Testosterone (CHEM003243)

IdentificationTaxonomyBiological PropertiesPhysical PropertiesToxicity ProfileSpectraConcentrationsLinksReferencesTargets (10)XML
Record Information
Version1.0
Creation Date2014-08-29 06:14:17 UTC
Update Date2026-04-17 17:50:25 UTC
Accession NumberCHEM003243
Identification
Common NameTestosterone
ClassSmall Molecule
DescriptionTestosterone is the most important androgen in potency and quantity•_Оa steroid sex hormone found in both men and women. Testosterone is synthesized and released by the Leydig cells that lie between the tubules and comprise less than 5% of the total testicular volume. testosterone diffuses into the seminiferous tubules where it is essential for maintaining spermatogenesis. Some binds to an androgen-binding protein (ABP) that is produced by the Sertoli cells and is homologous to the sex-hormone binding globulin that transports testosterone in the general circulation. The ABP carries testosterone in the testicular fluid where it maintains the activity of the accessory sex glands and may also help to retain testosterone within the tubule and bind excess free hormone. Some testosterone is converted to estradiol by Sertoli cell-derived aromatase enzyme. Leydig cell steroidogenesis is controlled primarily by luteinizing hormone with negative feedback of testosterone on the hypothalamic-pituitary axis. The requirement of spermatogenesis for high local concentrations of testosterone means that loss of androgen production is likely to be accompanied by loss of spermatogenesis. Indeed, if testicular androgen production is inhibited by the administration of exogenous androgens then spermatogenesis ceases. This is the basis of using exogenous testosterone as a male contraceptive. testosterone is converted to dihydrotestosterone by 5a-reductase type 2 (EC 1.3.1.22, SRD5A2), the androgen with the highest affinity for the androgen receptor. SRD5A2 deficiency illustrates the importance of dihydrotestosterone for external virilization, as individuals with this condition have normal male internal structures but their external genitalia are of female appearance. There is now clear evidence that the human fetal testis and also the fetal adrenal gland is capable of testosterone biosynthesis during the first trimester. Regardless of the source of androgen production, the target tissue responds by male sexual differentiation of the external genitalia by the end of the first trimester. It is clear that testicular damage may result in loss of testosterone production or the loss of spermatogenesis or both. Loss of androgen production results in hypogonadism, the symptoms of which reflect the functions of testosterone. Male hypogonadism is defined as failure of the testes to produce normal amounts of testosterone, combined with signs and symptoms of androgen deficiency. Systemic testosterone levels fall by about 1% each year in men. Therefore, with increasing longevity and the aging of the population, the number of older men with testosterone deficiency will increase substantially over the next several decades. Serum testosterone levels decrease progressively in aging men, but the rate and magnitude of decrease vary considerably. Approximately 1% of healthy young men have total serum testosterone levels below normal; in contrast, approximately 20% of healthy men over age 60 years have serum testosterone levels below normal. (1, 