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| Targets |
Inhibition of AKT activation (specifically phosphorylation at T308) by interfering with receptor tyrosine kinase (e.g., EGFR)-induced signaling pathways. [1]
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| ln Vitro |
Inducing DHT in human diabetes LNCaP cells and inhibiting their development are the two effects of delta-tocopherol (0-100 μM, 96 hours) on the cells[2]. In CWR-22Rv1/AR cells, delta-tocopherol (0-100 μM, 24 hours) suppresses the activation of androgen produced by DHT (10 nM) and its downstream target PSA [2]. In MCF-7 cells and MDA-MB-231 cells, delta-tocopherol (10 μM, 1-4 days) lowers estrogen-induced cyclin D1 and c-Myc levels [3].
In previous studies using prostate cancer cell lines, δ-Tocopherol attenuated growth factor-induced AKT activation, inhibited cell proliferation, and induced apoptosis. It was more effective than α-tocopherol or γ-tocopherol in these activities. [1] |
| ln Vivo |
Ptenp−/− mice treated with 0.2% food supplementation of delta-tocopherol for 28 weeks do not develop liver tumors [1]. Five weeks of 0.2% diet-based delta-tocopherol suppresses MCF-7 Xenograft tumor growth.
Dietary supplementation with 0.2% δ-Tocopherol significantly inhibited the development of prostate adenocarcinoma in prostate-specific Pten-deficient (Pten p-/-) mice. When feeding began at 12 weeks of age, δ-Tocopherol reduced adenocarcinoma multiplicity by 42.7% at 40 weeks of age. [1] When feeding began earlier, at 6 weeks of age, δ-Tocopherol reduced adenocarcinoma multiplicity by 53.3% at 40 weeks of age. [1] Immunohistochemical analysis of prostate tissues from treated mice showed that δ-Tocopherol reduced the levels of phosphorylated AKT (T308), decreased cell proliferation (as indicated by reduced Ki67-positive cells), and increased apoptosis (as indicated by increased cleaved-Caspase 3-positive cells). [1] In contrast, dietary supplementation with 0.2% α-Tocopherol did not significantly affect prostate adenocarcinoma multiplicity or the aforementioned molecular markers in the same mouse model. [1] Oxidative stress, assessed by 8-OH-dG and nitrotyrosine staining, was not significantly altered during tumorigenesis in this model and was not affected by δ-Tocopherol treatment. [1] |
| Animal Protocol |
Animal/Disease Models: MCF-7 orthotopic xenograft model [3]
Doses: 0.2% in diet Administration time: 5 weeks Experimental Results: Inhibit tumor growth by 58%. Prostate-specific Pten knockout mice (Pten p-/-) on an Fvb background were used. [1] Male Pten p-/- mice were randomly grouped starting at either 5 or 11 weeks of age and fed a standard AIN93M diet for 1 week for acclimation. [1] Experimental groups were then fed either the control AIN93M diet, or AIN93M diet supplemented with 0.2% purified δ-Tocopherol, or 0.2% purified α-Tocopherol. Diets were prepared commercially and stored under nitrogen at 4°C. [1] Feeding began at either 6 weeks or 12 weeks of age and continued until the study endpoint (e.g., 40 weeks of age). [1] Mice were housed under controlled conditions (temperature, humidity, light/dark cycle) with food and water provided ad libitum. From 16 weeks of age, male mice were singly housed. Body weight and food consumption were recorded weekly. [1] At the endpoint, mice were euthanized by CO2 asphyxiation. Blood was collected via cardiac puncture for serum. The entire prostate was excised, fixed in 10% PBS-buffered formalin, and processed for paraffin embedding. [1] Prostate tissues were meticulously dissected into different lobes (anterior, ventral, dorsal, lateral) under a microscope for separate histological processing and analysis. [1] Histopathological characterization (H&E staining) and immunohistochemical staining (for pAKT, Ki67, cleaved Caspase-3, 8-OH-dG, nitrotyrosine) were performed on tissue sections according to standard protocols. Lesions (LG-PIN, HG-PIN, adenocarcinoma) were scored based on established consensus criteria. [1] IHC staining quantification was performed using a digital slide scanner system. For pAKT, staining intensity was normalized to total cell number. For Ki67 and cleaved Caspase-3, the percentage of positively stained cells was calculated. [1] |
| ADME/Pharmacokinetics |
All forms of tocopherol can be absorbed by the liver. Hepatic α-tocopherol transfer proteins preferentially transfer α-tocopherol, rather than γ- and δ-tocopherol, into the blood, resulting in higher levels of α-tocopherol in the blood and tissues than δ-tocopherol. [1]
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| References |
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| Additional Infomation |
δ-Tocopherol is a tocopherol in which the 8-position of the chromanol core is substituted with a methyl group. It is mainly found in corn oil and soybean oil. δ-Tocopherol is a plant metabolite and food antioxidant belonging to vitamin E and tocopherol.
