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    Endogenous Metabolite
  3. DHEA

DHEA (Synonyms: Prasterone; Dehydroisoandrosterone; Dehydroepiandrosterone)

Cat. No.: HY-14650 Purity: >98.0%
Handling Instructions

DHEA (Prasterone) is one of the most abundant steroid hormones. DHEA (Prasterone) mediates its action via multiple signaling pathways involving specific membrane receptors and via transformation into androgen and estrogen derivatives (e.g., androgens, estrogens, 7α and 7β DHEA, and 7α and 7β epiandrosterone derivatives) acting through their specific receptors.

For research use only. We do not sell to patients.

DHEA Chemical Structure

DHEA Chemical Structure

CAS No. : 53-43-0

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Based on 1 publication(s) in Google Scholar

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Description

DHEA (Prasterone) is one of the most abundant steroid hormones. DHEA (Prasterone) mediates its action via multiple signaling pathways involving specific membrane receptors and via transformation into androgen and estrogen derivatives (e.g., androgens, estrogens, 7α and 7β DHEA, and 7α and 7β epiandrosterone derivatives) acting through their specific receptors.

IC50 & Target

Human Endogenous Metabolite

 

In Vitro

DHEA (Prasterone) is an effective antiapoptotic factor, reversing the serum deprivation-induced apoptosis in prostate cancer cells (DU145 and LNCaP cell lines) as well as in colon cancer cells (Caco2 cell line). DHEA (Prasterone) significantly reduces serum deprivation-induced apoptosis in all 3 cancer cell types, quantitated with the APOPercentage assay (apoptosis is reduced from 0.587±0.053 to 0.142±0.0016 or 0.059±0.002 after treatment for 12 hours with DHEA or NGF, respectively; n=3, P<0.01), and by flow cytometry analysis (FACS) for DU145 cells. The antiapoptotic effect of DHEA is dose dependent with an EC50 at nanomolar concentrations (EC50: 11.2±3.6 nM and 12.4±2.2 nM in DU145 and Caco2 cells, respectively)[1]. DHEA (Prasterone) is the principal sex steroid precursor in humans and can be converted directly to androgens. DHEA (Prasterone) (≥1 μM) causes a dose-dependent inhibition of Chub-S7 proliferation, as assessed by thymidine incorporation assays. DHEA (Prasterone) treatment inhibits expression of the key glucocorticoid-regulating genes H6PDH (≥100 nM) and HSD11B1 (≥1 μM) in differentiating preadipocytes in a dose-dependent manner. In keeping with this finding, DHEA (Prasterone) treatment (≥1 μM) results in a marked reduction in 11β-HSD1 oxoreductase activity (≥1 μM) and a concurrent increase in dehydrogenase activity at the highest DHEA dose used (25 μM DHEA) in differentiated adipocytes[2].

In Vivo

DHEA (Prasterone) in the diet (0.45 % w/w) of male B6 mice (groups of five mice) treated for 8 weeks led to significant decreases in body temperature compared with mice fed the control AIN-76A diet. A similar comparison indicated that control and pair-fed mice are also significantly different. Animals fed DHEA (Prasterone) have significantly lower temperatures than mice fed the control diet 26/29 times tested; mice pair fed to those on the DHEA (Prasterone) diet are less affected, with 8/29 values significantly lower than in mice fed AIN-76A ad libitum. The temperatures of mice fed DHEA (Prasterone) or pair fed to DHEA (Prasterone) are significantly different 21/29 times tested. Body weights are significantly greater in mice fed the control diet than in mice fed DHEA or pair fed to DHEA (Prasterone). Food intake (grams per day) from cages are averaged for each week (n=7), except for Week 9 (n=3). The amount of food intake is significantly decreased in mice fed DHEA (Prasterone). By design, mice pair fed to DHEA (Prasterone) ate about the same amount. Thus, it appears that DHEA (Prasterone) reduces body temperature by food restriction and by a separate mechanism[3].

Clinical Trial
Molecular Weight

288.42

Formula

C₁₉H₂₈O₂

CAS No.

53-43-0

SMILES
Shipping

Room temperature in continental US; may vary elsewhere

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 50 mg/mL (173.36 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 3.4672 mL 17.3358 mL 34.6717 mL
5 mM 0.6934 mL 3.4672 mL 6.9343 mL
10 mM 0.3467 mL 1.7336 mL 3.4672 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (8.67 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (8.67 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (8.67 mM); Clear solution

*All of the co-solvents are provided by MCE.
References
Cell Assay
[2]

Chub-S7 preadipocytes and human primary preadipocytes are seeded into a 24-well plate at densities 1×105 and 2.5×105 respectively. Following overnight culture, medium is supplemented with DHEA, androstenediol, or DHEA (Prasterone) (0-100 μM). Following 24-, 48-, or 72 h incubation, cell proliferation is assessed by incubation with radiolabeled thymidine (0.2 μCi/well) for the final 6 h of culture. Proteins are precipitated with TCA, and cells are scraped in NaOH. The respective content of radiolabeled nuclear material in the resulting lysates is analyzed by scintillation counting[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration
[3]

Mice[3]
Mice are fed Purina Lab Chow until the start of experiments (Day 0). Groups of five mice are then fed pelleted AIN-76A diet containing either no additive or DHEA (0.45% w/w) between 0900 and 1000 hr. Diets are stored at 4°C for no longer than six months to maintain optimal activity. Mice are given the diets ad libitum, except for mice that are pair fed to mice treated with DHEA (Prasterone). The amounts of AIN-76A diet the pair-fed mice received are determined by the weight of food consumed by the DHEA-fed mice on a daily basis. Body weights (grams) are measured at different time points starting at Day 1 and ending at Day 59. Daily food intakes (grams per day) are determined by weighing the food consumed per cage of five mice. The mean±SEM values are calculated for weeks 1 to 8 (n=7); week 9 had only 3 days.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

References

Purity: >98.0%

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DHEA
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HY-14650
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