2). In men, testosterone is produced primarily by the Leydig (interstitial) cells of the testes when stimulated by luteinizing hormone (LH). It functions to stimulate spermatogenesis, promote physical and functional maturation of spermatozoa, maintain accessory organs of the male reproductive tract, support development of secondary sexual characteristics, stimulate growth and metabolism throughout the body and influence brain development by stimulating sexual behaviors and sexual drive. In women, testosterone is produced by the ovaries (25%), adrenals (25%) and via peripheral conversion from androstenedione (50%). Testerone in women functions to maintain libido and general wellbeing. Testosterone exerts a negative feedback mechanism on pituitary release of LH and follicle-stimulating hormone (FSH). Testosterone may be further converted to dihydrotestosterone or estradiol depending on the tissue
Contaminant Sources
  • FooDB Chemicals
  • HMDB Contaminants - Urine
  • STOFF IDENT Compounds
  • T3DB toxins
  • ToxCast & Tox21 Chemicals
Contaminant Type
  • Androgen
  • Animal Toxin
  • Drug
  • Ester
  • Food Toxin
  • Metabolite
  • Natural Compound
  • Organic Compound
Chemical Structure
Thumb
MOLSDFPDBSMILESInChI
Synonyms
ValueSource
17beta-Hydroxy-4-androsten-3-oneChEBI
4-Androsten-17beta-ol-3-oneChEBI
AndrodermChEBI
TestosteronChEBI
TestosteronaChEBI
TestosteronumChEBI
AndrogelKegg
AxironKegg
StriantKegg
TestimKegg
17b-Hydroxy-4-androsten-3-oneGenerator
17Β-hydroxy-4-androsten-3-oneGenerator
4-Androsten-17b-ol-3-oneGenerator
4-Androsten-17β-ol-3-oneGenerator
(+)-TestosteroneHMDB
(+-)-8-Iso-testosteroneHMDB
(+-)-RetrotestosteroneHMDB
(+-)-TestosteroneHMDB
(17b)-17-Hydroxy-androst-4-en-3-oneHMDB
13-Iso-testosteroneHMDB
17-Hydroxy-10,13-dimethyl-1,2,6,7,8,9,10,11,12,13,14,15,16,17-tetradecahydro-cyclopenta[a]phenanthren-3-oneHMDB
17-Hydroxy-androst-4-en-3-oneHMDB
17-Hydroxy-D4-androsten-3-oneHMDB
17a-Hydroxy-(13a)-androst-4-en-3-oneHMDB
17a-Hydroxy-13a-androst-4-en-3-oneHMDB
17a-Hydroxy-14b-androst-4-en-3-oneHMDB
17a-Hydroxy-androst-4-en-3-oneHMDB
17b-Hydroxy-(10a)-androst-4-en-3-oneHMDB
17b-Hydroxy-(13a)-androst-4-en-3-oneHMDB
17b-Hydroxy-(8a)-androst-4-en-3-oneHMDB
17b-Hydroxy-(8a,10a)-androst-4-en-3-oneHMDB
17b-Hydroxy-(9b)-androst-4-en-3-oneHMDB
17b-Hydroxy-(9b,10a)-androst-4-en-3-oneHMDB
17b-Hydroxy-13a-androst-4-en-3-oneHMDB
17b-Hydroxy-8a-androst-4-en-3-oneHMDB
17b-Hydroxy-androst-4-en-3-ONHMDB
17b-Hydroxy-androst-4-en-3-oneHMDB
17b-Hydroxy-D4-androsten-3-oneHMDB
17b-Hydroxyandrost-4-en-3-oneHMDB
17b-Hydroxyandrost-4-ene-3-oneHMDB
17b-TestosteroneHMDB
4-Androsten-3-one-17b-olHMDB
8-Iso-testosteroneHMDB
9b,10a-TestosteroneHMDB
9b-TestosteroneHMDB
AndrolinHMDB
AndronaqHMDB
AndropatchHMDB
Androst-4-en-17b-ol-3-oneHMDB
Androst-4-ene-17b-ol-3-oneHMDB
AndrusolHMDB
Cristerona THMDB
D4-Androsten-17b-ol-3-oneHMDB
EpitestosteronHMDB
Geno-cristaux gremyHMDB
HomosteronHMDB
HomosteroneHMDB
LumitestosteronHMDB
MertestateHMDB
NeotestisHMDB
OretonHMDB
OrquisteronHMDB
PerandrenHMDB
Percutacrine androgeniqueHMDB
PrimotestHMDB
PrimotestonHMDB
rac-17b-Hydroxy-(13a)androst-4-en-3-oneHMDB
rac-17b-Hydroxy-(8a)-androst-4-en-3-oneHMDB
rac-17b-Hydroxy-(9b,10a)androst-4-en-3-oneHMDB
rac-17b-Hydroxy-androst-4-en-3-oneHMDB
RelibraHMDB
RetrotestosteroneHMDB
SustanonHMDB
SustanoneHMDB
Sustason 250HMDB
Synandrol FHMDB
TeslenHMDB
TestandroneHMDB
TesticulosteroneHMDB
TestobaseHMDB
