α-tocopherol.
[A32447]
Half-life
The elimination half-life ranged from 2.44 to 3.02 hours for δ-tocopherol, γ-tocopherol, and β-tocopherol.
[A32447]
[A32447]
Protein binding
There has not been described a specific plasma transport protein for tocopherol but it is thought that it is highly bound to lipoproteins such as VLDL, HDL and chylomicrons.
[A32451]
[A32451]
Volume of distribution
The apparent volume of distribution was 0.284 ± 0.021 mL for δ-tocopherol, 0.799 ± 0.047 mL for γ-tocopherol, and 0.556 ± 0.046 mL for β-tocopherol.
[A32447]
[A32447]
Metabolism
Excess tocopherol is converted into their corresponding carboxyethylhydroxychroman (CEHC), based on the isomer of tocopherol.
[A32448]
More deeply, the metabolism of tocopherol begins with the hepatic metabolism which is led by a CYP4F2/CYP3A4-dependent ω-hydroxylation of the side chains which leads to the formation of 13'-carboxychromanol. The metabolic pathway is followed by five cycles of β-oxidation. The β-oxidation cycles function by shortening the side chains, the first cycle results in the formation of carboxydimethyldecylhydroxychromanol followed by carboxymethyloctylhydroxychromanol.
These two metabolites are categorized as long-chain metabolites and they are not excreted in the urine. Some intermediate-chain metabolites that are products of two rounds of β-oxidation are carboxymethylhexylhydroxychromanol and carboxymethylbutylhydroxychromanol. These intermediate-chain metabolites can be found in human feces and urine.
The catabolic end-product of tocopherols, as stated before, is CEHC which can be largely found in urine and feces.
[A32451]
Two new metabolites have been detected in human and mice feces. These new metabolites are 12'-hydroxychromanol and 11'-hydroxychromanol. Because of their chemistry, it is thought that these metabolites can be the evidence for a ω-1 and ω-2 hydroxylation which leads to an impaired oxidation of 12'-OH followed side-chain truncation.
[A32451]
[A32448]
More deeply, the metabolism of tocopherol begins with the hepatic metabolism which is led by a CYP4F2/CYP3A4-dependent ω-hydroxylation of the side chains which leads to the formation of 13'-carboxychromanol. The metabolic pathway is followed by five cycles of β-oxidation. The β-oxidation cycles function by shortening the side chains, the first cycle results in the formation of carboxydimethyldecylhydroxychromanol followed by carboxymethyloctylhydroxychromanol.
These two metabolites are categorized as long-chain metabolites and they are not excreted in the urine. Some intermediate-chain metabolites that are products of two rounds of β-oxidation are carboxymethylhexylhydroxychromanol and carboxymethylbutylhydroxychromanol. These intermediate-chain metabolites can be found in human feces and urine.
The catabolic end-product of tocopherols, as stated before, is CEHC which can be largely found in urine and feces.
[A32451]
Two new metabolites have been detected in human and mice feces. These new metabolites are 12'-hydroxychromanol and 11'-hydroxychromanol. Because of their chemistry, it is thought that these metabolites can be the evidence for a ω-1 and ω-2 hydroxylation which leads to an impaired oxidation of 12'-OH followed side-chain truncation.
[A32451]
Route of elimination
The pharmacokinetic profile of tocopherol indicates a longer time of excretion for tocopherols when compared to tocotrienols.
[A32447]
The different conjugated metabolites are excreted in the urine or feces depending on the length of their side-chain.
[A32448]
Due to their polarity, intermediate-chain metabolites and short-chain metabolites are excreted via urine as glucoside conjugates. A mixture of all the metabolites and precursors can be found in feces. The long-chain metabolites correspond to >60% of the total metabolites in feces.
It is estimated that the fecal excretion accounts for even 80% of the administered dose.
[A32451]
[A32447]
The different conjugated metabolites are excreted in the urine or feces depending on the length of their side-chain.
[A32448]
Due to their polarity, intermediate-chain metabolites and short-chain metabolites are excreted via urine as glucoside conjugates. A mixture of all the metabolites and precursors can be found in feces. The long-chain metabolites correspond to >60% of the total metabolites in feces.
It is estimated that the fecal excretion accounts for even 80% of the administered dose.
[A32451]
Clearance
Clearance ranged from 0.081 to 0.190 L/h for δ-tocopherol, γ-tocopherol, and β-tocopherol.
[A32447]
[A32447]
Drug targets(1)
Metabolizing enzymes(2)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP4F2Cytochrome P450 4F2
substrate
CYP3A4Cytochrome P450 3A4
substrate
Transporters(7)
Proteins that transport this drug across cell membranes
Alpha-tocopherol transfer protein
TTPA
substrate
Specific functionlipid transfer activity
Cellular location
Cytoplasm
General function & pharmacology
Binds alpha-tocopherol, enhances its transfer between separate membranes, and stimulates its release from liver cells .
