alpha-Tocopherol acetate

Identification

Summary

alpha-Tocopherol acetate is a form of vitamin E used to treat and prevent vitamin deficiencies.

Brand Names

Infuvite, Infuvite Pediatric, Mvc-fluoride, Pregvit

Generic Name

alpha-Tocopherol acetate

DrugBank Accession Number

DB14003

Background

Alpha-tocopherol is the primary form of vitamin E that is preferentially used by the human body to meet appropriate dietary requirements. In particular, the RRR-alpha-tocopherol (or sometimes called the d-alpha-tocopherol stereoisomer) stereoisomer is considered the natural formation of alpha-tocopherol and generally exhibits the greatest bioavailability out of all of the alpha-tocopherol stereoisomers. Moreover, RRR-alpha-tocopherol acetate is a relatively stabilized form of vitamin E that is most commonly used as a food additive when needed ².

Alpha-tocopherol acetate is subsequently most commonly indicated for dietary supplementation in individuals who may demonstrate a genuine deficiency in vitamin E. Vitamin E itself is naturally found in various foods, added to others, or used in commercially available products as a dietary supplement. The recommended dietary allowances (RDAs) for vitamin E alpha-tocopherol are: males = 4 mg (6 IU) females = 4 mg (6 IU) in ages 0-6 months, males = 5 mg (7.5 IU) females = 5 mg (7.5 IU) in ages 7-12 months, males = 6 mg (9 IU) females = 6 mg (9 IU) in ages 1-3 years, males = 7 mg (10.4 IU) females = 7 mg (10.4 IU) in ages 4-8 years, males = 11 mg (16.4 IU) females = 11 mg (16.4 IU) in ages 9-13 years, males = 15 mg (22.4 IU) females = 15 mg (22.4 IU) pregnancy = 15 mg (22.4 IU) lactation = 19 mg (28.4 IU) in ages 14+ years ⁵. Most individuals obtain adequate vitamin E intake from their diets; genuine vitamin E deficiency is considered to be rare.

Nevertheless, vitamin E is known to be a fat-soluble antioxidant that has the capability to neutralize endogenous free radicals. This biologic action of vitamin E consequently continues to generate ongoing interest and study in whether or not its antioxidant abilities may be used to help assist in preventing or treating a number of different conditions like cardiovascular disease, ocular conditions, diabetes, cancer and more. At the moment however, there exists a lack of formal data and evidence to support any such additional indications for vitamin E use.

Type

Small Molecule

Groups

Approved

Synonyms

• Tocopherol acetate
• Tocopherol acetate, unspecified
• Tocopheryl acetate
• Vitamin E (alpha tocopherol acetate)
• Vitamin E acetate
• Vitamin E acetate, unspecified form

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Pharmacology

Indication

The primary health-related use for which alpha-tocopherol acetate is formally indicated is as a dietary supplement for patients who demonstrate a genuine vitamin E deficiency. At the same time, vitamin E deficiency is generally quite rare but may occur in premature babies of very low birth weight (< 1500 grams), individuals with fat-malabsorption disorders (as fat is required for the digestive tract to absorb vitamin E), or individuals with abetalipoproteinemia - a rare, inherited disorder that causes poor absorption of dietary fat - who require extremely large doses of supplemental vitamin E daily (around 100 mg/kg or 5-10 g/day) ⁵. In all such cases, alpha-tocopherol is largely the preferred form of vitamin E to be administered.

Elsewhere, vitamin E's chemical profile as a fat-soluble antioxidant that is capable of neutralizing free radicals in the body continues to generate ongoing interest and study regarding how and whether or not the vitamin can help prevent or delay various chronic diseases associated with free radicals or other potential biological effects that vitamin E possesses like cardiovascular diseases, diabetes, ocular conditions, immune illnesses, cancer, and more ⁴. None of these ongoing studies have yet to elucidate any formally significant evidence, however ⁴.

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Used in combination to treat	Deficiency, vitamin a	Combination Product in combination with: Vitamin A (DB00162)	••• •••
Used in combination to prevent	Vitamin deficiency		••••••••••••			•••••••••
Used in combination to treat	Vitamin e deficiency	Combination Product in combination with: Vitamin A (DB00162)	••• •••

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Associated Therapies

• Deficiency, Vitamin D
• Nutritional supplementation

Contraindications & Blackbox Warnings

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Pharmacodynamics

Of the eight separate variants of vitamin E, alpha-tocopherol is the predominant form of vitamin E in human and animal tissues, and it has the highest bioavailability ⁶. This is because the liver preferentially resecretes only alpha-tocopherol by way of the hepatic alpha-tocopherol transfer protein (alpha-TTP); the liver metabolizes and excretes all the other vitamin E variants, which is why blood and cellular concentrations of other forms of vitamin E other than alpha-tocopherol are ultimately lower ⁵.