TestodermHMDB
TestogelHMDB
TestolentHMDB
TestolinHMDB
TestoproponHMDB
TestosteroidHMDB
Testoviron scheringHMDB
Testoviron THMDB
Testro aqHMDB
TestroneHMDB
TestrylHMDB
TostrelleHMDB
TostrexHMDB
ViatrelHMDB
VirormoneHMDB
VirosteroneHMDB
AndrotopHMDB
CEPA brand OF testosteroneHMDB
HisteroneHMDB
SmithKline beecham brand OF testosteroneHMDB
Solvay brand OF testosteroneHMDB
SterotateHMDB
17-beta-Hydroxy-8 alpha-4-androsten-3-oneHMDB
AstraZeneca brand OF testosteroneHMDB
Bartor brand OF testosteroneHMDB
Dr. kade brand OF testosteroneHMDB
Ferring brand OF testosteroneHMDB
Hauck brand OF testosteroneHMDB
Pasadena brand OF testosteroneHMDB
Testosterone sulfateHMDB
Ulmer brand OF testosteroneHMDB
Unimed brand OF testosteroneHMDB
Watson brand OF testosteroneHMDB
17-beta-Hydroxy-4-androsten-3-oneHMDB
8 IsotestosteroneHMDB
8-IsotestosteroneHMDB
Auxilium pharmaceuticals inc. brand OF testosteroneHMDB
Faulding brand OF testosteroneHMDB
Paladin brand OF testosteroneHMDB
Schering brand OF testosteroneHMDB
17 beta Hydroxy 4 androsten 3 oneHMDB
17 beta Hydroxy 8 alpha 4 androsten 3 oneHMDB
GlaxoSmithKline brand OF testosteroneHMDB
Ortho brand OF testosteroneHMDB
TestopelHMDB
Chemical FormulaC19H28O2
Average Molecular Mass288.424 g/mol
Monoisotopic Mass288.209 g/mol
CAS Registry Number58-22-0
IUPAC Name(1S,2R,10R,11S,14S,15S)-14-hydroxy-2,15-dimethyltetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadec-6-en-5-one
Traditional Name(1S,2R,10R,11S,14S,15S)-14-hydroxy-2,15-dimethyltetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadec-6-en-5-one
SMILES[H][C@@]12CC[C@H](O)[C@@]1(C)CC[C@@]1([H])[C@@]2([H])CCC2=CC(=O)CC[C@]12C
InChI IdentifierInChI=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/h11,14-17,21H,3-10H2,1-2H3/t14-,15-,16-,17-,18-,19-/m0/s1
InChI KeyMUMGGOZAMZWBJJ-DYKIIFRCSA-N
Chemical Taxonomy
Description belongs to the class of organic compounds known as androgens and derivatives. These are 3-hydroxylated C19 steroid hormones. They are known to favor the development of masculine characteristics. They also show profound effects on scalp and body hair in humans.
KingdomOrganic compounds
Super ClassLipids and lipid-like molecules
ClassSteroids and steroid derivatives
Sub ClassAndrostane steroids
Direct ParentAndrogens and derivatives
Alternative Parents
Substituents
  • Androgen-skeleton
  • 3-oxo-delta-4-steroid
  • 3-oxosteroid
  • Hydroxysteroid
  • Oxosteroid
  • 17-hydroxysteroid
  • Delta-4-steroid
  • Cyclohexenone
  • Cyclic alcohol
  • Secondary alcohol
  • Ketone
  • Cyclic ketone
  • Organooxygen compound
  • Alcohol
  • Carbonyl group
  • Organic oxygen compound
  • Hydrocarbon derivative
  • Organic oxide
  • Aliphatic homopolycyclic compound
Molecular FrameworkAliphatic homopolycyclic compounds
External Descriptors
Biological Properties
StatusDetected and Not Quantified
OriginEndogenous
Cellular Locations
  • Cytoplasm
  • Endoplasmic reticulum
  • Extracellular
  • Membrane
Biofluid LocationsNot Available
Tissue Locations
  • Brain
  • Gonads
  • Hypothalamus
  • Muscle
  • Sperm
  • Testes
Pathways
NameSMPDB LinkKEGG Link
Androgen and Estrogen MetabolismSMP00068 map00150
Adrenal Hyperplasia Type 3 or Congenital Adrenal Hyperplasia due to 21-hydroxylase DeficiencySMP00373 Not Available
Aromatase deficiencySMP00565 Not Available
ApplicationsNot Available
Biological Roles
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite powder.
