D-α-Tocopherol succinate

530.78

530.78

4038233

224-403-8

LU4B53JYVE

TSCA listed

DTXSID2026151

White or off-white

2936280000

286nm(EtOH)(lit.)

72.8

11.88

D-alpha-tocopheryl acid succinate is a white powder. (NTP, 1992)

1.002±0.06 g/cm3(Predicted)

~76 °C(lit.)

625.8±55.0 °C(Predicted)

187.0±25.0 °C

1.498

H2O: less than 0.1 mg/mL at 64° F (NTP, 1992)

2-8°C

0Pa at 20℃

LD50 oral in rat: > 7gm/kg

Not classified

Little or no odor

4.35±0.17(Predicted)

Insoluble in water.

Acids, Carboxylic

Vitamin E succinate is an ester. Esters react with acids to liberate heat along with alcohols and acids. Strong oxidizing acids may cause a vigorous reaction that is sufficiently exothermic to ignite the reaction products. Heat is also generated by the interaction of esters with caustic solutions. Flammable hydrogen is generated by mixing esters with alkali metals and hydrides.

-20°C

NONH for all modes of transport

1

EJ9984000

Stable under normal temperatures and pressures.

Flash point data for Vitamin E succinate are not available; however, Vitamin E succinate is probably combustible.

Fires involving this compound should be controlled using a Halon, carbon dioxide, or dry chemical extinguisher. (NTP, 1992)

SMALL SPILLS AND LEAKAGE: You should dampen the solid spill material with acetone, then transfer the dampened material to a suitable container. Use absorbent paper dampened with acetone to pick up any remaining material. Seal your contaminated clothing and the adsorbent paper in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with acetone followed by washing with a strong soap and water solution. Do not reenter the contaminate area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should store this material in a refrigerator. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

_In addition to any following information, owing to alpha-Tocopherol succinate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._ It is generally believed that alpha-tocopherol succinate is ultimately de-esterified or cleaved to provide alpha-tocopherol once administered to the human body. It is consequently expected that pharmacodynamics and pharmacokinetics similar to that of alpha-tocopherol to be followed.

_In addition to any following information, owing to alpha-Tocopherol succinate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._ It is generally believed that alpha-tocopherol succinate is ultimately de-esterified or cleaved to provide alpha-tocopherol once administered to the human body. It is consequently expected that pharmacodynamics and pharmacokinetics similar to that of alpha-tocopherol to be followed. Bound to beta-lipoproteins in blood.

The primary health-related use for which alpha-tocopherol succinate 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). 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. None of these ongoing studies have yet to elucidate any formally significant evidence, however. Similarly, more effective clinical trials are necessary to confirm what has only been accrued as preliminary data when it comes to studies proposing the demonstration of alpha-tocopherol succinate's capability to act as an anti-cancer therapy or as a regulator of inflammation.

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. 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. 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. 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 and has been reported to demonstrate approximately twice the systemic availability of all-rac-tocopherol. 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. Subsequently, without further evidence to suggest otherwise, alpha-tocpherol succinate is generally believed to undergo a logical de-esterification in the gastrointestinal tract before being subsequently absorbed as free tocopherol.

Naturally occurring or synthetic substances that inhibit or retard oxidation reactions. They counteract the damaging effects of oxidation in animal tissues. (See all compounds classified as Antioxidants.)|Organic substances that are required in small amounts for maintenance and growth, but which cannot be manufactured by the human body. (See all compounds classified as Vitamins.)

_In addition to any following information, owing to alpha-Tocopherol succinate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._ It is generally believed that alpha-tocopherol succinate is ultimately de-esterified or cleaved to provide alpha-tocopherol once administered to the human body. It is consequently expected that pharmacodynamics and pharmacokinetics similar to that of alpha-tocopherol to be followed. 50 to 80% absorbed from gastrointestinal tract.|_In addition to any following information, owing to alpha-Tocopherol succinate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._ It is generally believed that alpha-tocopherol succinate is ultimately de-esterified or cleaved to provide alpha-tocopherol once administered to the human body. It is consequently expected that pharmacodynamics and pharmacokinetics similar to that of alpha-tocopherol to be followed.

_In addition to any following information, owing to alpha-Tocopherol succinate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._ It is generally believed that alpha-tocopherol succinate is ultimately de-esterified or cleaved to provide alpha-tocopherol once administered to the human body. It is consequently expected that pharmacodynamics and pharmacokinetics similar to that of alpha-tocopherol to be followed. Hepatic.

_In addition to any following information, owing to alpha-Tocopherol succinate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._ It is generally believed that alpha-tocopherol succinate is ultimately de-esterified or cleaved to provide alpha-tocopherol once administered to the human body. It is consequently expected that pharmacodynamics and pharmacokinetics similar to that of alpha-tocopherol to be followed.

Without further evidence to suggest otherwise, alpha-tocpherol succinate is generally believed to undergo a logical de-esterification in the gastrointestinal tract before being subsequently absorbed as free tocopherol. The free alpha-tocopherol is therefore available and capable of the following activities. 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. These unshared electrons are highly energetic and react rapidly with oxygen to form reactive oxygen species (ROS). In doing so, free radicals are capable of damaging cells, which may facilitate their contribution to the development of various diseases. 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. 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. Specifically, vitamin E is a chain-breaking antioxidant that prevents the propagation of free radical reactions. The vitamin E molecule is specifically a peroxyl radical scavenger and especially protects polyunsaturated fatty acids within endogenous cell membrane phospholipids and plasma lipoproteins. Peroxyl free radicals react with vitamin E a thousand times more rapidly than they do with the aforementioned polyunsaturated fatty acids. Furthermore, the phenolic hydroxyl group of tocopherol reacts with an organic peroxyl radical to form an organic hydroperoxide and tocopheroxyl radical. 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. 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. 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. 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. 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. Vitamin E also upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase-1. 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. Furthermore, vitamin E can inhibit platelet adhesion, aggregation, and platelet release reactions. 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. 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. 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. 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. 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. 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. 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. 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. 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) on which to suggest the use of vitamin E could formally benefit in any of these proposed indications. Furthermore, there are ongoing studies that demonstrate alpha-tocopherol succinate's unique possession of capabilities that allow it to induce differentiation, inhibit proliferation and apoptosis in cancer cells, enhance the growth-inhibitory effect of ionizing radiation, hyperthermia, and some chemotherapeutic agents and biological response modifiers on tumor cells, all the while protecting normal cells against any adverse effects. Despite being able to demonstrate such effects on animal and human cells in culture, the value of these effects has not drawn significant attention from researchers and clinicians and nor has the specific mechanisms of action been elucidated. Additionally, other studies have also shown that alpha-tocopherol succinate seemingly possesses an ability exclusive from other tocopherol esters to inhibit and minimize prostaglandin E2 production in human lung epithelial cells. Considering increased prostaglandin E2 production has been observed frequently in lung cancer patients, there may be another avenue in which alpha-tocopherol succinate may be able to treat lung cancer. Nevertheless, the possibility of such activity requires further elucidation.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

3,4-Dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1-benzopyran-6-ol

Butanedioic acid, 1-[(2R)-3,4-dihydro-2,5,7,8-tetramethyl-2-[(4R,8R)-4,8,12-trimethyltridecyl]-2H-1-benzopyran-6-yl] ester: ACTIVE