An official website of the United States government

Methandrostenolone

PubChem CID
6300
Structure
Methandrostenolone_small.png
Methandrostenolone_3D_Structure.png
Methandrostenolone__Crystal_Structure.png
Molecular Formula
Synonyms
  • METHANDROSTENOLONE
  • Metandienone
  • Methandienone
  • 72-63-9
  • Dianabol
Molecular Weight
300.4 g/mol
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Dates
  • Create:
    2005-03-26
  • Modify:
    2025-01-25
Description
Methandrostenolone is an organic molecular entity.
Metandienone is an orally active anabolic androgenic steroid. It was introduced to the market in the 1960s but later discontinued and withdrawn from the market. Although it is prohibited in and outside competition by the World Anti-Doping Agency, metandienone continues to be marketed and misused as a performance-enhancing drug in sports. In the US, metandienone is a controlled substance under the Controlled Substances Act.
METHANDROSTENOLONE is a small molecule drug with a maximum clinical trial phase of IV. It was withdrawn in at least one region.
See also: Epimethandienone (annotation moved to).

1 Structures

1.1 2D Structure

Chemical Structure Depiction
Methandrostenolone.png

1.2 3D Conformer

1.3 Crystal Structures

CCDC Number
Crystal Structure Data
Crystal Structure Depiction
Crystal Structure Depiction

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

(8R,9S,10R,13S,14S,17S)-17-hydroxy-10,13,17-trimethyl-7,8,9,11,12,14,15,16-octahydro-6H-cyclopenta[a]phenanthren-3-one
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)

2.1.2 InChI

InChI=1S/C20H28O2/c1-18-9-6-14(21)12-13(18)4-5-15-16(18)7-10-19(2)17(15)8-11-20(19,3)22/h6,9,12,15-17,22H,4-5,7-8,10-11H2,1-3H3/t15-,16+,17+,18+,19+,20+/m1/s1
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.3 InChIKey

XWALNWXLMVGSFR-HLXURNFRSA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.4 SMILES

C[C@]12CC[C@H]3[C@H]([C@@H]1CC[C@]2(C)O)CCC4=CC(=O)C=C[C@]34C
Computed by OEChem 2.3.0 (PubChem release 2024.12.12)

2.2 Molecular Formula

C20H28O2
Computed by PubChem 2.2 (PubChem release 2021.10.14)

2.3 Other Identifiers

2.3.1 CAS

2.3.2 European Community (EC) Number

2.3.3 UNII

2.3.4 ChEBI ID

2.3.5 ChEMBL ID

2.3.6 DrugBank ID

2.3.7 DSSTox Substance ID

2.3.8 HMDB ID

2.3.9 KEGG ID

2.3.10 Lipid Maps ID (LM_ID)

2.3.11 Metabolomics Workbench ID

2.3.12 NCI Thesaurus Code

2.3.13 Nikkaji Number

2.3.14 NSC Number

2.3.15 Wikidata

2.3.16 Wikipedia

2.4 Synonyms

2.4.1 MeSH Entry Terms

  • Dehydromethyltestosterone
  • Dianabol
  • Metanabol
  • Metandienone
  • Methandienone
  • Methandrostenolone
  • Nerobol

2.4.2 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

Property Name
Molecular Weight
Property Value
300.4 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
XLogP3
Property Value
3.6
Reference
Computed by XLogP3 3.0 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Donor Count
Property Value
1
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Acceptor Count
Property Value
2
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Rotatable Bond Count
Property Value
0
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Exact Mass
Property Value
300.208930132 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Monoisotopic Mass
Property Value
300.208930132 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Topological Polar Surface Area
Property Value
37.3 Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Heavy Atom Count
Property Value
22
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
0
Reference
Computed by PubChem
Property Name
Complexity
Property Value
589
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Isotope Atom Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Atom Stereocenter Count
Property Value
6
Reference
Computed by PubChem
Property Name
Undefined Atom Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Covalently-Bonded Unit Count
Property Value
1
Reference
Computed by PubChem
Property Name
Compound Is Canonicalized
Property Value
Yes
Reference
Computed by PubChem (release 2021.10.14)