Experimental Properties
PropertyValue
Melting Point155°C
Boiling PointNot Available
Solubility23.4 mg/L (at 25°C)
Predicted Properties
PropertyValueSource
Water Solubility0.033 g/LALOGPS
logP2.99ALOGPS
logP3.37ChemAxon
logS-3.9ALOGPS
pKa (Strongest Acidic)19.09ChemAxon
pKa (Strongest Basic)-0.88ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count2ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area37.3 ŲChemAxon
Rotatable Bond Count0ChemAxon
Refractivity84.43 m³·mol⁻¹ChemAxon
Polarizability33.88 ųChemAxon
Number of Rings4ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleNoChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash KeyView
GC-MSGC-MS Spectrum - GC-MS (1 TMS)splash10-004i-3910000000-d6ace9b7f8aff4dd46d0Spectrum
GC-MSGC-MS Spectrum - GC-MS (2 TMS)splash10-053u-1920200000-db3504f562c54e6e1bbbSpectrum
GC-MSGC-MS Spectrum - GC-MS (1 MEOX; 1 TMS)splash10-004l-3910000000-b43cd1ee268a855c8aa0Spectrum
GC-MSGC-MS Spectrum - GC-MS (1 MEOX; 1 TMS)splash10-004l-3910000000-356ddfa8ddf8e551278dSpectrum
GC-MSGC-MS Spectrum - EI-B (Non-derivatized)splash10-0597-7920000000-dde7fba02fcbcec2d665Spectrum
GC-MSGC-MS Spectrum - EI-B (Non-derivatized)splash10-05fs-4920000000-ccd839134de79f179f9eSpectrum
GC-MSGC-MS Spectrum - EI-B (Non-derivatized)splash10-00ds-0950000000-c65fc8043083ad93d169Spectrum
GC-MSGC-MS Spectrum - GC-MS (Non-derivatized)splash10-004i-3910000000-d6ace9b7f8aff4dd46d0Spectrum
GC-MSGC-MS Spectrum - GC-MS (Non-derivatized)splash10-053u-1920200000-db3504f562c54e6e1bbbSpectrum
GC-MSGC-MS Spectrum - GC-MS (Non-derivatized)splash10-004l-3910000000-b43cd1ee268a855c8aa0Spectrum
GC-MSGC-MS Spectrum - GC-MS (Non-derivatized)splash10-004l-3910000000-356ddfa8ddf8e551278dSpectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, Positivesplash10-074i-0390000000-09e2a725ebd92c93dc88Spectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (1 TMS) - 70eV, Positivesplash10-001j-3349000000-75c3f3e0341bb42eb819Spectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, PositiveNot AvailableSpectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (TMS_1_2) - 70eV, PositiveNot AvailableSpectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (TBDMS_1_1) - 70eV, PositiveNot AvailableSpectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (TBDMS_1_2) - 70eV, PositiveNot AvailableSpectrum
LC-MS/MSLC-MS/MS Spectrum - Quattro_QQQ 10V, Positive (Annotated)splash10-000i-0090000000-914b212f1dbb7fb7b1acSpectrum
LC-MS/MSLC-MS/MS Spectrum - Quattro_QQQ 25V, Positive (Annotated)splash10-052b-9800000000-d2e38d44d2f16d0a4203Spectrum
LC-MS/MSLC-MS/MS Spectrum - Quattro_QQQ 40V, Positive (Annotated)splash10-052b-9300000000-6830823fa12b40e784a2Spectrum
LC-MS/MSLC-MS/MS Spectrum - EI-B (JEOL JMS-01-SG-2) , Positivesplash10-0597-7920000000-dde7fba02fcbcec2d665Spectrum
LC-MS/MSLC-MS/MS Spectrum - EI-B (HITACHI RMU-6E) , Positivesplash10-05fs-4920000000-ccd839134de79f179f9eSpectrum
LC-MS/MSLC-MS/MS Spectrum - EI-B (HITACHI M-80) , Positivesplash10-00ds-0950000000-48c1f79091d708072f30Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0a4j-6900000000-3d818ffe03ecd499e078Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0a4j-7900000000-6db3d23d98d548cbbfaaSpectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0ukj-2690000000-14b953cb16c53d1e2744Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0uka-2790000000-dcd6839af64c3ef6006eSpectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0006-0090000000-b5f0189f1d6f21b90673Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0006-0090000000-21e1bde01931b051a4a3Spectrum
LC-MS/MSLC-MS/MS Spectrum - 30V, Positivesplash10-0fe1-0940000000-acd7cb439468ece54d34Spectrum
LC-MS/MSLC-MS/MS Spectrum - 50V, Positivesplash10-00am-0900000000-9f695ef54b7a75aa0ca5Spectrum
