Endogenous Metabolite
No direct receptor target; DHEA acetate is hydrolyzed to DHEA in vivo. DHEA is then converted to active androgens (testosterone, DHT) via 3β-HSD and 17β-HSD, and to estrogens via aromatase. It also acts as a neurosteroid, modulating GABA-A and NMDA receptors indirectly. Its effects on aggression are thought to be mediated through androgen receptor activation following conversion.

Dehydroepiandrosterone (DHEA) is a testosterone/oestrogen precursor and known modulator of vertebrate aggression. [1]
Dehydroepiandrosterone (DHEA), the most abundant sex steroid, is primarily secreted by the adrenal gland and a precursor hormone used by athletes for performance enhancement. [2]
In vitro, DHEA acetate is used as a substrate for steroidogenic enzymes in cell cultures of adrenocortical, testicular, and ovarian cells. It is converted to DHEA and subsequently to androstenedione, testosterone, and estradiol, which can be measured by ELISA or LC-MS. In neuronal cultures, DHEA acetate (and its metabolites) can enhance neurite outgrowth and protect against excitotoxicity, effects attributed to neurosteroid activity rather than direct receptor binding.

In lab-simulated territorial invasions, dehydroepiandrosterone implants heighten hostility. Higher expression of aromatase mRNA was observed in the preoptic area (POA), periventricular nucleus of the medial striatum (pvMSt), and ventromedial hypothalamus (VMH) of birds whose brains had been implanted with dehydroepiandrosterone. There is more hormone receptor mRNA expression. Aromatase expression in POA and androgen receptor expression in pvMSt are both increased by DHEA, which is in line with previously documented seasonal increases in both markers linked to naturally increasing DHEA levels [1]. In comparison to the SC group, the addition of DHEA (10.2 mg/kg) alone dramatically enhanced the mice's body weight (BW), muscle weight, testosterone levels, and muscle and liver glycogen content [2].
In vivo, DHEA acetate acts as a prohormone, raising circulating DHEA and its downstream steroid levels upon oral or intraperitoneal administration. In rodent studies, it has been shown to modulate aggressive behavior, with effects dependent on dose and sex. It also influences immune function, bone density, and cognitive performance in aging models, though results are sometimes contradictory. It is not used therapeutically in this ester form.

Cell-free assays for steroidogenic enzyme activity: incubate DHEA acetate with recombinant or microsomal preparations of 3β-HSD, aromatase, or 17β-HSD, and measure product formation (androstenedione, testosterone, estradiol) by RIA or LC-MS. For receptor binding, use radiolabeled DHEA or its metabolites to study displacement at androgen or estrogen receptors, though DHEA acetate itself has low direct affinity.

Cells expressing steroidogenic enzymes (e.g., H295R adrenocortical cells) are treated with DHEA acetate (0.1–100 µM) for 24–72 h. Steroid concentrations in media are measured by ELISA. For neuroprotection, neuronal cells (e.g., PC12) are exposed to DHEA acetate prior to glutamate or oxidative stress; cell viability is measured by MTT or LDH. Neurite outgrowth is quantified by image analysis.

In the present study, nonbreeding male song sparrows were captured and held in the laboratory under short days (8 : 16 h light/dark cycle) and implanted with s.c. DHEA-filled or empty (control) implants for 14 days. DHEA implants increased aggression in a laboratory-based simulated territorial intrusion. Brains of DHEA-implanted birds showed higher aromatase mRNA expression in the preoptic area (POA) and higher androgen receptor mRNA expression in the periventricular nucleus of the medial striatum (pvMSt) and ventromedial nucleus of the hypothalamus. The DHEA-induced increases in aromatase expression in the POA and androgen receptor expression in the pvMSt are consistent with previously reported seasonal increases in these markers associated with naturally elevated DHEA levels. This suggests that DHEA facilitates seasonal increases in aggression in nonbreeding male song sparrows by up-regulating steroid signalling/synthesis machinery in a brain region-specific fashion. [1]

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The objective of the study is to investigate the effects of DHEA supplementation combined with WBV training on body composition, exercise performance, and physical fatigue-related biochemical responses and testosterone content in young-adult C57BL/6 mice. In this study, male C57BL/6 mice were divided into four groups (n = 8 per group) for 6-weeks treatment: sedentary controls with vehicle (SC), DHEA supplementation (DHEA, 10.2 mg/kg), WBV training (WBV; 5.6 Hz, 2 mm, 0.13 g), and WBV training with DHEA supplementation (WBV+DHEA; WBV: 5.6 Hz, 2 mm, 0.13 g and DHEA: 10.2 mg/kg). Exercise performance was evaluated by forelimb grip strength and exhaustive swimming time, as well as changes in body composition and anti-fatigue levels of serum lactate, ammonia, glucose, creatine kinase (CK), and blood urea nitrogen (BUN) after a 15-min swimming exercise. In addition, the biochemical parameters and the testosterone content were measured at the end of the experiment. Six-week DHEA supplementation alone significantly increased mice body weight (BW), muscle weight, testosterone level, and glycogen contents (liver and muscle) when compared with SC group. DHEA supplementation alone had no negative impact on all tissue and biochemical profiles, but could not improve exercise performance. However, WBV+DHEA supplementation also significantly decreased BW, testosterone level and glycogen content of liver, as well as serum lactate and ammonia levels after the 15-min swimming exercise when compared with DHEA supplementation alone. Although DHEA supplementation alone had no beneficial effect in the exercise performance of mice, the BW, testosterone level and glycogen content significantly increased. On the other hand, WBV training combined with DHEA decreased the BW gain, testosterone level and glycogen content caused by DHEA supplementation. Therefore, WBV training could inhibit DHEA supplementation to synthesis the testosterone level or may decrease the DHEA supplement absorptive capacity in young-adult mice. [2]
In vivo, DHEA acetate is administered orally (10–100 mg/kg) or intraperitoneally (1–10 mg/kg) to rodents. Blood samples are collected at various time points to measure steroid hormone levels by RIA. Behavioral tests (resident-intruder, open field, forced swim) assess aggression, anxiety, or depression-like behavior. Bone density is measured by DEXA, and cognition by Morris water maze. Tissue steroid levels can be measured by LC-MS.