3.2 Experimental Properties

3.2.1 Physical Description

Solid

3.2.2 Color / Form

Crystals from acetone and ether
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1064
WHITE CRYSTALS OR WHITE, CRYSTALLINE POWDER
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 930

3.2.3 Odor

ODORLESS
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 930

3.2.4 Melting Point

163-164 °C
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1064
163.5 °C

3.2.5 Solubility

SOL IN ALC, CHLOROFORM, GLACIAL ACETIC ACID; SLIGHTLY SOL IN ETHER; INSOL IN WATER
Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 930

3.2.6 Optical Rotation

Specific optical rotation: 0 at 26 °C/D (1.15%, chloroform)
The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976., p. 776

3.3 SpringerMaterials Properties

3.4 Chemical Classes

3.4.1 Drugs

Pharmaceutical
S120 | DUSTCT2024 | Substances from Second NORMAN Collaborative Dust Trial | DOI:10.5281/zenodo.13835254
Pharmaceuticals -> Synthetic Cannabinoids or Psychoactive Compounds
S58 | PSYCHOCANNAB | Synthetic Cannabinoids and Psychoactive Compounds | DOI:10.5281/zenodo.3247723

3.4.2 Endocrine Disruptors

Potential endocrine disrupting compound
S109 | PARCEDC | List of 7074 potential endocrine disrupting compounds (EDCs) by PARC T4.2 | DOI:10.5281/zenodo.10944198

3.4.3 Lipids

Lipids -> Sterol Lipids [ST] -> Steroids [ST02] -> C19 steroids (androgens) and derivatives [ST0202]

4 Spectral Information

4.1 1D NMR Spectra

4.1.1 1H NMR Spectra

Source of Spectrum
Sigma-Aldrich Co. LLC.
Source of Sample
Sigma-Aldrich Co. LLC.
Catalog Number
318132
Copyright
Copyright © 2021-2024 Sigma-Aldrich Co. LLC. - Database Compilation Copyright © 2021 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail

4.1.2 13C NMR Spectra

1 of 2
Copyright
Copyright © 2016-2024 W. Robien, Inst. of Org. Chem., Univ. of Vienna. All Rights Reserved.
Thumbnail
Thumbnail
2 of 2
Copyright
Copyright © 2016-2024 W. Robien, Inst. of Org. Chem., Univ. of Vienna. All Rights Reserved.
Thumbnail
Thumbnail

4.2 Mass Spectrometry

4.2.1 GC-MS

1 of 3
View All
NIST Number
43678
Library
Main library
Total Peaks
247
m/z Top Peak
122
m/z 2nd Highest
121
m/z 3rd Highest
43
Thumbnail
Thumbnail
2 of 3
View All
Source of Spectrum
Mass Spectrometry Committee of the Toxicology Section of the American Academy of Forensic Sciences
Copyright
Copyright © 2012-2024 John Wiley & Sons, Inc. Portions provided by AAFS, Toxicology Section. All Rights Reserved.
Thumbnail
Thumbnail

4.2.2 LC-MS

1 of 8
View All
Authors
da Silva KM, Iturrospe E, van de Lavoir M, Robeyns R, University of Antwerp, Belgium
Instrument
Agilent 6560 QTOF
Instrument Type
LC-ESI-QTOF
MS Level
MS2
Ionization Mode
POSITIVE
Ionization
ESI
Collision Energy
20 eV
Fragmentation Mode
CID
Column Name
Direct injection
Retention Time
0.154 min
Precursor m/z
301.2162
Precursor Adduct
[M+H]+
Top 5 Peaks

121.0648 999

149.1326 248

93.0693 185

107.0852 127

81.07 93

Thumbnail
Thumbnail
License
CC BY
2 of 8
View All
Authors
da Silva KM, Iturrospe E, van de Lavoir M, Robeyns R, University of Antwerp, Belgium
Instrument
Agilent 6560 QTOF
Instrument Type
LC-ESI-QTOF
MS Level
MS2
Ionization Mode
POSITIVE
Ionization
ESI
Collision Energy
10 eV
Fragmentation Mode
CID
Column Name
Direct injection
Retention Time
0.180 min
Precursor m/z
301.2162
Precursor Adduct
[M+H]+
Top 5 Peaks