LC-MS/MSLC-MS/MS Spectrum - 55V, Positivesplash10-0a4j-6900000000-cc148be066f76bf120a2Spectrum
LC-MS/MSLC-MS/MS Spectrum - 80V, Positivesplash10-0a4j-8900000000-5a1a78a963c17ee2f26bSpectrum
LC-MS/MSLC-MS/MS Spectrum - 35V, Positivesplash10-0ukj-2690000000-075abfa2a19ae84712fbSpectrum
LC-MS/MSLC-MS/MS Spectrum - 55V, Positivesplash10-0uka-2790000000-528f02372cf3ac228b4aSpectrum
LC-MS/MSLC-MS/MS Spectrum - 35V, Positivesplash10-052k-7950000000-7505adc1ceff21713130Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-00dr-0190000000-4b469479ef097f60ed90Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-00dr-0390000000-8bebba5f70c72e80b630Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-0udi-5890000000-46ba5a59d051001f2a63Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-000i-0090000000-3c963477109db1f6b39eSpectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-000i-0090000000-87d4a2534cd39e8c54a8Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-0abc-1190000000-abbd0808a06f67c1f6fcSpectrum
MSMass Spectrum (Electron Ionization)splash10-00dv-5940000000-5e22fba0c369374c75dfSpectrum
1D NMR1H NMR SpectrumNot AvailableSpectrum
1D NMR1H NMR SpectrumNot AvailableSpectrum
1D NMR13C NMR SpectrumNot AvailableSpectrum
2D NMR[1H,13C] 2D NMR SpectrumNot AvailableSpectrum
Toxicity Profile
Route of ExposureEndogenous, Injection
Mechanism of ToxicityTestosterone is considered an anabolic steroid. It plays a key role in the development of male reproductive tissues such as the testis and prostate as well as promoting secondary sexual characteristics such as increased muscle, bone mass, and the growth of body hair. High levels of testosterone can lead to masculinization in females or premature puberty in young boys. Chronically high levels in adults increase the incidence of heart attack, stroke and blood clots by lowering the level of HDL (good cholesterol) and increasing the level of LDL (bad cholesterol). Chronic high use of anabolic steroids (such as testosterone) appears to lead to cardiac myopathy and weakening the left ventricle. The development of breast tissue in males, a condition called gynecomastia (which is usually caused by high levels of circulating estradiol), arises because of increased conversion of testosterone to estradiol by the enzyme aromatase. Reduced sexual function and temporary infertility can also occur in males. The mechanism of testosterone’s action is as follows: Free testosterone is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5-alpha reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of testosterone. Once bound, the ligand-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
MetabolismTestosterone is metabolized to 17-keto steroids through two different pathways. The major active metabolites are estradiol and dihydrotestosterone (DHT). Route of Elimination: About 90% of a dose of testosterone given intramuscularly is excreted in the urine as glucuronic and sulfuric acid conjugates of testosterone and its metabolites; about 6% of a dose is excreted in the feces, mostly in the unconjugated form. Half Life: 10-100 minutes
Toxicity ValuesNot Available
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesTo be used as hormone replacement or substitution of diminished or absent endogenous testosterone. Use in males: For management of congenital or acquired hypogonadism, hypogonadism associated with HIV infection, and male climacteric (andopause). Use in females: For palliative treatment of androgen-responsive, advanced, inoperable, metastatis (skeletal) carcinoma of the breast in women who are 1-5 years postmenopausal; testosterone esters may be used in combination with estrogens in the management of moderate to severe vasomotor symptoms associated with menopause in women who do not respond to adequately to estrogen therapy alone.