PMID:7887897
Binds both phosphatidylinositol 3,4-bisphosphate and phosphatidylinositol 4,5-bisphosphate; the resulting conformation change is important for the release of the bound alpha-tocopherol (By similarity)
PMID:7887897
Binds both phosphatidylinositol 3,4-bisphosphate and phosphatidylinositol 4,5-bisphosphate; the resulting conformation change is important for the release of the bound alpha-tocopherol (By similarity)
SEC14-like protein 4
SEC14L4
substrate
Specific functionlipid binding
General function & pharmacology
Probable hydrophobic ligand-binding protein; may play a role in the transport of hydrophobic ligands like tocopherol, squalene and phospholipids
SEC14-like protein 2
SEC14L2
substrate
Specific functionphospholipid binding
Cellular location
Cytoplasm
General function & pharmacology
Carrier protein. Binds to some hydrophobic molecules and promotes their transfer between the different cellular sites. Binds with high affinity to alpha-tocopherol.
Also binds with a weaker affinity to other tocopherols and to tocotrienols. May have a transcriptional activatory activity via its association with alpha-tocopherol. Probably recognizes and binds some squalene structure, suggesting that it may regulate cholesterol biosynthesis by increasing the transfer of squalene to a metabolic active pool in the cell
Also binds with a weaker affinity to other tocopherols and to tocotrienols. May have a transcriptional activatory activity via its association with alpha-tocopherol. Probably recognizes and binds some squalene structure, suggesting that it may regulate cholesterol biosynthesis by increasing the transfer of squalene to a metabolic active pool in the cell
SEC14-like protein 3
SEC14L3
substrate
Specific functionlipid binding
General function & pharmacology
Probable hydrophobic ligand-binding protein; may play a role in the transport of hydrophobic ligands like tocopherol, squalene and phospholipids
Apolipoprotein B receptor
APOBR
transporter
Specific functionvery-low-density lipoprotein particle receptor activity
Cellular location
Cell membrane
General function & pharmacology
Macrophage receptor that binds to the apolipoprotein B48 (APOB) of dietary triglyceride (TG)-rich lipoproteins (TRL) or to a like domain of APOB in hypertriglyceridemic very low density lipoprotein (HTG-VLDL). Binds and internalizes TRL when out of the context of the macrophage. May provide essential lipids to reticuloendothelial cells.
Could also be involved in foam cell formation with elevated TRL and remnant lipoprotein (RLP). Mediates the rapid high-affinity uptake of chylomicrons (CM), HTG-VLDL, and trypsinized (tryp) VLDL devoid of APOE in vitro in macrophages
Could also be involved in foam cell formation with elevated TRL and remnant lipoprotein (RLP). Mediates the rapid high-affinity uptake of chylomicrons (CM), HTG-VLDL, and trypsinized (tryp) VLDL devoid of APOE in vitro in macrophages
Scavenger receptor class B member 1
SCARB1
transporter
Specific function1-phosphatidylinositol binding
Cellular location
Cell membrane
General function & pharmacology
Receptor for different ligands such as phospholipids, cholesterol ester, lipoproteins, phosphatidylserine and apoptotic cells .
PMID:12016218 PMID:12519372 PMID:21226579
Receptor for HDL, mediating selective uptake of cholesteryl ether and HDL-dependent cholesterol efflux .
PMID:26965621
Also facilitates the flux of free and esterified cholesterol between the cell surface and apoB-containing lipoproteins and modified lipoproteins, although less efficiently than HDL. May be involved in the phagocytosis of apoptotic cells, via its phosphatidylserine binding activity PMID:12016218
PMID:12016218 PMID:12519372 PMID:21226579
Receptor for HDL, mediating selective uptake of cholesteryl ether and HDL-dependent cholesterol efflux .
PMID:26965621
Also facilitates the flux of free and esterified cholesterol between the cell surface and apoB-containing lipoproteins and modified lipoproteins, although less efficiently than HDL. May be involved in the phagocytosis of apoptotic cells, via its phosphatidylserine binding activity PMID:12016218
ATP-dependent translocase ABCB1
ABCB1
transporter
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
Carriers(2)
Proteins that carry this drug through the body
Very low-density lipoprotein receptor
VLDLR
binder
Specific functionapolipoprotein binding
Cellular location
Cell membrane
General function & pharmacology
Multifunctional cell surface receptor that binds VLDL and transports it into cells by endocytosis and therefore plays an important role in energy metabolism. Also binds to a wide range of other molecules including Reelin/RELN or apolipoprotein E/APOE-containing ligands as well as clusterin/CLU .
