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Details

Stereochemistry ABSOLUTE
Molecular Formula C27H46O2
Molecular Weight 402.6529
Optical Activity UNSPECIFIED
Defined Stereocenters 3 / 3
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of .DELTA.-TOCOPHEROL

SMILES

CC(C)CCC[C@@H](C)CCC[C@@H](C)CCC[C@]1(C)CCC2=C(O1)C(C)=CC(O)=C2

InChI

InChIKey=GZIFEOYASATJEH-VHFRWLAGSA-N
InChI=1S/C27H46O2/c1-20(2)10-7-11-21(3)12-8-13-22(4)14-9-16-27(6)17-15-24-19-25(28)18-23(5)26(24)29-27/h18-22,28H,7-17H2,1-6H3/t21-,22-,27-/m1/s1

HIDE SMILES / InChI

Molecular Formula C27H46O2
Molecular Weight 402.6529
Charge 0
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 3 / 3
E/Z Centers 0
Optical Activity UNSPECIFIED

Description

δ-Tocopherol (δ-T) is a chiral organic molecule belonging to the group of tocopherol, that vary in their degree of methylation of the phenol moiety of the chromanol ring. It was revealed, that δ-Tocopherol had a more potent anticancer activity in solid tumors compared to the other tocopherols, δ-T possessed antileukemic activity of in acute myeloid leukemia (AML). δ-T induced tumor cell death through peroxisome proliferator-activated receptor γ (PPAR-γ) induction, cyclin-D1 inhibition, and modulation of redox balance. In addition, on animal models was found, that δ-tocopherol was more active than α- or γ-tocopherol in inhibiting lung tumor growth, possibly through trapping reactive oxygen and nitrogen species and inducing apoptosis.

Approval Year

Targets

Primary TargetPharmacologyConditionPotency

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
Unknown
Primary
Unknown

PubMed

Sample Use Guides

In Vivo Use Guide
xenograft model mice: diets supplemented with δ-tocopherol at 0.17% and 0.3%) for 49 days
Route of Administration: Oral
In Vitro Use Guide
Effects of δ-T (δ-Tocopherol) on Acute Myeloid Leukemia (AML) cells. Jurkat, TOM-1, K-562, KG-1, THP-1, and UMCL01-101 cell lines were incubated with increasing concentrations of δ-T (0-200 µM) for 72 hours. Cell viability was quantified using a tetrazolium dye reduction assay. Apoptotic induction and cell cycle arrest explained the efficacy of δ-T against KG-1 cells. The mechanism of cell growth inhibition of δ-T was through downregulation of cyclin-D1 and a set of homeobox proteins (HOXA9, PBX1, and Cdx2) that have a well-documented role in the pathobiology of AML.
Substance Class Chemical
Record UNII
JU84X1II0N
Record Status Validated (UNII)
Record Version