| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| 1g |
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| 2g |
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| 5g |
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| 10g |
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Purity: ≥98%
Dehydroepiandrosterone (trans-Dehydroandrosterone; DHEA; Prasterone; Psicosterone; EL-10; GL-701; IP-1001; NSC-9896; PB-007; SH-K-04828; Androstenolone; Diandrone) is an endogenous steroidal hormone acting as an androgen receptor antagonist and an estrogen receptor agonist. DHEA is acts as a metabolic intermediate in the biosynthesis of estrogen and androgen. Also, DHEA has a variety of potential biological effects by binding to nuclear and cell surface receptors and acts as a neurosteroid. DHEA significantly increased neural stem cells growth when grew with leukemia inhibitory factor and EGF.
| Targets |
Hormone; Endogenous Metabolite
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| ln Vitro |
DHEA (Prasterone) is a potent antiapoptotic agent, correcting 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 activity of DHEA is dose dependent with an EC50 at nanomolar doses (EC50: 11.2±3.6 nM and 12.4±2.2 nM in DU145 and Caco2 cells, respectively)[1] DHEA (Prasterone) is the major sex steroid precursor in humans and can be converted directly to androgens. DHEA (Prasterone) (≥1 μM) produces a dose-dependent suppression of Chub-S7 proliferation, as determined by thymidine incorporation tests. (Prasterone) administration decreases expression of the important glucocorticoid-regulating genes H6PDH (≥100 nM) and HSD11B1 (≥1 μM) in differentiating preadipocytes in a dose-dependent manner. In accord with this discovery, DHEA (Prasterone) treatment (≥1 μM) leads in a considerable reduction in 11β-HSD1 oxoreductase activity (≥1 μM) and a contemporaneous increase in dehydrogenase activity at the highest DHEA dose utilized (25 μM DHEA) in differentiated adipocytes[2].
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| ln Vivo |
When male B6 mice (groups of five mice) were given DHEA (Prasterone) in their diet (0.45% w/w) for eight weeks, their body temperatures significantly decreased as compared to mice given the control AIN-76A diet. Comparing control and pair-fed mice revealed significant differences as well. 26 out of 29 times that the animals were tested, the mice fed DHEA (Prasterone) had significantly lower temperatures than the mice fed the control diet; the mice fed in pairs to the DHEA (Prasterone) group showed less of an impact, with 8 out of 29 values being significantly lower than the mice fed AIN-76A ad libitum. There is a significant difference in the temperatures of mice fed DHEA (Prasterone) or in pairs fed DHEA (Prasterone) across 21 out of 29 tests. Mice fed the control diet had much larger body weights than mice fed DHEA or mice fed in pairs to DHEA (Prasterone). With the exception of Week 9 (n=3), the average daily food intake (grams) from cages is calculated for each week (n=7). When mice are fed DHEA (Prasterone), their food intake is markedly reduced. Mice pairs that were fed DHEA (Prasterone) were intended to eat roughly the same amount. Therefore, it would seem that both a different mechanism and food restriction are how DHEA (Prasterone) lowers body temperature[3].
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| Enzyme Assay |
In addition, we have recently reported that dehydroepiandrosterone (DHEA) can control cell fate, activating nerve growth factor (NGF) receptors, namely tropomyosin-related kinase (Trk)A and p75 neurotrophin receptor, in primary neurons and in PC12 tumoral cells. NGF was recently involved in cancer cell proliferation and apoptosis. In the present study, we explored the cross talk between androgens (testosterone and DHEA) and NGF in regulating apoptosis of prostate and colon cancer cells. DHEA and NGF strongly blunted serum deprivation-induced apoptosis, whereas testosterone induced apoptosis of both cancer cell lines. The antiapoptotic effect of both DHEA and NGF was completely reversed by testosterone. In line with this, DHEA or NGF up-regulated, whereas testosterone down-regulated, the expression of TrkA receptor. The effects of androgens were abolished in both cell lines in the presence of TrkA inhibitor. DHEA induced the phosphorylation of TrkA and the interaction of p75 neurotrophin receptor with its effectors, Rho protein GDP dissociation inhibitor and receptor interacting serine/threonine-protein kinase 2. Conversely, testosterone was unable to activate both receptors. Testosterone acted as a DHEA and NGF antagonist, by blocking the activation of both receptors by DHEA or NGF. Our findings suggest that androgens may influence hormone-sensitive tumor cells via their cross talk with NGF receptors. The interplay between steroid hormone and neurotrophins signaling in hormone-dependent tumors offers new insights in the pathophysiology of these neoplasias[1].
