Dehydroepiandrosterone sulfate sodium
Based on 4 publication(s) in Google Scholar
Dehydroepiandrosterone sulfate (DHEA sulfate; Prasterone sulfate) sodium salt is a neurosteroid and the main secretion product of the adrenal gland. Dehydroepiandrosterone sulfate sodium salt has both non-competitive antagonist activity of GABAA receptor and agonist activity of σ1 receptor. Dehydroepiandrosterone sulfate sodium salt can partially penetrate the blood-brain barrier, inhibit GABAA receptor-mediated chloride influx, enhance NMDA receptor activity through σ1 receptors, exert anti-inflammatory, anti-glucocorticoid and antidepressant effects, and increase convulsive sensitivity. Dehydroepiandrosterone sulfate sodium salt participates in neuroprotection, neurite growth regulation and catecholamine secretion regulation, and can be used in the study of depression, post-traumatic stress disorder (PTSD), Alzheimer's disease, etc. Dehydroepiandrosterone sulfate sodium salt may also be a biomarker for cardiovascular disease mortality, and its concentration is independently and negatively correlated with mortality.
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- Purity : 99.96%
- CAS No.: 1099-87-2
- 화학식: C19H27NaO5S
- 분자량:390.47
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보관:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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Biological Activity
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Chemical Information
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용액&용해도
- Protocol
- 순도&문서
- References
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Publications Citing Use of MedChemExpress (MCE) Dehydroepiandrosterone sulfate sodium
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Cell Proliferation/Viability Assay
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Cell Proliferation/Viability Assay
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IF
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Cell Migration/Invasion Assay
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Bio/Physico-chemical Assay
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Biological Activity
제품 설명
IC50 & Target
[1]|
Human Endogenous Metabolite |
PPARα |
Sigma 1 Receptor |
In Vitro
Dehydroepiandrosterone sulfate sodium salt (0.1 nM-10 μM; 2-24 h) increases neuronal survival in embryonic rat cortical cell hypoxia assay, with significant effects at 10 μM[1].
Dehydroepiandrosterone sulfate sodium salt (0.1-10 μM) protects neurons in rat cerebellar granule cell oxygen-glucose deprivation assay in a dose-dependent manner, with almost complete protection at 10 μM[1].
Dehydroepiandrosterone sulfate sodium salt (DHEAS) (1 μM-1 mM; 48 h) inhibits TNF-α-induced VCAM-1, IL-8, and ICAM-1 expression in human aortic endothelial cell inflammation assay, and inhibits NF-κB activity via activation of PPARα[5].
Dehydroepiandrosterone sulfate sodium salt (DHEAS) (10-7-10-5 M; 96 h) inhibits LIF-induced proliferation of juvenile bovine chromaffin cells and enhances EGF-induced proliferation of adult bovine chromaffin cells in a proliferation assay[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Human aortic endothelial cells (HAECs)
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Concentration:0.1 μM-1 mM
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Incubation Time:48 hours
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Result:Had no significant effect on cell viability, as over 95% of cells remained viable across all concentrations tested, comparable to vehicle control.
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Cell Line:Human aortic endothelial cells (HAECs)
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Concentration:1 mM
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Incubation Time:48 hours (pretreatment) + 4 hours (TNF-α stimulation)
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Result:Significantly reduced TNF-α-induced IL-8 and ICAM-1 mRNA expression by 5-fold and 2-fold, respectively, compared to TNF-α alone.
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Cell Line:Human aortic endothelial cells (HAECs)
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Concentration:1-1000 μM
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Incubation Time:48 hours
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Result:Increased IκB-α protein levels in a dose-dependent manner, with maximal induction at 1000 μM, correlating with NF-κB inhibition.
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Cell Line:Juvenile/adult bovine chromaffin cells
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Concentration:10-7-10-5 M
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Incubation Time:96 hours
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Result:Did not affect basal proliferation but inhibited LIF-induced proliferation by 30% at 10-5 M.
In adult cells, enhanced EGF-induced proliferation by 25% at 10-5 M, without effect at lower concentrations.
In Vivo
Dehydroepiandrosterone sulfate (DHEAS) (converted from 2 mg/kg Dehydroepiandrosterone intraperitoneally; once daily; 13 days) can shorten the immobility time in the forced swim test in the male FSL rat model of depression, but when used in combination with electroconvulsive shock (ECS), it offsets the antidepressant effect of ECS[8].
Dehydroepiandrosterone sulfate (DHEAS) (10 mg/kg; subcutaneous injection; once daily; 4 weeks) sodium salt enhances the seizure sensitivity of Laka mice in the pentylenetetrazol-induced seizure model, as shown by a decrease in the half effective dose of seizure (ED50 from 67.6 mg/kg to 48.6 mg/kg) and a shortens seizure latency, an effect that is reversed by Progesterone (HY-N0437) or Dizocilpine (HY-15084B)[9].
