General
Preferred name
Vitamin E
Synonyms
Tocopherol (vit e) ()
E-Caps ()
Fort-E-Vite Plus ()
Tocopheryl Acetate, dl-Alpha ()
Natopherol ()
Davina ()
Bio-E-Vit ()
Sigma ()
Tocopheryl Acetate, d-Alpha ()
Eprolin ()
Tocopheryl Acid Succinate, d-Alpha ()
Harris ()
Fort-E-Vite 1000 ()
Fort-E-Vite ()
Fort-E-Vite Super Plus ()
Alpha-tocopherol ()
Jarrow For ()
(+)-¦Á-Tocopherol ()
D-¦Á-Tocopherol ()
¦Á-Vitamin E ()
??-Vitamin E ()
Dexrabeprazole Sodium ()
D-??-Tocopherol ()
ALPHA-TOCOPHEROL ()
5,7,8-Trimethyltocol ()
(+)-alpha-Tocopherol ()
Tocofersolan ()
(+)-??-Tocopherol ()
Tocopherol (R,S) ()
5,7,8-Trimethyltocol(+)-alpha-Tocopherol ()
rel-(+)-¦Á-Tocopherol ()
rel-D-¦Á-Tocopherol ()
rel-¦Á-Vitamin E ()
vitamin-E ()
α-Vitamin E ()
rel-α-Vitamin E ()
(+)-α-Tocopherol ()
D-α-Tocopherol ()
rel-D-α-Tocopherol ()
Alpha Tocopherol ()
Tocopherol ()
Aquasol E ()
E307 ()
P&D ID
PD010193
CAS
59-02-9
11105-14-9
10191-41-0
2074-53-5
Tags
natural product
drug
available
Approved by
FDA
Drug Status
nutraceutical
withdrawn
approved
vet_approved
Drug indication
Cardiovascular disease
Vitamin E Supplement
Structure
Probe scores
P&D probe-likeness score
[[ v.score ]]%
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
METABOLISM Alpha and gamma tocopherol are undergo beta oxidation and a process mediated by cytochrome P450s such as CYP4F2, CYP3A4, and CYP3A5[A176155]. These processes convert alpha and gamma tocopherol to alpha-CEHC (2,5,7,8-tetramethyl-2-(2’-carboxyethyl)-6-hydroxychroman) and gamma-CEHC (2,7,8-trimethyl-2-(2’-carboxyethyl)-6-hydroxychroman) respectively, however the full process is not known[A176155].
ABSORPTION 10-33% of deuterium labelled vitamin E is absorbed in the small intestine[A176110,L3063]. Absorption of Vitamin E is dependant upon absorption of the fat in which it is dissolved[L3063,A176104]. For patients with poor fat absorption, a water soluble form of vitamin E may need to be substituted such as tocopheryl polyethylene glycol-1000 succinate[L3063].; ; In other studies the oral bioavailability of alpha-tocopherol was 36%, gamma-tocotrienol was 9%[A32447]. The time to maximum concentration was 9.7 hours for alpha-tocopherol and 2.4 hours for gamma-tocotrienol[A32447].
MOA The mechanism of action for most of vitamin E's effects are still unknown[A176104,A176107]. Vitamin E is an antioxidant, preventing free radical reactions with cell membranes[A176360]. Though in some cases vitamin E has been shown to have pro-oxidant activity[A176360].; ; One mechanism of vitamin E's antioxidant effect is in the termination of lipid peroxidation[A176363]. Vitamin E reacts with unstable lipid radicals, producing stable lipids and a relatively stable vitamin E radical[A176363]. The vitamin E radical is then reduced back to stable vitamin E by reaction with ascorbate or glutathione[A176363].
HALF-LIFE 44 hours in premature neonates given a 20mg/kg intramuscular injection[A176113]. 12 minutes in intravenous injection of intestinal lymph[A176363].
ABSORPTION 10-33% of deuterium labelled vitamin E is absorbed in the small intestine[A176110,L3063]. Absorption of Vitamin E is dependant upon absorption of the fat in which it is dissolved[L3063,A176104]. For patients with poor fat absorption, a water soluble form of vitamin E may need to be substituted such as tocopheryl polyethylene glycol-1000 succinate[L3063]. In other studies the oral bioavailability of alpha-tocopherol was 36%, gamma-tocotrienol was 9%[A32447]. The time to maximum concentration was 9.7 hours for alpha-tocopherol and 2.4 hours for gamma-tocotrienol[A32447].