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| Cell Assay |
Glucocorticoids increase adipocyte proliferation and differentiation, a process underpinned by the local reactivation of inactive cortisone to active cortisol within adipocytes catalyzed by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). The adrenal sex steroid precursor dehydroepiandrosterone (DHEA) has been shown to inhibit 11β-HSD1 in murine adipocytes; however, rodent adrenals do not produce DHEA physiologically. Here, we aimed to determine the effects and underlying mechanisms of the potential antiglucocorticoid action of DHEA and its sulfate ester DHEAS in human preadipocytes. Utilizing a human subcutaneous preadipocyte cell line, Chub-S7, we examined the metabolism and effects of DHEA in human adipocytes, including adipocyte proliferation, differentiation, 11β-HSD1 expression, and activity and glucose uptake. DHEA, but not DHEAS, significantly inhibited preadipocyte proliferation via cell cycle arrest in the G1 phase independent of sex steroid and glucocorticoid receptor activation. 11β-HSD1 oxoreductase activity in differentiated adipocytes was inhibited by DHEA. DHEA coincubated with cortisone significantly inhibited preadipocyte differentiation, which was assessed by the expression of markers of early (LPL) and terminal (G3PDH) adipocyte differentiation. Coincubation with cortisol, negating the requirement for 11β-HSD1 oxoreductase activity, diminished the inhibitory effect of DHEA. Further consistent with glucocorticoid-opposing effects of DHEA, insulin-independent glucose uptake was significantly enhanced by DHEA treatment. DHEA increases basal glucose uptake and inhibits human preadipocyte proliferation and differentiation, thereby exerting an antiglucocorticoid action. DHEA inhibition of the amplification of glucocorticoid action mediated by 11β-HSD1 contributes to the inhibitory effect of DHEA on human preadipocyte differentiation[2].
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| Animal Protocol |
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| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Following a 50-mg DHEA PO dose in cynomolgus monkeys, systemic availability was only 3.1 +/- 0.4%. [PMID: 12970301] Metabolism / Metabolites Hepatic. As shown by their high conversion ratios (in a study involving cynomolgus monkeys), the major circulating metabolites of DHEA are DHEA-S, androsterone glucuronide, and androstane-3 alpha,17 beta-diol-glucuronide. [PMID: 12970301] Dehydroisoandrosterone has known human metabolites that include 3,16-Dihydroxyandrost-5-en-17-one, 3,7-Dihydroxy-10,13-dimethyl-1,2,3,4,7,8,9,11,12,14,15,16-dodecahydrocyclopenta[a]phenanthren-17-one, and Dehydroisoandrosterone 3-glucuronide. Biological Half-Life 12 hours |
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| Toxicity/Toxicokinetics |
man TDLo oral 10 mg/kg/2W-I CARDIAC: ARRHYTHMIAS (INCLUDING CHANGES IN CONDUCTION) Annals of Internal Medicine., 129(588), 1998
rat LD50 oral >10 gm/kg British UK Patent Application., #2208473 rat LD50 subcutaneous 1 gm/kg British UK Patent Application., #2208473 mouse LD50 oral >10 gm/kg British UK Patent Application., #2208473 mouse LD50 subcutaneous 900 mg/kg British UK Patent Application., #2208473 |
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| References |
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| Additional Infomation |
Pharmacodynamics
DHEA is naturally produced from cholesterol through two cytochrome P450 enzymes. Cholesterol is converted to pregnenolone by the enzyme P450 scc (side chain cleavage); then another enzyme, CYP17A1, converts pregnenolone to 17α-Hydroxypregnenolone and then to DHEA. DHEA is increased by exercise and calorie restriction. Some theorize that the increase in endogenous DHEA brought about by calorie restriction is partially responsible for the longer life expectancy known to be associated with calorie restriction. |
| Molecular Formula |
C19H28O2
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| Molecular Weight |
288.43
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| Exact Mass |
288.208
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| Elemental Analysis |
C, 79.12; H, 9.79; O, 11.09
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| CAS # |
53-43-0
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| Related CAS # |
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| PubChem CID |
5881
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| Appearance |
White to off-white solid powder
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| Density |
1.1±0.1 g/cm3
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| Boiling Point |
426.7±45.0 °C at 760 mmHg
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| Melting Point |
146-151ºC
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| Flash Point |
182.1±21.3 °C
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| Vapour Pressure |
0.0±2.3 mmHg at 25°C
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| Index of Refraction |
1.560
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| LogP |
3.42
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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 |
0
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| Heavy Atom Count |
21
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| Complexity |
508
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| Defined Atom Stereocenter Count |
6
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| SMILES |
C[C@]12CC[C@H]3[C@H]([C@@H]1CCC2=O)CC=C4[C@@]3(CC[C@@H](C4)O)C
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| InChi Key |
FMGSKLZLMKYGDP-USOAJAOKSA-N
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| InChi Code |
InChI=1S/C19H28O2/c1-18-9-7-13(20)11-12(18)3-4-14-15-5-6-17(21)19(15,2)10-8-16(14)18/h3,13-16,20H,4-11H2,1-2H3/t13-,14-,15-,16-,18-,19-/m0/s1
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| Chemical Name |
(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
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| Synonyms |
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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 |
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| 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) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (8.67 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. Solubility in Formulation 2: ≥ 2.5 mg/mL (8.67 mM) (saturation unknown) in 10% EtOH + 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 25.0 mg/mL clear EtOH 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: ≥ 2.5 mg/mL (8.67 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: ≥ 2.5 mg/mL (8.67 mM) (saturation unknown) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. 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. Solubility in Formulation 5: ≥ 1.25 mg/mL (4.33 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 12.5 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 6: ≥ 1.25 mg/mL (4.33 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 12.5 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. Solubility in Formulation 7: 5 mg/mL (17.34 mM) in Cremophor EL (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.4670 mL | 17.3352 mL | 34.6705 mL | |
| 5 mM | 0.6934 mL | 3.4670 mL | 6.9341 mL | |
| 10 mM | 0.3467 mL | 1.7335 mL | 3.4670 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.
Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1852-7. |
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The effects of DHEA on the lesions induced by NMDA infused into the hippocampus of rats. Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1852-7. |
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