121.0651 999

149.1328 858

283.2057 309

301.2174 241

147.0808 120

Thumbnail
Thumbnail
License
CC BY

4.2.3 Other MS

Other MS
MASS: 54951 (NIST/EPA/MSDC Mass Spectral Data Base, 1990 Version

4.3 UV Spectra

Max absorption: 245 nm (epsilon= 15,600)
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1064
UV: 1896 (Absorption Spectra in the UV and visible Regions, Academic Press, New York)
Lide, D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. Volume I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V1: 228

4.4 IR Spectra

4.4.1 FTIR Spectra

1 of 2
Technique
KBr WAFER
Source of Sample
Unknown
Copyright
Copyright © 1980, 1981-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail
2 of 2
Instrument Name
Bio-Rad FTS
Technique
KBr1 0.53mg
Source of Spectrum
Forensic Spectral Research
Source of Sample
Steraloids
Catalog Number
A0130-020
Lot Number
L1407
Copyright
Copyright © 2008-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail

4.4.2 ATR-IR Spectra

Instrument Name
Bio-Rad FTS
Technique
ATR-Neat (DuraSamplIR II)
Source of Spectrum
Forensic Spectral Research
Source of Sample
Steraloids Inc.
Catalog Number
A0130-020
Lot Number
L1407
Copyright
Copyright © 2009-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail

4.5 Raman Spectra

Technique
FT-Raman
Source of Spectrum
Forensic Spectral Research
Source of Sample
Steraloids Inc.
Catalog Number
A0130-020
Lot Number
L1407
Copyright
Copyright © 2012-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail

6 Chemical Vendors

7 Drug and Medication Information

7.1 Therapeutic Uses

Anabolic Steroids
National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)
A two compartment, double-blind, randomized, parallel study was performed comparing methandrostenolone with placebo in the treatment of osteoporosis. The duration of the study was 24 mo. Dependent parameters included total body calcium (TBCa), measured by neutron activation analysis: bone mineral content of the radius (BMC), measured by photon absorptiometry; and total body potassium (TBK), measured by total body counting. A significant increase in TBK occurred in the treated group, primarily in the first 6 mo; thereafter the TBK remained fairly constant. No significant changes in bone mass occurred, except the 6 mo TBCa measurement increased by 11 grams for the methandrostenolone group and decreased by 6 grams for the placebo group (p = .05). Other evidence also suggests that anabolic steroids may not produce sustained uncoupling of bone formation and bone resorption in osteoporosis. If methandrostenolone is capable of producing an increment in bone mass in osteoporosis, it was not readily observable with the sensitivity of the techniques employed in this study
Aloia JF et al; Metabolism 30 (11): 1076-9 (1981)
VET: orally, to increase nitrogen retention and increase serum protein values aiding in tissue repair and decrease healing time after surgery, burns, or skin grafts. Also in geriatric states, debilitation, and after chronic infections. As aid in calcium retention in senile, corticosteroid induced, or idiopathic osteoporosis.
Rossoff, I.S. Handbook of Veterinary Drugs. New York: Springer Publishing Company, 1974., p. 346

7.2 Drug Warnings

Use of anabolic steroids by athletes is not recommended. Objective evidence is conflicting and inconclusive as to whether these medications significantly increase athletic performance by increasing muscle strength. Weight gains reported by athletes are due in part to fluid retention, which is a potentially hazardous side effect of anabolic steroid therapy. The risk of other unwanted effects, such as testicular atrophy and suppression of spermatogenesis in males; menstrual disturbances and virilization, such as deepening of voice, development of acne, and unnatural growth of body hair in females; peliosis hepatis or other hepatotoxicity; and hepatic cancer outweigh any possible benefit received from anabolic steroids and make their use in athletes inappropriate. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 140
Hepatocellular carcinoma has been associated rarely with long-term, high-dose anabolic steroid therapy. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
Hepatic neoplasms have been associated rarely with long-term, high-dose anabolic steroid therapy. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
FDA Pregnancy Category X. /CONTRAINDICATED IN PREGNANCY. Studies in animals and or humans, or investigational or post-marketing reports, have demonstrated positive evidence of fetal abnormalities or risk which clearly outweighs any possible benefit to the patient./
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
For more Drug Warnings (Complete) data for METHANDROSTENOLONE (19 total), please visit the HSDB record page.