TOXICITY There is no data available for effects in pregnancy, breast feeding, hepatic impairment, or renal impairment. However, it appears that the process of vitamin E elimination is strict and self regulating enough that vitamin E toxicity is exceedingly rare[A176137,A176210]. Studies showing adverse effects from excess vitamin E generally involve people consuming more than 1000mg/day for weeks to months[L3063].
ROE Alpha tocopherol is excreted in urine as well as bile in the feces mainly as a carboxyethyl-hydrochroman (CEHC) metabolite, but it can be excreted in it's natural form [A176137].
INDICATION Vitamin E supplementation is indicated for treatment of vitamin E deficiency which can occur in cystic fibrosis, cholestasis and severe liver disease, abetalipoproteinemia or simply poor diet[A176104,L3063].
MOA The mechanism of action for most of vitamin E's effects are still unknown[A176104,A176107]. Vitamin E is an antioxidant, preventing free radical reactions with cell membranes[A176360]. Though in some cases vitamin E has been shown to have pro-oxidant activity[A176360]. One mechanism of vitamin E's antioxidant effect is in the termination of lipid peroxidation[A176363]. Vitamin E reacts with unstable lipid radicals, producing stable lipids and a relatively stable vitamin E radical[A176363]. The vitamin E radical is then reduced back to stable vitamin E by reaction with ascorbate or glutathione[A176363].
PHARMACODYNAMICS Vitamin E is a collective term used to describe 8 separate fat soluble antioxidants, most commonly alpha-tocopherol[A176104]. Vitamin E acts to protect cells against the effects of free radicals, which are potentially damaging by-products of the body's metabolism. Vitamin E deficiency is seen in persons with abetalipoproteinemia, premature, very low birth weight infants (birth weights less than 1500 grams, or 3½ pounds), cystic fibrosis, and cholestasis and severe liver disease[A176104]. Preliminary research suggests vitamin E may help prevent or delay coronary heart disease and protect against the damaging effects of free radicals, which may contribute to the development of chronic diseases such as cancer[A237]. It also protects other fat-soluble vitamins (A and B group vitamins) from destruction by oxygen[A239]. Low levels of vitamin E have been linked to increased incidence of breast and colon cancer[L5725].
Cell lines
1
Organisms
4
Compound Sets
14
Drug Repurposing Hub
DrugBank
DB00163
DrugBank Approved Drugs
DB00163
DrugCentral
4280
DrugCentral Approved Drugs
4280
DrugMAP
DMZC90K
DrugMAP Approved Drugs
DMZC90K
JUMP-Target 1 Compound Set
14985
MedChem Express Bioactive Compound Library
HY-N0683
HY-N0683A
NPC Screening Collection
Other bioactive compounds
ReFrame library
TargetMol Bioactive Compound Library
T1648
Withdrawn 2.0
w189
External IDs
46
Properties
(calculated by RDKit )
Molecular Weight
430.38
Hydrogen Bond Acceptors
2
Hydrogen Bond Donors
1
Rotatable Bonds
12
Ring Count
2
Aromatic Ring Count
1
cLogP
8.84
TPSA
29.46
Fraction CSP3
0.79
Chiral centers
3.0
Largest ring
6.0
QED
0.36
Structural alerts
1
Singlet oxygen quenching
Nuisance compounds in cellular assays
Related compounds
Custom attributes
(extracted from source data)
Pathway
NF-¦ÊB
Cytoskeletal Signaling
Metabolism
oxidation-reduction
Anti-infection
Apoptosis
Immunology/Inflammation
Metabolic Enzyme/Protease
NF-κB
Target
GST Mu 3
GST omega-1
GSTP
SEC14-like protein
PKC
VE
ALOX5, DGKA, NR1I2, PPP2CA, PPP2CB, PRKCA, PRKCB, SEC14L2, SEC14L3, SEC14L4
PRKCB
Bacterial
Endogenous Metabolite
Ferroptosis
Influenza Virus
Reactive Oxygen Species
MOA
LDL oxidation inhibitor, PKC inhibitor
ATC
A11HA03
Toxicity type
hepatic
Source data