Furthermore, the term alpha-tocopherol generally refers to a group of eight possible stereoisomers which is often called all-rac-tocopherol for being a racemic mixture of all eight stereoisomers ^4,6. Of the eight stereoisomers, the RRR-alpha-tocopherol - or sometimes referred to as the d-alpha-tocopherol - stereoisomer is the naturally occurring form of alpha-tocopherol that is perhaps best recognized by the alpha-TTP ^4,6 and has been reported to demonstrate approximately twice the systemic availability of all-rac-tocopherol ⁶.

As a result, often times (but certainly not always) the discussion of vitamin E - at least within the context of using the vitamin for health-related indications - is generally in reference to the use of RRR- or d-alpha-tocopherol.

Mechanism of action

Vitamin E's antioxidant capabilities are perhaps the primary biological action associated with alpha-tocopherol. In general, antioxidants protect cells from the damaging effects of free radicals, which are molecules that consist of an unshared electron ⁵. These unshared electrons are highly energetic and react rapidly with oxygen to form reactive oxygen species (ROS) ⁵. In doing so, free radicals are capable of damaging cells, which may facilitate their contribution to the development of various diseases ⁵. Moreover, the human body naturally forms ROS when it converts food into energy and is also exposed to environmental free radicals contained in cigarette smoke, air pollution, or ultraviolet radiation from the sun ⁵. It is believed that perhaps vitamin E antioxidants might be able to protect body cells from the damaging effects of such frequent free radical and ROS exposure ⁵.

Specifically, vitamin E is a chain-breaking antioxidant that prevents the propagation of free radical reactions ⁴. The vitamin E molecule is specifically a peroxyl radical scavenger and especially protects polyunsaturated fatty acids within endogenous cell membrane phospholipids and plasma lipoproteins ⁴. Peroxyl free radicals react with vitamin E a thousand times more rapidly than they do with the aforementioned polyunsaturated fatty acids ⁴. Furthermore, the phenolic hydroxyl group of tocopherol reacts with an organic peroxyl radical to form an organic hydroperoxide and tocopheroxyl radical ⁴. This tocopheroxyl radical can then undergo various possible reactions: it could (a) be reduced by other antioxidants to tocopherol, (b) react with another tocopheroxyl radical to form non-reactive products like tocopherol dimers, (c) undergo further oxidation to tocopheryl quinone, or (d) even act as a prooxidant and oxidize other lipids ⁴.

In addition to the antioxidant actions of vitamin E, there have been a number of studies that report various other specific molecular functions associated with vitamin E ⁴. For example, alpha-tocopherol is capable of inhibiting protein kinase C activity, which is involved in cell proliferation and differentiation in smooth muscle cells, human platelets, and monocytes ⁴. In particular, protein kinase C inhibition by alpha-tocopherol is partially attributable to its attenuating effect on the generation of membrane-derived dialglycerol, a lipid that facilitates protein kinase C translocation, thereby increasing its activity ⁴.

In addition, vitamin E enrichment of endothelial cells downregulates the expression of intercellular cell adhesion molecule (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), thereby decreasing the adhesion of blood cell components to the endothelium ⁴.

Vitamin E also upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase-1 ⁴. The increased expression of these two rate-limiting enzymes in the arachidonic acid cascade explains the observation that vitamin E, in a dose-dependent fashion, enhanced the release of prostacyclin, a potent vasodilator and inhibitor of platelet aggregation in humans ⁴.

Furthermore, vitamin E can inhibit platelet adhesion, aggregation, and platelet release reactions ⁴. The vitamin can also evidently inhibit the plasma generation of thrombin, a potent endogenous hormone that binds to platelet receptors and induces aggregation of platelets ⁴. Moreover, vitamin E may also be able to decrease monocyte adhesion to the endothellium by downregulating expression of adhesion molecules and decreasing monocyte superoxide production ⁴.