8 Pharmacology and Biochemistry

8.1 MeSH Pharmacological Classification

Anabolic Agents
These compounds stimulate anabolism and inhibit catabolism. They stimulate the development of muscle mass, strength, and power. (See all compounds classified as Anabolic Agents.)

8.2 ATC Code

A - Alimentary tract and metabolism

A14 - Anabolic agents for systemic use

A14A - Anabolic steroids

A14AA - Androstan derivatives

A14AA03 - Metandienone

D - Dermatologicals

D11 - Other dermatological preparations

D11A - Other dermatological preparations

D11AE - Androgens for topical use

D11AE01 - Metandienone

8.3 Absorption, Distribution and Excretion

It is not known whether anabolic steroids are distributed into breast milk. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
After oral administration of nerobol, only small amount of its metabolites could be detected in urine of control or patients with hepatic diseases. Half-life of nerobol was greater in patients with cirrhosis than in controls.
Bodrogi L et al; Acta Pharm Hung 49(5): 194 (1979)

8.4 Metabolism / Metabolites

The phase I and phase II metabolism of the anabolic steroid methandrostenolone was investigated following oral administration to a standardbred gelding. In the phase I study, metabolites were isolated from the urine by solid-phase extraction, deconjugated by acid catalysed methanolysis and converted to their O-methyloxime trimethylsilyl derivatives. GC-MS analysis indicated the major metabolic processes to be sequential reduction of the A-ring and hydroxylation at C6 and C16. In the phase II study, unconjugated, beta-glucuronidated and sulfated metabolites were fractionated and deconjugated using a combination of liquid-liquid extraction, enzyme hydrolysis, solid-phase extraction and acid catalysed methanolysis. Derivatization followed by GC-MS analysis revealed extensive conjugation to both glucuronic and sulfuric acids, with only a small proportion of metabolites occurring in unconjugated form.
McKinney AR et al; J Chromatogr B Biomed Sci Appl 765 (1): 71-9 (2001)
After oral administration of methandrostenolone to rats small amounts excreted in urine but no metabolites. Larger amounts excreted in feces and 2 components identified as 17alpha-methyl-5beta-androstane-3alpha,17beta-diol and 17alpha-methyl-5alpha-androstane-3beta,17beta-diol.
Steel JW, Schlunegger UP; Can J Pharm Sci 14(2): 50 (1979)
Monolayer cultures of bovine hepatocytes were used to investigate the biotransformation of methandienone in vitro. After incubation of bovine hepatocytes with methandienone, samples were taken at different times. The samples were treated with deconjugation enzymes and extracted with diethyl ether. The metabolites formed were converted to their trimethylsilylether derivatives. By using gas chromatography-mass spectrometry with electron impact and chemical ionisation, several metabolites were identified. After 24 h of incubation with bovine hepatocytes, 83% of the parent compound was converted to its metabolites. The major metabolite found was 6-beta-hydroxymethandienone with a yield of 24%. This compound was identified after comparison with an authentic sample of 6 beta-hydroxymethandienone, which was synthesized chemically.
Hooijerink D et al; Analyst 123 (12): 2637-41(1998)
The expression of the cytochrome P450IIIA4 gene in the Saccharomyces cerevisiae yeast using the shuttle vector pYeDP1-8/2 has been carried out. The microsomal fraction isolated from the transformed yeast cells was used for biotransformation of the anabolic steroid hormone-methandrostenolone. The microsomal oxidation products were analyzed by HPLC and two-dimensional TLC. It was shown that microsomes of the yeasts expressing human cytochrome P450IIIA4 catalyze the methandrostenolone conversion into its 6 beta-hydroxy derivative. An identical product is formed via a reaction catalyzed by human liver microsomes. The use of the heterological system of cytochrome P450IIIA4 expression has made it possible to establish its role in methandrostenolone metabolism. The experimental system simulates the first phase of the drug biotransformation in liver cells.
Krynetskii Elu et al; Biokhimiia 59 (2): 282-7 (1994)
For more Metabolism/Metabolites (Complete) data for METHANDROSTENOLONE (6 total), please visit the HSDB record page.

