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Details

Stereochemistry ABSOLUTE
Molecular Formula C19H28O2
Molecular Weight 288.4244
Optical Activity UNSPECIFIED
Defined Stereocenters 6 / 6
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of DIHYDROANDROSTENEDIONE

SMILES

[H][C@@]12CCC(=O)[C@@]1(C)CC[C@@]3([H])[C@@]2([H])CC[C@@]4([H])CC(=O)CC[C@]34C

InChI

InChIKey=RAJWOBJTTGJROA-WZNAKSSCSA-N
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/h12,14-16H,3-11H2,1-2H3/t12-,14-,15-,16-,18-,19-/m0/s1

HIDE SMILES / InChI

Molecular Formula C19H28O2
Molecular Weight 288.4244
Charge 0
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 6 / 6
E/Z Centers 0
Optical Activity UNSPECIFIED

Description

Dihydroandrostenedione (Androstanedione) is a steroid metabolite and a precursor of both testosterone and estrone normally produced by the adrenal gland and gonads and is converted to testosterone through the action of 17β-hydroxysteroid dehydrogenase, which is found in most body tissues. Androstenedione is also produced by some plants and has recently been marketed as a product for increasing blood testosterone concentrations to be used as a natural alternative to anabolic steroid use. However, androstenedione administration during resistance training did not significantly alter the serum testosterone concentration in normotestosterogenic young men. The increased muscle size and strength observed with resistance training were also not augmented with androstenedione administration. The use of androstenedione increased the serum concentrations of estradiol and estrone, suggesting an increased aromatization of the ingested androstenedione and/or testosterone derived from the exogenous androstenedione. The use of androstenedione was associated with decreased levels of HDL-C. These data provide evidence that androstenedione does not enhance adaptations to resistance training and may result in potentially serious adverse health consequences in young men.

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency
20.0 nM [IC50]

Conditions

ConditionModalityTargetsHighest PhaseProduct
Diagnostic
Unknown

PubMed

Patents

Sample Use Guides

In Vivo Use Guide
During weeks 1, 2, 4, 5, 7, and 8, the men were randomized to either androstenedione, 300 mg/d (n = 10), or placebo (n = 10).
Route of Administration: Oral
In Vitro Use Guide
Ishikawacells were treated with increasing concentrations of A4 (Androstanedione) (0-1000 pmol) for 4 days. Cell proliferation was measured by the (4,5-dimethylthiaxol-2-yi)-2,5-diphenyltetraxolium bromide (MTT) assay. Apoptosis was analyzed through Annexin-V/propidium iodide (PI) staining and flow cytometry: 17β-hydroxy steroid dehydrogenase type 1 (17β-HSD1) and aromatase mRNA expression was measured by reverse transcription-polymerase chain reaction (RT-PCR). Western blotting was used to detect cell signaling expressions of Akt/MAPK. A4 treatment (1 nM) decreased cell proliferation and increased apoptosis, as demonstrated by MTT and flow cytometry or related gene expression. The cellular responses induced by A4 treatment were mediated by activation of the Akt and MAPK signaling pathway. Treatment had no effect on 17β-HSD1 and aromatase expression.
Substance Class Chemical
Record UNII
2KR72RNR8Z
Record Status Validated (UNII)
Record Version