Given these proposed biological activities of vitamin E, the substance continues to generate ongoing interest and studies in whether or not vitamin E can assist in delaying or preventing various diseases with any one or more of its biologic actions. For instance, studies continue to see whether vitamin E's ability to inhibit low-density lipoprotein oxidation can aid in preventing the development of cardiovascular disease or atherogenesis ⁴.

Similarly, it is also believed that if vitamin E can decrease the chance of cardiovascular disease then it can also decrease the chance of related diabetic disease and complications ⁴. In much the same way, it is also believed that perhaps the antioxidant abilities of vitamin E can neutralize free radicals that are constantly reacting and damaging cellular DNA ⁴. Furthermore, it is also believed that free radical damage does contribute to protein damage in the ocular lens - another free radical-mediated condition that may potentially be prevented by vitamin E use ⁴. Where it is also suggested that various central nervous system disorders like Parkinson's disease, Alzheimer's disease, Down's syndrome, and Tardive Dyskinesia possess some form of oxidative stress component, it is also proposed that perhaps vitamin E use could assist with its antioxidant action ⁴.

There have also been studies that report the possibility of vitamin E supplementation can improve or reverse the natural decline in cellular immune function in healthy, elderly individuals ⁴.

As of this time however, there is either only insufficient data or even contradicting data (where certain doses of vitamin E supplementation could even potentially increase all-cause mortality) ¹ on which to suggest the use of vitamin E could formally benefit in any of these proposed indications.

Target	Actions	Organism
AFree radicals	binder	Humans

Absorption

When vitamin E is ingested, intestinal absorption plays a principal role in limiting its bioavailability ². It is known that vitamin E is a fat-soluble vitamin that follows the intestinal absorption, hepatic metabolism, and cellular uptake processes of other lipophilic molecules and lipids ². The intestinal absorption of vitamin E consequently requires the presence of lipid-rich foods ².

In particular, stable alpha-tocopherol acetate undergoes hydrolysis by bile acid-dependant lipase in the pancreas or by an intestinal mucosal esterase ². Subsequent absorption in the duodenum occurs by way of transfer from emulsion fat globules to water-soluble multi- and unilamellar vesicles and mixed micelles made up of phospholipids and bile acids ². As the uptake of vitamin E into enterocytes is less efficient compared to other types of lipids, this could potentially explain the relatively low bioavailability of vitamin E ². Alpha-tocopherol acetate itself is embedded in matrices where its hydrolysis and its uptake by intestinal cells are markedly less efficient than in mixed micelles ². Subsequently, the intestinal cellular uptake of vitamin E from mixed micelles follows in principle two different pathways across enterocytes: (a) via passive diffusion, and (b) via receptor-mediated transport with various cellular transports like scavenger receptor class B type 1, Niemann-Pick C1-like protein, ATP-binding cassette (ABC) transporters ABCG5/ABCG8, or ABCA1, among others ².

Vitamin E absorption from the intestinal lumen is dependent upon biliary and pancreatic secretions, micelle formation, uptake into enterocytes, and chylomicron secretion ⁴. Defects at any step can lead to impaired absorption. ⁴. Chylomicron secretion is required for vitamin E absorption and is a particularly important factor for efficient absorption. All of the various vitamin E forms show similar apparent efficiencies of intestinal absorption and subsequent secretion in chylomicrons ⁴. During chylomicron catabolism, some vitamin E is distributed to all the circulating lipoproteins ⁴.

Chylomicron remnants, containing newly absorbed vitamin E, are then taken up by the liver ⁴. Vitamin E is secreted from the liver in very low density lipoproteins (VLDLs). Plasma vitamin E concentrations depend upon the secretion of vitamin E from the liver, and only one form of vitamin E, alpha-tocopherol, is ever preferentially resecreted by the liver ⁴. The liver is consequently responsible for discriminating between tocopherols and the preferential plasma enrichment with alpha-tocopherol ⁴. In the liver, the alpha-tocopherol transfer protein (alpha-TTP) likely is in charge of the discriminatory function, where RRR- or d-alpha-tocopherol possesses the greatest affinity for alpha-TTP ⁴.

It is nevertheless believed that only a small amount of administered vitamin E is actually absorbed. In two individuals with gastric carcinoma and lymphatic leukemia, the respective fractional absorption in the lymphatics was only 21 and 29 percent of label from meals containing alpha-tocopherol and alpha-tocopheryl acetate, respectively ⁴.