8.5 Mechanism of Action

Anabolic steroids reverses catabolic processes and negative nitrogen balance by promoting protein anabolism and stimulating appetite if there is concurrently a proper intake of calories and proteins. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
...Methandrostenolone, was shown to influence cardiac growth in immature male rats by affecting protein synthesis and degradation. The nature of cardiac responses to androgen appear to depend on the prevailing experimental conditions. Protein synthesis was inhibited in the castrate rat and was stimulated by subsequent treatment with androgen. Under conditions of induced overgrowth of the ventricles, androgens gave rise to an attenuation of the effects of aortic constriction on ventricular mass and blood pressure involving smaller changes in protein synthesis and proteolysis. Concentrations of testosterone receptors in ventricular cytosol further indicated that the myocardium is more sensitive to androgen action during the prepubertal phase of the life-span. Changes in amount and properties of the receptors showed them to be functional and responsive to castration, aortic constriction, and administration of the androgens. The androgens affected cardiac protein balance by stimulating the incorporation of radiolabelled amino acid into protein in vivo. They also appeared to influence proteolytic processes involving lysosomal hydrolase activities, but their actions were either stimulatory or inhibitory depending on the internal environment. The heart is a target organ for several hormones including androgen, and our findings fortify the notion that hormone action needs to be investigated alone and in association with other endocrines.
Kinson GA et al; Can J Physiol Pharmacol 69 (11): 1698-704 (1991)
The effects of treating groups of rats with four different anabolic androgenic steroids (AAS) (testosterone, nandrolone, methandrostenolone, and oxymetholone) on 5-hydroxytryptamine (5-HT) and dopamine (DA) neurones in different brain regions were examined. The AAS was injected six times with 1 week's interval and the rats were sacrificed 2 days after the final injection. 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured. The effect on DA and 5-HT synthesis rate was analysed as the accumulation of 3,4-dihydroxyphenyl-alanine (DOPA) and 5-hydroxytryptophan (5-HTP), respectively, after inhibition of the amino acid decarboxylase with NSD-1015 (3-hydroxy-benzylhydrazine dihydrochloride). Additionally, the monoamine oxidase (MAO) activity was analysed in the hypothalamus. The DOPAC+HVA/DA ratio was increased in the striatum in all treatment groups. However, the synthesis rate of DA was significantly increased only in the methandrostenolone treated group. The 5-HIAA/5-HT ratio was increased in all treatment groups in the hippocampus, in the frontal cortex in the methandrostenolone-treated animals and in the hypothalamus in the testosterone- and oxymetholone-treated rats, while the 5-HT synthesis rate was not affected by the AAS-treatments. The MAO-A activity was increased in the oxymetholone-treated rats while the other treatment groups were unaffected. The MAO-B activity was not changed. The results indicate that relatively high doses of AAS increase dopaminergic and 5-hydroxytryptaminergic metabolism in male rat brain, probably due to enhanced turnover in these monaminergic systems.
Thiblin I et al; British Journal of Pharmacology 126: 1301-1306 (1999)
Long-term treatment of female rats with the anabolic steroid hormone Methandrostenolone results in a conspicuous increase of intermediate sized, nonmyofibrillar filaments in muscle cells of the left cardiac ventricle, as revealed by electron microscopy. These filaments, measuring 70 - 110 A in diameter, form a characteristic network at the Z-level of the sarcomere, either encircling or penetrating the Z-bands, and appear to insert into the nuclear membrane. The T-system is accompanied by the filaments adjacent to the site of the couplings. Here they are attached to subsarcolemmal electron-dense patches, which may be Z-line precursor material. The filaments may function as a cytoskeleton, to provide passive support in the mechanism of contraction and to mediate nucleo-sarcolemmal and nucleo-myofibrillar exchange.
Behrendt H; Cell Tissue Res 180 (3): 303-15 (1977)

8.6 Human Metabolite Information

8.6.1 Cellular Locations

Membrane

9 Use and Manufacturing

9.1 Uses

EPA CPDat Chemical and Product Categories
The Chemical and Products Database, a resource for exposure-relevant data on chemicals in consumer products, Scientific Data, volume 5, Article number: 180125 (2018), DOI:10.1038/sdata.2018.125
MEDICATION (VET)
MEDICATION