δ-Tocopherol has been reported to be found in Guarea kunthiana, soybean (Glycine max) and other organisms with relevant data. δ-Tocopherol is a naturally occurring fat-soluble vitamin E with high oral bioavailability and is mainly found in soybean oil and corn oil, and has potential antioxidant activity. Although the exact mechanism of action of δ-Tocopherol has not been fully elucidated, it appears to have the ability to scavenge free radicals, thereby protecting cells from oxidative damage. δ-Tocopherol is a form of vitamin E found in some plant oils and nuts. It is methylated at the 8-position of the chromanol ring. [1] Unlike α-Tocopherol, δ-Tocopherol can effectively scavenge both reactive oxygen species and reactive nitrogen species. [1] In the Pten p-/- prostate cancer model, the anticancer activity of δ-tocopherol appears to be primarily achieved through inhibition of AKT activation rather than through its antioxidant activity. This is because oxidative stress is not a major driver in this particular gene model. [1] This study suggests that δ-tocopherol may alter lipid membrane properties, interfere with the endocytosis of growth factor receptors (e.g., EGFR) and subsequent AKT pathway activation. [1] The results suggest that δ-tocopherol has the potential to prevent prostate cancer driven by PTEN deficiency/AKT activation, a common alteration in human prostate cancer. [1] |
| Molecular Formula |
C27H46O2
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|---|---|
| Molecular Weight |
402.6529
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| Exact Mass |
402.35
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| CAS # |
119-13-1
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| PubChem CID |
92094
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| Appearance |
Colorless to light yellow liquid
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| Density |
0.935 g/cm3
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| Boiling Point |
504.3ºC at 760 mmHg
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| Melting Point |
< 25 °C
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| Flash Point |
200.1ºC
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| Vapour Pressure |
8.54E-11mmHg at 25°C
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| Index of Refraction |
1.494
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| LogP |
8.223
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
12
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| Heavy Atom Count |
29
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| Complexity |
448
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| Defined Atom Stereocenter Count |
3
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| SMILES |
O1C2C(C([H])([H])[H])=C([H])C(=C([H])C=2C([H])([H])C([H])([H])[C@@]1(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])[C@]([H])(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])[C@]([H])(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])C([H])(C([H])([H])[H])C([H])([H])[H])O[H]
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| InChi Key |
GZIFEOYASATJEH-VHFRWLAGSA-N
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| InChi Code |
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
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| Chemical Name |
(2R)-2,8-dimethyl-2-[(4R,8R)-4,8,12-trimethyltridecyl]-3,4-dihydrochromen-6-ol
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~50 mg/mL (~124.18 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (5.17 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (5.17 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (5.17 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4835 mL | 12.4177 mL | 24.8355 mL | |
| 5 mM | 0.4967 mL | 2.4835 mL | 4.9671 mL | |
| 10 mM | 0.2484 mL | 1.2418 mL | 2.4835 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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