Molecular formula C21H30O3, MW 330.46. Appearance: white to off-white crystalline powder. Solubility: soluble in DMSO, ethanol, chloroform; practically insoluble in water. Melting point ~170-172°C. Store at room temperature in a dry, dark place. Purity ≥98%. For injection, dissolve in vegetable oil or cyclodextrin-based vehicles. Stable under normal storage; protect from light and moisture.

No specific toxicity data available for DHEA acetate, but DHEA is generally well-tolerated at physiological doses. High doses may cause hormonal side effects including acne, hirsutism, and menstrual irregularities. Androgenic effects may occur in women. Long-term safety of high-dose DHEA supplementation is not established. It is not FDA-approved for any indication.

[1]. Dehydroepiandrosterone (DHEA) heightens aggression and increases androgen receptor and aromatase mRNA expression in the brain of a male songbird. J Neuroendocrinol. 2016 Nov 2.

[2]. Dehydroepiandrosterone Supplementation Combined with Whole-Body Vibration Training Affects Testosterone Level and Body Composition in Mice. Int J Med Sci. 2016 Sep 16;13(10):730-740.

Prasterone acetate is a steroid ester. Dehydroepiandrosterone (DHEA) is a precursor of testosterone/estrogen and a known regulator of aggression in vertebrates. Male songbirds (Melospiza melodia morphna) exhibit higher aggression during the breeding and non-breeding seasons, when circulating DHEA levels are higher; while during molting, DHEA levels are lower and aggression is lower. We have previously demonstrated that the expression of androgen receptor and aromatase mRNA is higher in brain regions associated with reproductive and aggressive behavior during both the breeding and/or non-breeding seasons, but the potential role of DHEA in mediating these seasonal variations remains unclear. [1] Dehydroepiandrosterone (DHEA) is the most abundant sex steroid, primarily secreted by the adrenal glands, and is a precursor hormone used by athletes to enhance athletic performance. Whole-body vibration (WBV) is a well-known low-resistance exercise that allows the body to automatically adapt to the rapid, repetitive vibrations of a vibration platform, making it a simple and convenient exercise for older adults. However, the potential effects of combining DHEA supplementation with WBV training on body composition, athletic performance, and hormone regulation remain unclear. [2]
DHEA acetate is a research chemical used primarily as a synthetic intermediate for steroidal pharmaceuticals. It is also used in studies of endocrine function, aging, and behavior. It is not intended for human supplementation. In many countries, DHEA is regulated as a dietary supplement, but the acetate form is not commonly used. No clinical trials have been conducted with this specific ester.

C₂₁H₃₀O₃

330.46

330.219

853-23-6

14709

White to off-white solid powder

1.1±0.1 g/cm3

434.8±45.0 °C at 760 mmHg

168-170ºC

188.1±28.8 °C

0.0±1.0 mmHg at 25°C

1.541

4.28

0

3

2

24

606

6

CC(=O)O[C@H]1CC[C@@]2([C@H]3CC[C@]4([C@H]([C@@H]3CC=C2C1)CCC4=O)C)C

NCMZQTLCXHGLOK-ZKHIMWLXSA-N

InChI=1S/C21H30O3/c1-13(22)24-15-8-10-20(2)14(12-15)4-5-16-17-6-7-19(23)21(17,3)11-9-18(16)20/h4,15-18H,5-12H2,1-3H3/t15-,16-,17-,18-,20-,21-/m0/s1

[(3S,8R,9S,10R,13S,14S)-10,13-dimethyl-17-oxo-1,2,3,4,7,8,9,11,12,14,15,16-dodecahydrocyclopenta[a]phenanthren-3-yl] acetate

DHEA acetate; Dehydroepiandrosterone acetate; 853-23-6; Dehydroisoandrosterone 3-acetate; Prasterone acetate; Dehydroisoandrosterone acetate; Dehydroepiandrosterone 3-acetate; trans-Dehydroandrosterone acetate; Androst-5-en-17-one, 3-(acetyloxy)-, (3b)-; Dehydroepiandrosterone 3-acetate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~14.29 mg/mL (~43.24 mM)
H2O : < 0.1 mg/mL

Solubility in Formulation 1: ≥ 1.43 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 14.3 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.

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Solubility in Formulation 2: ≥ 1.43 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 14.3 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.

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Solubility in Formulation 3: ≥ 1.43 mg/mL (4.33 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 14.3 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)