Additionally, after feeding three separate single doses of 125 mg, 250 mg, and 500 mg to a group of healthy males, the observed plasma peak concentrations (ng/mL) were 1822 +/- 48.24, 1931.00 +/- 92.54, and 2188 +/- 147.61, respectively ⁷.

Volume of distribution

When three particular doses alpha-tocopherol were administered to healthy male subjects, the apparent volumes of distribution (ml) observed were: (a) at a single administered dose of 125 mg, the Vd/f was 0.070 +/- 0.002, (b) at dose 250. mg, the Vd/f was 0.127 +/- 0.004, and (c) at dose 500 mg, the Vd/f was 0.232 +/- 0.010 ⁷.

Protein binding

Data regarding the protein binding of alpha-tocopherol is not readily accessible at the moment. In fact, the existence of alpha-tocopherol binding proteins in tissues other than the liver is involved in ongoing investigations ⁴.

Metabolism

Primary hepatic metabolism of alpha-tocopherol begins in the endoplasmic reticulum with CYP4F2/CYP3A4 dependent ω-hydroxylation of the aliphatic side-chain, which forms the 13’-hydroxychromanol (13’-OH) metabolite ². Next, peroxisome ω-oxidation results in 13’-carboxychromanol (13’-COOH) ². Following these two steps are five consecutive β-oxidation reactions which serve to shorten the alpha-tocopherol metabolite side-chains ². The first of these β-oxidations occurs still in the peroxisome environment, generating carboxydimethyldecylhydroxychromanol (CDMDHC, 11’-COOH) ². Then, in the mitochondrion, the second β-oxidation step forms the carboxymethyloctylhydroxychromanol (CDMOHC, 9’-COOH) metabolite ². Since both CDMDHC and CDMOHC possess a side-chain length of between 13 to 9 carbon units, they are considered long-chain metabolites. The hydrophobicity of these long-chain metabolites means they are not excreted in the urine but have been found in human microsomes, serum, and feces ². The next two β-oxidation reactions, still within the mitochondrion environment, produce two intermediate chain metabolites: carboxymethylhexylhydroxychromanol (CDMHHC, 7’-COOH), followed by carboxymethylbutylhydroxychromanol (CMBHC, 5’-COOH) ². Both of these intermediate chain metabolites are found in human plasma, feces, and urine ². Finally, the last mitochrondrion β-oxidation generates the catabolic end product of alpha-tocopherol metabolism: carboxyethyl-hydroxychromans (CEHC, 3'-COOH), which is considered a short-chain metabolite ². CEHC has been observed in human plasma, serum, urine, and feces ².

Hover over products below to view reaction partners

• alpha-Tocopherol acetate
  • 13'-hydroxychromanol
    • 13'-carboxychromanol
      • CDMDHC
        • CDMOHC
          • CDMHHC
            • CMBHC
              • CEHC

Route of elimination

The major route of excretion of ingested vitamin E is fecal elimination because of its relatively low intestinal absorption ⁴. Excess alpha-tocopherol, as well as forms of vitamin E not preferentially used, are probably excreted unchanged in bile ⁴.

Half-life

The apparent half-life of RRR- or d-alpha-tocopherol in normal subjects is approximately 48 hours ⁴.

Clearance

When three specific doses of 125 mg, 250 mg, and 500 mg of alpha-tocopherol were administered as single doses to a group of healthy males, the resultant times of clearance observed, respectively, were: 0.017 +/- 0.015 l/h, 0.011 +/- 0.001 l/h, and 0.019 +/- 0.001 l/h ⁷.

Adverse Effects

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Toxicity

Tocopherols are considered as non-toxic but if very high doses (approximately >2 g/kg/day) are administered, there are reports of hemorrhagic activity ³. Reproductive and developmental toxicity tests are negative ³. These negative results were also observed in the analysis of mutagenicity and carcinogenicity ³. The majority of these tests were animal feeding studies ³.

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Not Available

Interactions

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

• Approved
• Vet approved
• Nutraceutical
• Illicit
• Withdrawn
• Investigational
• Experimental
• All Drugs

Drug	Interaction
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Orlistat	Orlistat can cause a decrease in the absorption of alpha-Tocopherol acetate resulting in a reduced serum concentration and potentially a decrease in efficacy.

Food Interactions

No interactions found.