9.2 Methods of Manufacturing

Preparation by microbial dehydrogenation of 17alpha-methyltestosterone.
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1064
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1064
Preparation: ... Wettstein et al, US 2900398 (1959 to Ciba).
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1064

9.3 Formulations / Preparations

METHANDROSTENOLONE, NF (DIANABOL), TABLETS: 2.5 & 5 MG.
Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975., p. 1462

9.4 General Manufacturing Information

While data specific to methandrostenolone were not available(SRC, 2005), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2).
(1) Heberer T; Tox Lett 131: 5-17 (2002)
(2) Koplin DW et al; Environ Sci Toxicol 36: 1202-211 (2002)
Daily oral administration of anabolic steroid, methandienone, to mink improved fur quality.
Westermarck H et al; Effect of Methandienone on Fur Quality & Reproduction of Mink; Zentralbl Veterinaermed, Reihe a 26(9) 752 (1979)
This is a controlled substance (anabolic steroid)... .
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1064
Synthetic analogs of androgens have been used by professional, as well as amateur, athletes for possible performance enhancement.
Donahue JL, Lowenthal DT; Am J Ther 7: 365-73 (2000)
Anabolic Steroid Control Act of 2004. Public Law 108-358 (October 22, 2004)... includes /methandrostenolone/ as an anabolic steroid
US Gov Print Off; National Archives and Records Administration. Catalog of Public and Private Laws - 108th Congress. Pub.L. 108-358. Available from, as of Jun 2, 2005: https://www.access.gpo.gov/nara/publaw/108publ.html

10 Identification

10.1 Clinical Laboratory Methods

HPLC can be useful for routine surveillance of anabolic drug abuse in sports.
Frischkorn CG B, Frischkorn HE; Investigations of Anabolic Drug Abuse in Athletics & Cattle Feed. Ii. Specific Determination of Methandienone (Dianabol) in Urine in Nanogram Amounts; J Chromatogr 151(3) 331 (1978)
Computerized method simultaneously detected five 17alpha-me anabolic steroids excreted in human urine.
Bertrand M et al; GC-MS Approach For Detection & Characterization of Anabolic Steroids & Their Metabolites in Biological Fluids at Major International Sporting Events; Farm Tijdschr Belg 55(3) 85 (1978)
Screening of anabolic steroids /including methandrostenolone/ in horse urine by liquid chromatography-tandem mass spectrometry.
Yu NH et al; J Pharm Biomed Anal 37 (5): 1031-8 (2005)

11 Safety and Hazards

11.1 Hazards Identification

11.1.1 GHS Classification

Note
This chemical does not meet GHS hazard criteria for 79.1% (91 of 115) of all reports. Pictograms displayed are for 20.9% (24 of 115) of reports that indicate hazard statements.
Pictogram(s)
Health Hazard
Signal
Danger
GHS Hazard Statements

H360 (20.9%): May damage fertility or the unborn child [Danger Reproductive toxicity]

H362 (20.9%): May cause harm to breast-fed children [Reproductive toxicity, effects on or via lactation]

Precautionary Statement Codes

P203, P260, P263, P264, P270, P280, P318, P405, and P501

(The corresponding statement to each P-code can be found at the GHS Classification page.)

ECHA C&L Notifications Summary

Aggregated GHS information provided per 115 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Reported as not meeting GHS hazard criteria per 91 of 115 reports by companies. For more detailed information, please visit ECHA C&L website.

There is 1 notification provided by 24 of 115 reports by companies with hazard statement code(s).

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown.

11.1.2 Hazard Classes and Categories

Repr. 1A (20.9%)

Lact. (20.9%)

11.2 Accidental Release Measures

11.2.1 Disposal Methods

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

11.3 Regulatory Information

11.3.1 FDA Requirements

Schedules of controlled substances are established by section 202 of the Controlled Substances Act (21 U.S.C. 812). Schedule III shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation containing any quantity of the following substances, including its salts, isomers, and salts of isomers whenever the existence of such salts of isomers is possible within the specific chemical designation. DEA Code #: 4000; Drug class: anabolic steroids.
21 CFR 1308.13(f); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of June 1, 2005: https://www.ecfr.gov