Chronic treatment with Dehydroepiandrosterone sulfate sodium salt for 4 weeks significantly reduces the body weight of mice in the pentylenetetrazol-induced seizure model[9].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Albino Guinea Pig Noise-Induced Cochlear Injury Model (250-350 g): 2 kHz pure tone (120-125 dB SPL for 10 min) induced cochlear injury[7]
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Dosage:1 mg/kg Dehydroepiandrosterone sulfate
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Administration:Intravenous injection, single dose immediately before acoustic overexposure
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Result:Significantly improved cochlear function 1 week after acoustic exposure, reducing CAP threshold shifts and increasing DPOAE amplitude compared to control groups. The protective effect was observed at 1 mg/kg but not at 0.1 mg/kg, with no significant effect immediately after exposure.
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Animal Model:Flinder Sensitive Line (FSL) Rat Model of Depression (male, 200-220 g, 6-8 weeks old): forced swim test (FST) assay[8]
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Dosage:2 mg/kg Dehydroepiandrosterone (converted to Dehydroepiandrosterone sulfate)
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Administration:Intraperitoneal injection, daily for 13 days
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Result:Chronic Dehydroepiandrosterone administration (converted to Dehydroepiandrosterone sulfate) alone reduced immobility time in FST, mimicking antidepressant effects. However, combined treatment with electroconvulsive shock (ECS) abolished this effect, with immobility time significantly increased compared to DHEA or ECS alone, indicating DHEAS may antagonize ECS efficacy.
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Animal Model:Mouse Pentylenetetrazol-Induced Seizure Model (20-25 g): Pentylenetetrazol-induced tonic convulsions[9]
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Dosage:10 mg/kg Dehydroepiandrosterone sulfate
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Administration:Subcutaneous injection, daily for 4 weeks
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Result:Chronic treatment shifted pentylenetetrazol dose-response curves leftward, reducing ED50 for convulsions and shortening latency to seizure onset, indicating enhanced seizure sensitivity. This proconvulsant effect was prevented by co-treatment with progesterone or dizocilpine, linking it to GABAA receptor antagonism and NMDA receptor activation.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
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| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 1099-87-2
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Appearance Solid
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분자량 390.47
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화학식 C19H27NaO5S
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Color White to off-white
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SMILES
C[C@]1([C@](CC2)([H])[C@]3([H])CC=C4C[C@@H](OS(=O)(O[Na])=O)CC[C@]4(C)[C@@]3([H])CC1)C2=O
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Synonyms
DHEA sulfate sodium; Prasterone sulfate sodium
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Structure Classification
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Initial Source
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선적
Room temperature in continental US; may vary elsewhere.
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보관
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications (4)
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Journal Impact Factor
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Most Recent
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Cell Metab
Sensing steroid hormone 17α-hydroxypregnenolone by GPR56 enables protection from ferroptosis-induced liver injury. [Abstract]2024 Nov 5;36(11):2402-2418.e10. PMID: 39389061 -
Nat Chem Biol
2022 Nov;18(11):1196-1203. PMID: 35982227 -
Eur J Pharmacol
18β-Glycyrrhetinic acid synergizes with enzalutamide to counteract castration-resistant prostate cancer by inhibiting OATP2B1 uptake of dehydroepiandrosterone sulfate. [Abstract]2024 Nov 15:983:176995. PMID: 39277096
Dehydroepiandrosterone sulfate sodium purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2024 Nov 15:983:176995. [Abstract]
CCK8 assay was conducted to determine the viability of LNCap and 22RV1 cells treated with Dehydroepiandrosterone sulfate (DHEAS) (0, 2.5, 5, and 10 μM) for 48 h in a normal cultivation environment and an androgen-deprived environment. The results showed that DHEAS had no significant effect on cell proliferation in the FBS group.
Dehydroepiandrosterone sulfate sodium purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2024 Nov 15:983:176995. [Abstract]
A CCK8 assay was conducted to determine the viability of LNCap and 22RV1 cells treated with Dehydroepiandrosterone sulfate (DHEAS, 2.5-10 μM) for 2, 4, and 6 days in an androgen-deprived environment. DHEAS promoted the proliferation of LNCap and 22RV1 cells in the androgen deprivation environment. When treated with 10 μM DHEAS, the proliferation rate of LNCap and 22RV1 cells was higher than that recorded in the blank control group. The proliferation rate of LNCap and 22RV1 cells increased by 21.8% and 20.8%, respectively, on day 6.
Dehydroepiandrosterone sulfate sodium purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2024 Nov 15:983:176995. [Abstract]
Immunofluorescence was used to demonstrate the co-localization of androgen receptor (AR) in 22RV1 cells treated with 18β-GA (40 μM) and ENZ (40 μM) for 24 h after Dehydroepiandrosterone sulfate (DHEAS, 10 μM) stimulation.
