Vitamin E

Research use only, not for human use.

A generic descriptor for all tocopherols and tocotrienols that exhibit alpha-tocopherol activity.

A generic descriptor for all tocopherols and tocotrienols that exhibit alpha-tocopherol activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of isoprenoids. (In Vitro):α-Vitamin E ((+)-α-Tocopherol) is a peroxyl radical scavenger. The importance of this function is to maintain the integrity of long-chain polyunsaturated fatty acids in the membranes of cells and thus maintain their bioactivity.α-Vitamin E ((+)-α-Tocopherol) has been described to inhibit PKC in various cell types with consequent inhibition of platelet aggregation, endothelial cell nitric oxide production and superoxide production in neutrophils and macrophages. α-Vitamin E ((+)-α-Tocopherol) exposure induced the activation of both the MAP kinase and PI3 kinase (PI3K) pathways, suggesting that it is the oxidative stress that up-regulates kinase pathways and the antioxidant action of α-tocopherol protects the cell membrane fatty acids.α-Vitamin E ((+)-α-Tocopherol) has proposed benefits for influenza virus A infection, as well as possible activity against hepatitis B and C. α-Vitamin E shows proviral effects, particularly in HEK293T/17 cells. (In Vivo):α-Vitamin E ((+)-α-Tocopherol) prevents the increase in the pro-inflammatory cytokines IL-1, IL-6, and IFN-γ mRNA and protein compared with the ischemic-reperfused myocardium from untreated pigs and compared to the non-injured area.α-Vitamin E (D-α-Tocopherol; intraperitoneal injection or oral administration) treatment induces an amelioration of diabetic nephropathy in mice through the activation of diacylglycerol kinase α (DGKα) and the prevention of podocyte loss.

α-Vitamin E ((+)-α-Tocopherol) is a peroxyl radical scavenger. The importance of this function is to maintain the integrity of long-chain polyunsaturated fatty acids in the membranes of cells and thus maintain their bioactivity. α-Vitamin E ((+)-α-Tocopherol) has been described to inhibit PKC in various cell types with consequent inhibition of platelet aggregation, endothelial cell nitric oxide production and superoxide production in neutrophils and macrophages. α-Vitamin E ((+)-α-Tocopherol) exposure induced the activation of both the MAP kinase and PI3 kinase (PI3K) pathways, suggesting that it is the oxidative stress that up-regulates kinase pathways and the antioxidant action of α-tocopherol protects the cell membrane fatty acids. α-Vitamin E ((+)-α-Tocopherol) has proposed benefits for influenza virus A infection, as well as possible activity against hepatitis B and C. α-Vitamin E shows proviral effects, particularly in HEK293T/17 cells.

α-Vitamin E ((+)-α-Tocopherol) prevents the increase in the pro-inflammatory cytokines IL-1, IL-6, and IFN-γ mRNA and protein compared with the ischemic-reperfused myocardium from untreated pigs and compared to the non-injured area. α-Vitamin E (D-α-Tocopherol; intraperitoneal injection or oral administration) treatment induces an amelioration of diabetic nephropathy in mice through the activation of diacylglycerol kinase α (DGKα) and the prevention of podocyte loss.

alpha-Tocopherol | D-alpha tocopherol | Mixed tocopherols

Cytoskeleton/Cell Adhesion Molecules

GST

GST Mu 3| GST omega-1| GSTP| SEC14-like protein| PKC| VE

Other Indications

——

59-02-9

430.71

C29H50O2

>98% (HPLC)

DMSO: 10 mM

OC1=C(C)C(CC[C@](CCC[C@H](C)CCC[C@H](C)CCCC(C)C)(C)O2)=C2C(C)=C1C

(R)-2,5,7,8-tetramethyl-2-((4R,8R)-4,8,12-trimethyltridecyl)chroman-6-ol

(-20℃)

With Ice Pack

≥ 2 years