PMID:24381170 PMID:30873003
In the off-state of the pathway, forms homooligomers or heterooligomers with LRP8 .
PMID:30873003
Upon binding to ligands, homooligomers are rearranged to higher order receptor clusters that transmit the extracellular RELN signal to intracellular signaling processes by binding to DAB1 .
PMID:30873003
This interaction results in phosphorylation of DAB1 leading to the ultimate cell responses required for the correct positioning of newly generated neurons. Later, mediates a stop signal for migrating neurons, preventing them from entering the marginal zone (By similarity)
PMID:24381170 PMID:30873003
In the off-state of the pathway, forms homooligomers or heterooligomers with LRP8 .
PMID:30873003
Upon binding to ligands, homooligomers are rearranged to higher order receptor clusters that transmit the extracellular RELN signal to intracellular signaling processes by binding to DAB1 .
PMID:30873003
This interaction results in phosphorylation of DAB1 leading to the ultimate cell responses required for the correct positioning of newly generated neurons. Later, mediates a stop signal for migrating neurons, preventing them from entering the marginal zone (By similarity)
Low-density lipoprotein receptor
LDLR
binder
Specific functionamyloid-beta binding
Cellular location
Cell membrane
General function & pharmacology
Binds low density lipoprotein /LDL, the major cholesterol-carrying lipoprotein of plasma, and transports it into cells by endocytosis. In order to be internalized, the receptor-ligand complexes must first cluster into clathrin-coated pits. Forms a ternary complex with PGRMC1 and TMEM97 receptors which increases LDLR-mediated LDL internalization PMID:30443021
Scientific references(9)
Das Gupta S., Suh N.
Tocopherols in cancer: An update.
Molecular Nutr Food Research
2016 Jun60(6):1354-63. doi: 10.1002/mnfr.201500847. Epub 2016 Feb 2
Mathur P., Ding Z., Saldeen T., Mehta J.L.
Tocopherols in the Prevention and Treatment of Atherosclerosis and Related Cardiovascular Disease.
Clinical Cardiology
2015 Sep38(9):570-6. doi: 10.1002/clc.22422. Epub 2015 Aug 14
Kim H.J., Giovannucci E., Rosner B., Willett W.C., Cho E.
Longitudinal and secular trends in dietary supplement use: Nurses' Health Study and Health Professionals Follow-Up Study, 1986-2006.
Journal Academy Nutr Diet
2014 Mar114(3):436-43. doi: 10.1016/j.jand.2013.07.039. Epub 2013 Oct 9
Chew E.Y., Clemons T.E., Agron E., Sperduto R.D., Sangiovanni J.P., Kurinij N., Davis M.D.
Long-term effects of vitamins C and E, beta-carotene, and zinc on age-related macular degeneration: AREDS report no.
35
Ophthalmology. 2013 Aug120(8):1604-11.e4. doi: 10.1016/j.ophtha.2013.01.021. Epub 2013 Apr 10
Traber M.G., Atkinson J.
Vitamin E, antioxidant and nothing more.
Free Radic Biological Medicine
2007 Jul 143(1):4-15. doi: 10.1016/j.freeradbiomed.2007.03.024. Epub 2007 Mar 31
Qureshi A.A., Khan D.A., Silswal N., Saleem S., Qureshi N.
Evaluation of Pharmacokinetics, and Bioavailability of Higher Doses of Tocotrienols in Healthy Fed Humans.
Journal Clinical Experimental Cardiolog
2016 Apr7(4). doi: 10.4172/2155-9880.1000434. Epub 2016 Apr 28
Brigelius-Flohe R., Traber M.G.
Vitamin E: function and metabolism.
The FASEB Journal
199913(10):1145-1155. doi: 10.1096/fasebj.13.10.1145
Schmolz L., Birringer M., Lorkowski S., Wallert M.
Complexity of vitamin E metabolism.
World Journal Biological Chemistry
2016 Feb 267(1):14-43. doi: 10.4331/wjbc.v7.i1.14
Zondlo Fiume M.
Final report on the safety assessment of Tocopherol, Tocopheryl Acetate, Tocopheryl Linoleate, Tocopheryl Linoleate/Oleate, Tocopheryl Nicotinate, Tocopheryl Succinate, Dioleyl Tocopheryl Methylsilanol, Potassium Ascorbyl Tocopheryl Phosphate, and Tocophersolan.
International Journal Toxicology
200221 Suppl 3:51-116. doi: 10.1080/10915810290169819
ATC classification(1 code)
ATC A11HA03
Affected organisms(1)
Humans and other mammals
Experimental properties(2)
Commercial products(100)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
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Updated 26 days ago(8 Mar 2026)