12 Toxicity

12.1 Toxicological Information

12.1.1 Toxicity Summary

IDENTIFICATION: Methandienone is an anabolic steroid. Origin of the substance: Naturally-occuring anabolic steroids are synthesized in the testis, ovary and adrenal gland from cholesterol via pregnenolone. Synthetic anabolic steroids are based on the principal male hormone testosterone, modified in one of three ways: alkylation of the 17-carbon; esterification of the 17-OH group and modification of the steroid nucleus. Indications: The only legitimate therapeutic indications for anabolic steroids are: replacement of male sex steroids in men who have androgen deficiency, for example as a result of loss of both testes; the treatment of certain rare forms of aplastic anemia which are or may be responsive to anabolic androgens; the drugs have been used in certain countries to counteract catabolic states, for example after major trauma. HUMAN EXPOSURE: Main risks and target organs: There is no serious risk from acute poisoning, but chronic use can cause harm. The main risks are those of excessive androgens: menstrual irregularities and virilization in women and impotence, premature cardiovascular disease and prostatic hypertrophy in men. Both men and women can suffer liver damage with oral anabolic steroids containing a substituted 17-alpha-carbon. Psychiatric changes can occur during use or after cessation of these agents. Summary of clinical effects: Acute overdosage can produce nausea and gastrointestinal upset. Chronic usage is thought to cause an increase in muscle bulk, and can cause an exageration of male characteristics and effects related to male hormones. Anabolic steroids can influence sexual function. They can also cause cardiovascular and hepatic damage. Acne and male- pattern baldness occur in both sexes; irregular menses, atrophy of the breasts, and clitoromegaly in women; and testicular atrophy and prostatic hypertrophy in men. Contraindications: Known or suspected cancer of the prostate or (in men) breast. Pregnancy or breast-feeding and known cardiovascular disease is a relative contraindication. Oral: Anabolic steroids can be absorbed from the gastrointestinal tract, but many compounds undergo such extensive first-pass metabolism in the liver that they are inactive. Those compounds in which substitution of the 17-carbon protects the compound from the rapid hepatic metabolism are active orally. Parenteral: Intramuscular or deep subcutaneous injection is the principal route of administration of all the anabolic steroids except the 17-alpha-substituted steroids which are active orally. Absorption by route of exposure: The absorption after oral dosing is rapid for testosterone and probably for other anabolic steroids, but there is extensive first-pass hepatic metabolism for all anabolic steroids except those that are substituted at the 17-alpha position. The rate of absorption from subcutaneous or intramuscular depots depends on the product and its formulation. Absorption is slow for the lipid-soluble esters such as the cypionate or enanthate, and for oily suspensions. Distribution by route of exposure: The anabolic steroids are highly protein bound, and is carried in plasma by a specific protein called sex-hormone binding globulin. Biological half-life by route of exposure: The metabolism of absorbed drug is rapid, and the elimination half-life from plasma is very short. The duration of the biological effects is therefore determined almost entirely by the rate of absorption from subcutaneous or intramuscular depots, and on the de-esterification which precedes it. Metabolism: Free (de-esterified) anabolic androgens are metabolized by hepatic mixed function oxidases. Elimination by route of exposure: After administration of radiolabelled testosterone, about 90% of the radioactivity appears in the urine, and 6% in the feces; there is some enterohepatic recirculation. Mode of action: Toxicodynamics: The toxic effects are an exaggeration of the normal pharmacological effects. Pharmacodynamics: Anabolic steroids bind to specific receptors present especially in reproductive tissue, muscle and fat. The anabolic steroids reduce nitrogen excretion from tissue breakdown in androgen deficient men. They are also responsible for normal male sexual differentiation. The ratio of anabolic (body-building) effects to androgenic (virilizing) effects may differ among the members of the class, but in practice all agents possess both properties to some degree. There is no clear evidence that anabolic steroids enhance overall athletic performance. Carcinogenicity: Anabolic steroids may be carcinogenic. They can stimulate growth of sex-hormone dependent tissue, primarily the prostate gland in men. Precocious prostatic cancer has been described after long-term anabolic steroid abuse. Cases where hepatic cancers have been associated with anabolic steroid