Minimum Risk LevelNot Available
Health EffectsIn women, excess testosterone may cause decreased breast size, a deep voice, increased genital size, irregular periods, oily skin, and unnatural hair growth. In men, excess testosterone may cause aggression, breast tenderness or enlargement, decreased testes size, and urinary urgency. Chronically high levels of testosterone are associated with at least 2 inborn errors of metabolism including: Adrenal Hyperplasia Type 3 and Aromatase deficiency.
SymptomsIn women, testosterone may cause decreased breast size, a deep voice, increased genital size, irregular periods, oily skin, and unnatural hair growth. In men, excess testosterone may cause aggression, premature baldness, breast tenderness or enlargement, decreased testes size, and urinary urgency.
TreatmentNot Available
Concentrations
Not Available
DrugBank IDDB00624
HMDB IDHMDB0000234
FooDB IDNot Available
Phenol Explorer IDNot Available
KNApSAcK IDC00003675
BiGG IDNot Available
BioCyc IDNot Available
METLIN IDNot Available
PDB IDNot Available
Wikipedia LinkTestosterone
Chemspider ID5791
ChEBI ID17347
PubChem Compound ID6013
Kegg Compound IDC00535
YMDB IDNot Available
ECMDB IDNot Available
References
Synthesis Reference

Merle G. Wovcha, Frederick J. Antosz, John M. Beaton, Alfred B. Garcia, Leo A. Kominek, “Process for preparing 9.alpha.-OH testosterone.” U.S. Patent US4221868, issued November, 1977.

MSDSLink
General References
1. Ercoli, Alberto; De Ruggieri, Pietro. An improved method of preparing testosterone, dihydrotestosterone, and some of their esters. Journal of the American Chemical Society (1953), 75 650-3.
2. Handelsman DJ: Clinical review: The rationale for banning human chorionic gonadotropin and estrogen blockers in sport. J Clin Endocrinol Metab. 2006 May;91(5):1646-53. Epub 2006 Feb 14.
3. Duschek EJ, Gooren LJ, Netelenbos C: Comparison of effects of the rise in serum testosterone by raloxifene and oral testosterone on serum insulin-like growth factor-1 and insulin-like growth factor binding protein-3. Maturitas. 2005 Jul 16;51(3):286-93.
4. Schaap LA, Pluijm SM, Smit JH, van Schoor NM, Visser M, Gooren LJ, Lips P: The association of sex hormone levels with poor mobility, low muscle strength and incidence of falls among older men and women. Clin Endocrinol (Oxf). 2005 Aug;63(2):152-60.
5. Kim YS, Zhang H, Kim HY: Profiling neurosteroids in cerebrospinal fluids and plasma by gas chromatography/electron capture negative chemical ionization mass spectrometry. Anal Biochem. 2000 Jan 15;277(2):187-95.
6. Huang I, Jones J, Khorram O: Human seminal plasma nitric oxide: correlation with sperm morphology and testosterone. Med Sci Monit. 2006 Mar;12(3):CR103-6. Epub 2006 Feb 23.
7. Hussein A, Ozgok Y, Ross L, Niederberger C: Clomiphene administration for cases of nonobstructive azoospermia: a multicenter study. J Androl. 2005 Nov-Dec;26(6):787-91; discussion 792-3.
8. Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, Hakkinen K: Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men. J Strength Cond Res. 2005 Aug;19(3):572-82.
9. Landman AD, Sanford LM, Howland BE, Dawes C, Pritchard ET: Testosterone in human saliva. Experientia. 1976;32(7):940-1.
