Dehydroepiandrosterone

Research use only, not for human use.

DHEA (Dehydroisoandrosterone) is an important endogenous steroid hormone.

DHEA (Dehydroisoandrosterone) is an important endogenous steroid hormone; DHEA also has a variety of potential biological effects in its own right, binding to an array of nuclear and cell surface receptors and acting as a neurosteroid.(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). 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. (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.

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). 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.

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.

Androstenolone | trans-Dehydroandrosterone | DHEA | Diandrone | NSC 9896 | Prasterone | Psicosterone

Endocrinology/Hormones

Androgen Receptor (AR)

Androgen Receptor

Endocrinology

——

53-43-0

288.42

C19H28O2

>98% (HPLC)

Ethanol: 57 mg/mL (197.62 mM); DMSO: 57 mg/mL (197.62 mM)

C[C@]1([C@](CC2)([H])[C@]3([H])CC=C4C[C@@H](O)CC[C@]4(C)[C@@]3([H])CC1)C2=O

(3S,8R,9S,10R,13S,14S)-3-hydroxy-10,13-dimethyl-1,2,3,4,7,8,9,10,11,12,13,14,15,16-tetradecahydro-17H-cyclopenta[a]phenanthren-17-one

(-20℃)

With Ice Pack

≥ 2 years