Products

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Active Moieties

Name	Kind	UNII	CAS	InChI Key
Vitamin E	prodrug	N9PR3490H9	59-02-9	GVJHHUAWPYXKBD-IEOSBIPESA-N

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Vitamin E Inj 100unit/ml	Liquid	100 unit / mL	Intramuscular	Kripps Pharmacy Ltd.	1986-12-31	Not applicable

Over the Counter Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Dl E 400 Cap 400unit	Capsule	400 unit / cap	Oral	Thorne Research Inc.	1984-12-31	1997-07-16
Formula S.D.	Tablet	100 unit / tab	Oral	Changes International	Not applicable	Not applicable
Intense Multi Ampoule Balm Collagen	Liquid	0.3 g/10g	Topical	Nature Republic Co., Ltd.	2022-03-01	Not applicable
One A Day With Non-medicinal Garlic	Tablet	100 unit / tab	Oral	Bayer Inc Consumer Care	2000-09-27	2002-08-01
Synthetic Vitamin E	Capsule	400 unit / cap	Oral	Quantofill Inc.	Not applicable	Not applicable

Mixture Products

Name	Ingredients	Dosage	Route	Labeller	Marketing Start	Marketing End	Region	Image
Adult Formula 50+	alpha-Tocopherol acetate (60 unit) + Ascorbic acid (120 mg) + Beta carotene (3000 unit) + Biotin (30 mcg) + Calcium (220 mg) + Cholecalciferol (400 unit) + Chromium (10 mcg) + Copper (2 mg) + Cyanocobalamin (25 mcg) + Folic acid (0.4 mg) + Iodine (0.15 mg) + Magnesium (100 mg) + Manganese (2.5 mg) + Molybdenum (10 mcg) + Nicotinamide (20 mg) + Calcium pantothenate (20 mg) + Potassium (37.5 mg) + Pyridoxine hydrochloride (6 mg) + Riboflavin (3.4 mg) + Selenium (10 mcg) + Thiamine hydrochloride (4.5 mg) + Vitamin A palmitate (3000 unit) + Zinc (15 mg)	Tablet	Oral	Wn Pharmaceuticals Ltd.	2002-04-25	2009-09-28
Adult Infuvite Multiple Vitamins	alpha-Tocopherol acetate (10 [iU]/10mL) + Ascorbic acid (200 mg/10mL) + Biotin (60 ug/10mL) + Cholecalciferol (200 [iU]/10mL) + Cyanocobalamin (5 ug/10mL) + Dexpanthenol (15 mg/10mL) + Riboflavin-5'-phosphate sodium salt dihydrate (3.6 mg/10mL) + Folic acid (600 ug/10mL) + Nicotinamide (40 mg/10mL) + Phylloquinone (150 ug/10mL) + Pyridoxine hydrochloride (6 mg/10mL) + Thiamine hydrochloride (6 mg/10mL) + Vitamin A palmitate (3300 [iU]/10mL)	Injection, solution	Intravenous	Sandoz Inc	2005-05-18	Not applicable
Adult Infuvite Multiple Vitamins	alpha-Tocopherol acetate (10 [iU]/10mL) + Ascorbic acid (200 mg/10mL) + Biotin (60 ug/10mL) + Cholecalciferol (200 [iU]/10mL) + Cyanocobalamin (5 ug/10mL) + Dexpanthenol (15 mg/10mL) + Riboflavin-5'-phosphate sodium salt dihydrate (3.6 mg/10mL) + Folic acid (600 ug/10mL) + Nicotinamide (40 mg/10mL) + Phylloquinone (150 ug/10mL) + Pyridoxine hydrochloride (6 mg/10mL) + Thiamine hydrochloride (6 mg/10mL) + Vitamin A palmitate (3300 [iU]/10mL)	Injection, solution	Intravenous	Sandoz Inc	2005-05-18	Not applicable
Adult Infuvite Multiple Vitamins	alpha-Tocopherol acetate (10 [iU]/10mL) + Ascorbic acid (200 mg/10mL) + Biotin (60 ug/10mL) + Cholecalciferol (200 [iU]/10mL) + Cyanocobalamin (5 ug/10mL) + Dexpanthenol (15 mg/10mL) + Riboflavin-5'-phosphate sodium salt dihydrate (3.6 mg/10mL) + Folic acid (600 ug/10mL) + Nicotinamide (40 mg/10mL) + Phylloquinone (150 ug/10mL) + Pyridoxine hydrochloride (6 mg/10mL) + Thiamine hydrochloride (6 mg/10mL) + Vitamin A palmitate (3300 [iU]/10mL)	Injection, solution	Intravenous	Sandoz Inc	2003-06-16	Not applicable
Adult Infuvite Multiple Vitamins	alpha-Tocopherol acetate (10 [iU]/10mL) + Ascorbic acid (200 mg/10mL) + Biotin (60 ug/10mL) + Cholecalciferol (200 [iU]/10mL) + Cyanocobalamin (5 ug/10mL) + Dexpanthenol (15 mg/10mL) + Riboflavin-5'-phosphate sodium salt dihydrate (3.6 mg/10mL) + Folic acid (600 ug/10mL) + Nicotinamide (40 mg/10mL) + Phylloquinone (150 ug/10mL) + Pyridoxine hydrochloride (6 mg/10mL) + Thiamine hydrochloride (6 mg/10mL) + Vitamin A palmitate (3300 [iU]/10mL)	Injection, solution	Intravenous	Sandoz Inc	2003-06-16	Not applicable