10. Knickmeyer RC, Wheelwright S, Taylor K, Raggatt P, Hackett G, Baron-Cohen S: Gender-typed play and amniotic testosterone. Dev Psychol. 2005 May;41(3):517-28.
11. Fejes I, Koloszar S, Szollosi J, Zavaczki Z, Pal A: Is semen quality affected by male body fat distribution? Andrologia. 2005 Oct;37(5):155-9.
12. Jarow JP, Zirkin BR: The androgen microenvironment of the human testis and hormonal control of spermatogenesis. Ann N Y Acad Sci. 2005 Dec;1061:208-20.
13. Rovensky J, Radikova Z, Imrich R, Greguska O, Vigas M, Macho L: Gonadal and adrenal steroid hormones in plasma and synovial fluid of patients with rheumatoid arthritis. Endocr Regul. 2004 Dec;38(4):143-9.
14. Klimek M, Pabian W, Tomaszewska B, Kolodziejczyk J: Levels of plasma ACTH in men from infertile couples. Neuro Endocrinol Lett. 2005 Aug;26(4):347-50.
15. Cutolo M, Sulli A, Capellino S, Villaggio B, Montagna P, Pizzorni C, Paolino S, Seriolo B, Felli L, Straub RH: Anti-TNF and sex hormones. Ann N Y Acad Sci. 2006 Jun;1069:391-400.
16. Schwarz S, Pohl P: Steroid hormones and steroid hormone binding globulins in cerebrospinal fluid studied in individuals with intact and with disturbed blood-cerebrospinal fluid barrier. Neuroendocrinology. 1992 Feb;55(2):174-82.
17. Shores MM, Matsumoto AM, Sloan KL, Kivlahan DR: Low serum testosterone and mortality in male veterans. Arch Intern Med. 2006 Aug 14-28;166(15):1660-5.
18. Bhasin S, Cunningham GR, Hayes FJ, Matsumoto AM, Snyder PJ, Swerdloff RS, Montori VM: Testosterone therapy in adult men with androgen deficiency syndromes: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2006 Jun;91(6):1995-2010. Epub 2006 May 23.
19. Archer JS, Love-Geffen TE, Herbst-Damm KL, Swinney DA, Chang JR: Effect of estradiol versus estradiol and testosterone on brain-activation patterns in postmenopausal women. Menopause. 2006 May-Jun;13(3):528-37.
20. Jarow JP, Wright WW, Brown TR, Yan X, Zirkin BR: Bioactivity of androgens within the testes and serum of normal men. J Androl. 2005 May-Jun;26(3):343-8.
21. Bridger T, MacDonald S, Baltzer F, Rodd C: Randomized placebo-controlled trial of metformin for adolescents with polycystic ovary syndrome. Arch Pediatr Adolesc Med. 2006 Mar;160(3):241-6.
22. Kazi M, Geraci SA, Koch CA: Considerations for the diagnosis and treatment of testosterone deficiency in elderly men. Am J Med. 2007 Oct;120(10):835-40.
23. Krone N, Hanley NA, Arlt W: Age-specific changes in sex steroid biosynthesis and sex development. Best Pract Res Clin Endocrinol Metab. 2007 Sep;21(3):393-401.
24. Authors unspecified: Contraceptive efficacy of testosterone-induced azoospermia in normal men. World Health Organization Task Force on methods for the regulation of male fertility. Lancet. 1990 Oct 20;336(8721):955-9.
25. Hoberman JM, Yesalis CE: The history of synthetic testosterone. Sci Am. 1995 Feb;272(2):76-81.
26. Freeman ER, Bloom DA, McGuire EJ: A brief history of testosterone. J Urol. 2001 Feb;165(2):371-3.
27. https://www.ncbi.nlm.nih.gov/pubmed/?term=10438974
28. https://www.ncbi.nlm.nih.gov/pubmed/?term=11786693
29. https://www.ncbi.nlm.nih.gov/pubmed/?term=18900503
30. https://www.ncbi.nlm.nih.gov/pubmed/?term=24498482