Dehydroepiandrosterone sulfate sodium purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2024 Nov 15:983:176995. [Abstract]
Transwell migration assay was performed to assess the migration ability of 22RV1 cells, and the cells were treated with 18β-GA (40 μM) and ENZ (40 μM) for 48 h. The results of the Transwell migration experiments suggested that Dehydroepiandrosterone sulfate (DHEAS, 10 μM; 48 h) increased the migration of 22RV1 cells compared to the rate of cell migration recorded in the control group, but the combined treatment using 18β-GA and ENZ significantly inhibited cell mobility.
Dehydroepiandrosterone sulfate sodium purchased from MedChemExpress. Usage Cited in: Eur J Pharmacol. 2024 Nov 15:983:176995. [Abstract]
The effects of 24 components found in traditional Chinese medicine (10 and 100 μM) on the uptake of Dehydroepiandrosterone sulfate (DHEAS, 10 μM) for 10 min were assessed in OATP2B1-HEK293 cells.
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용액&용해도
In Vitro:
DMSO : 100 mg/mL (256.10 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : 10 mg/mL (25.61 mM; Need ultrasonic)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.08 mg/mL (5.33 mM); Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.08 mg/mL (5.33 mM); Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocol
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
순도&문서
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Data Sheet (289 KB)
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Handling Instructions (2659 KB)
References
[1]. Baulieu EE, et al. Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging: contribution of the DHEAge Study to a sociobiomedical issue. Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4279-84. [Content Brief]
[2]. Maninger N, et al. Neurobiological and neuropsychiatric effects of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS). Front Neuroendocrinol. 2009 Jan;30(1):65-91. [Content Brief]
[3]. Dillon JS. Dehydroepiandrosterone, dehydroepiandrosterone sulfate and related steroids: their role in inflammatory, allergic and immunological disorders. Curr Drug Targets Inflamm Allergy. 2005 Jun;4(3):377-85. [Content Brief]
[4]. Barrett-Connor E, et al. A prospective study of dehydroepiandrosterone sulfate, mortality, and cardiovascular disease. N Engl J Med. 1986 Dec 11;315(24):1519-24. [Content Brief]
[5]. Altman R, et al. Inhibition of vascular inflammation by dehydroepiandrosterone sulfate in human aortic endothelial cells: roles of PPARalpha and NF-kappaB. Vascul Pharmacol. 2008 Feb-Mar;48(2-3):76-84. [Content Brief]
[6]. Sicard F, et al. Age-dependent regulation of chromaffin cell proliferation by growth factors, dehydroepiandrosterone (DHEA), and DHEA sulfate. Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):2007-12. [Content Brief]
[7]. Tabuchi K, et al. Dehydroepiandrosterone sulfate reduces acoustic injury of the guinea-pig cochlea. J Pharmacol Sci. 2005 Oct;99(2):191-4. [Content Brief]
[8]. Maayan R, et al. The involvement of dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) in blocking the therapeutic effect of electroconvulsive shocks in an animal model of depression. Eur Neuropsychopharmacol. 2005 May;15(3):253-62. [Content Brief]
[9]. Reddy DS, et al. Proconvulsant effects of neurosteroids pregnenolone sulfate and dehydroepiandrosterone sulfate in mice. Eur J Pharmacol. 1998 Mar 12;345(1):55-9. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| H2O / DMSO | 1 mM | 2.5610 mL | 12.8051 mL | 25.6102 mL | 64.0254 mL |
| 5 mM | 0.5122 mL | 2.5610 mL | 5.1220 mL | 12.8051 mL | |
| 10 mM | 0.2561 mL | 1.2805 mL | 2.5610 mL | 6.4025 mL | |
| 15 mM | 0.1707 mL | 0.8537 mL | 1.7073 mL | 4.2684 mL | |
| 20 mM | 0.1281 mL | 0.6403 mL | 1.2805 mL | 3.2013 mL | |
| 25 mM | 0.1024 mL | 0.5122 mL | 1.0244 mL | 2.5610 mL | |
| DMSO | 30 mM | 0.0854 mL | 0.4268 mL | 0.8537 mL | 2.1342 mL |
| 40 mM | 0.0640 mL | 0.3201 mL | 0.6403 mL | 1.6006 mL | |
| 50 mM | 0.0512 mL | 0.2561 mL | 0.5122 mL | 1.2805 mL | |
| 60 mM | 0.0427 mL | 0.2134 mL | 0.4268 mL | 1.0671 mL | |
| 80 mM | 0.0320 mL | 0.1601 mL | 0.3201 mL | 0.8003 mL | |
| 100 mM | 0.0256 mL | 0.1281 mL | 0.2561 mL | 0.6403 mL |
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Dehydroepiandrosterone sulfate sodium Related Classifications
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