Unapproved/Other Products

Name	Ingredients	Dosage	Route	Labeller	Marketing Start	Marketing End	Region	Image
Aronamin Gold	alpha-Tocopherol acetate (20 mg/1) + Ascorbic acid (70 mg/1) + Fursultiamine (50 mg/1) + Hydroxocobalamin acetate (5.22 ug/1) + Riboflavin tetrabutyrate (2.5 mg/1)	Tablet, film coated	Oral	OASIS TRADING	2018-11-20	Not applicable
Bacmin	alpha-Tocopherol acetate (30 [iU]/1) + Ascorbic acid (500 mg/1) + Biotin (150 ug/1) + Chromium Cr-51 chloride (0.1 mg/1) + Cupric oxide (3 mg/1) + Cyanocobalamin (50 ug/1) + Ferrous fumarate (27 mg/1) + Flavone (50 mg/1) + Folic acid (1 mg/1) + Magnesium oxide (50 mg/1) + Manganese gluconate (5 mg/1) + Nicotinamide (100 mg/1) + Calcium pantothenate (25 mg/1) + Pyridoxine hydrochloride (25 mg/1) + Riboflavin (20 mg/1) + Selenomethionine (50 ug/1) + Thiamine mononitrate (20 mg/1) + Vitamin A acetate (2000 [iU]/1) + Zinc oxide (22.5 mg/1)	Tablet, coated	Oral	Marnel Pharmaceuticals, Llc	2000-04-01	Not applicable
Cheee Gold Plus Tooth	alpha-Tocopherol acetate (0.13 g/130g) + Silicon dioxide (7.8 g/130g)	Paste, dentifrice	Oral	Nature Plus	2020-07-01	Not applicable
Chunzam Silk Amino Acid Tooth	alpha-Tocopherol acetate (0.1 g/100g) + Silicon dioxide (4 g/100g) + Sodium fluorophosphate (0.33 g/100g)	Paste, dentifrice	Dental	Chunzam Bio Co Ltd	2016-11-11	Not applicable
CitraNatal 90 DHA	alpha-Tocopherol acetate (30 [iU]/1) + Ascorbic acid (120 mg/1) + Calcium citrate tetrahydrate (160 mg/1) + Cupric oxide (2 mg/1) + Docusate sodium (50 mg/1) + Folic acid (1 mg/1) + Iron (90 mg/1) + Nicotinamide (20 mg/1) + Potassium triiodide (150 ug/1) + Pyridoxine hydrochloride (20 mg/1) + Riboprine (3.4 mg/1) + Thiamine chloride (3 mg/1) + Vitamin D (400 [iU]/1) + Zinc oxide (25 mg/1)	Tablet	Oral	Mission Pharmacal	2010-02-01	Not applicable

Categories

Drug Categories

• Antioxidants
• Benzopyrans
• Biological Factors
• Compounds used in a research, industrial, or household setting
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 Substrates
• Diet, Food, and Nutrition
• Food
• Heterocyclic Compounds, Fused-Ring
• Micronutrients
• P-glycoprotein substrates
• Physiological Phenomena
• Protective Agents
• Pyrans
• Tocopherols
• Vitamin E
• Vitamins
• Vitamins (Fat Soluble)

