CAS NO: | 53-43-0 |
包装 | 价格(元) |
10 mM * 1 mL in DMSO | 电议 |
100mg | 电议 |
250mg | 电议 |
500mg | 电议 |
1 g | 电议 |
5 g | 电议 |
生物活性 | 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 |
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体外研究 (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 genesH6PDH(≥100 nM) andHSD11B1(≥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]. | ||||||||||||||||
体内研究 (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-76Aad 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]. | ||||||||||||||||
分子量 | 288.42 | ||||||||||||||||
性状 | Solid | ||||||||||||||||
Formula | C19H28O2 | ||||||||||||||||
CAS 号 | 53-43-0 | ||||||||||||||||
中文名称 | 脱氢表雄酮;去氢表雄酮;脱氢表雄甾酮;脱氢异雄酮;反式-脱氢异雄甾酮;反式-脱氢雄甾酮;脱氢表雄至素酮 | ||||||||||||||||
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运输条件 | Room temperature in continental US; may vary elsewhere. | ||||||||||||||||
储存方式 |
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溶解性数据 | In Vitro: Ethanol : 50 mg/mL(173.36 mM;Need ultrasonic) DMSO : 50 mg/mL(173.36 mM;Need ultrasonic) H2O : 1 mg/mL(3.47 mM;Need ultrasonic) 配制储备液
* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 In Vivo: 请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用;
以下溶剂前显示的百
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