Classification

Not classified

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

9E8X80D2L0

CAS number

7695-91-2

References

General References

1. Miller ER 3rd, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E: Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med. 2005 Jan 4;142(1):37-46. Epub 2004 Nov 10. [Article]
2. Schmolz L, Birringer M, Lorkowski S, Wallert M: Complexity of vitamin E metabolism. World J Biol Chem. 2016 Feb 26;7(1):14-43. doi: 10.4331/wjbc.v7.i1.14. [Article]
3. 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. Int J Toxicol. 2002;21 Suppl 3:51-116. doi: 10.1080/10915810290169819. [Article]
4. Institute of Medicine (US) Panel on Dietary Antioxidants and Related Compounds (2000). Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academies Press (US). [ISBN:0309069491]
5. National Institute for Health [Link]
6. Cosmetic Ingredient Review: Safety Assessment of Tocopherols and Tocotrienols as Used in Cosmetics [Link]
7. Journal of Clinical & Experimental Cardiology: Pharmacokinetics and Bioavailability of Annatto δ-tocotrienol in Healthy Fed Subjects [Link]

External Links

RxNav

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MSDS

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Clinical Trials

Clinical Trials

Phase	Status	Purpose	Conditions	Count
4	Completed	Treatment	Hyperemesis Gravidarum / Morning Sickness / Nausea / Pregnancy / Vomiting	1
4	Completed	Treatment	Pregnancy	1
4	Unknown Status	Treatment	Hyperuricemia	1
3	Completed	Prevention	Postoperative pain	1
3	Completed	Prevention	Surgical Site Infections	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Syrup	Oral
Tablet, film coated	Oral
Solution	Intravenous	1.914 mg
Kit	Oral
Solution / drops	Nasal
Tablet, extended release	Oral
Patch	Transdermal
Paste, dentifrice	Dental
Tablet, effervescent	Oral
Injection, solution	Intramuscular	300 mg/2ml
Solution	Intramuscular	300 mg
Capsule	Oral	400 i.u.
Capsule	Oral
Tablet, chewable	Oral	100 mg
Paste, dentifrice	Topical
Solution / drops	Oral
Capsule, gelatin coated	Oral
Capsule, gelatin coated; kit; tablet	Oral
Tablet, coated	Oral
Liquid	Topical	0.3 g/10g
Cloth	Topical
Paste, dentifrice	Oral
Liquid	Intravenous
Liquid	Oral
Solution	Intravenous
Tablet, chewable	Oral
Tablet, sugar coated	Oral
Tablet	Oral
Capsule	Oral
Tablet	Oral	100 unit / tab
Paste	Dental
Powder
Patch	Topical
Injection, solution; kit	Intravenous
Injection, solution	Intravenous
Cream	Topical
Suspension / drops	Oral
Solution	Oral
Capsule, liquid filled; kit; tablet	Oral
Pill	Oral
Liquid	Topical
Lotion	Topical
Emulsion	Topical
Injection, powder, for solution	Intravenous	100 mg
Tablet	Oral	100 mg
Paste	Topical
Powder	Oral
Lozenge	Oral
Capsule	Oral	800 mg
Capsule	Oral	100 unit / cap
Capsule	Oral	400 mg / cap
Tablet	Oral	400 unit
Capsule	Oral	800 unit
Capsule	Oral	1000 unit / cap
Capsule	Oral	200 unit / cap
Capsule	Oral	200 unit
Capsule	Oral	400 unit / cap
Capsule	Oral	400 unit
Capsule	Oral	800 unit / cap
Tablet	Oral	400 unit / tab
Liquid	Intramuscular	100 unit / mL
Solution	Intramuscular	50 IU/1mL

Prices

Not Available

Patents

Not Available

Properties

State

Liquid

Experimental Properties

Property	Value	Source
melting point (°C)	10 degrees Celcius	MSDS
boiling point (°C)	>343 degrees Celcius	MSDS
water solubility	Insoluble in cold water and hot water	Not Available

Predicted Properties

Not Available

Predicted ADMET Features

Not Available

Spectra

Mass Spec (NIST)

Not Available

Spectra

Not Available

Chromatographic Properties

Collision Cross Sections (CCS)

Not Available

Targets

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1. Free radicals

Kind

Group

Organism

Humans

Pharmacological action

Yes

Actions

Binder

References

1. Institute of Medicine (US) Panel on Dietary Antioxidants and Related Compounds (2000). Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academies Press (US). [ISBN:0309069491]

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Drug created at March 25, 2018 20:54 / Updated at April 26, 2024 00:46