abuse have been reported. Teratogenicity: Androgen ingestion by a pregnant mother can cause virilization of a female fetus. Chronic poisoning: Ingestion: Hepatic damage, manifest as derangement of biochemical tests of liver function and sometimes severe enough to cause jaundice; virilization in women; prostatic hypertrophy, impotence and azoospermia in men; acne, abnormal lipids, premature cardiovascular disease (including stroke and myocardial infarction), abnormal glucose tolerance, and muscular hypertrophy in both sexes; psychiatric disturbances can occur during or after prolonged treatment. Parenteral exposure: Virilization in women; prostatic hypertrophy, impotence and azoospermia in men; acne, abnormal lipids, premature cardiovascular disease (including stroke and myocardial infarction), abnormal glucose tolerance, and muscular hypertrophy in both sexes. Psychiatric disturbances can occur during or after prolonged treatment. Hepatic damage is not expected from parenteral preparations. Course, prognosis, cause of death: Patients with symptoms of acute poisoning are expected to recover rapidly. Patients who persistently abuse high doses of anabolic steroids are at risk of death from premature heart disease or cancer, especially prostatic cancer. Non-fatal but long lasting effects include voice changes in women and fusion of the epiphyses in children. Other effects are reversible over weeks or months. Systematic description of clinical effects: Cardiovascular: Chronic ingestion of high doses of anabolic steroids can cause elevations in blood pressure, left ventricular hypertrophy and premature coronary artery disease. Neurological: Central nervous system: Stroke has been described in a young anabolic steroid abuser. Mania and psychotic symptoms of hallucination and delusion was described in anabolic steroid abusers. They also described depression after withdrawal from anabolic steroids. There is also considerable debate about the effects of anabolic steroids on aggressive behavior and on criminal behavior. Mood swings were significantly more common in normal volunteers during the active phase of a trial comparing methyltestosterone with placebo. Gastrointestinal: Acute ingestion of large doses can cause nausea and gastrointestinal upset. Hepatic: Orally active (17-alpha substituted) anabolic steroids can cause abnormalities of hepatic function, manifest as abnormally elevated hepatic enzyme activity in biochemical tests of liver function, and sometimes as overt jaundice. The histological abnormality of peliosis hepatitis has been associated with anabolic steroid use. Angiosarcoma and a case of hepatocellular carcinoma in an anabolic steroid user has been reported. Urinary: Men who take large doses of anabolic steroids can develop prostatic hypertrophy. Prostatic carcinoma has been described in young men who have abused anabolic steroids. Endocrine and reproductive systems: Small doses of anabolic steroids are said to increase libido, but larger doses lead to azoospermia and impotence. Testicular atrophy is a common clinical feature of long-term abuse of anabolic steroids, and gynacomastia can occur. Women develop signs of virilism, with increased facial hair, male pattern baldness, acne, deepening of the voice, irregular menses and clitoral enlargement. Dermatological: Acne occurs in both male and female anabolic steroids abusers. Women can develop signs of virilism, with increased facial hair and male pattern baldness. Eye, ear, nose, throat: local effects: Changes in the larynx in women caused by anabolic steroids can result in a hoarse, deep voice. The changes are irreversible. Metabolic: Fluid and electrolyte disturbances: Sodium and water retention can occur, and result in edema; hypercalcemia is also reported. Insulin resistance with a fall in glucose tolerance, and hypercholesterolemia with a fall in high density lipoprotein cholesterol, have been reported.
International Programme on Chemical Safety; Poisons Information Monograph: Methandienone (PIM 905) (1998) Available from, as of October 24, 2005: https://www.inchem.org/pages/pims.html

12.1.2 Acute Effects

12.1.3 Interactions

Anticoagulant effects of coumarin- or indandione-derivative or anti-inflammatory analgesics, nonsteroidal or salicylates, in therapeutic doses may be increased during concurrent use with anabolic steroids, especially 17-alpha-alkylated compounds, because of decreased procoagulant factor concentration caused by alteration of procoagulant factor synthesis or catabolism and increased receptor affinity for the anticoagulant; anticoagulant dosage adjustment based on prothrombin time determinations may be required during and following concurrent use with anabolic steroids. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
Concurrent use of antidiabetic agents, sulfonylurea or insulin with anabolic steroids may decrease blood glucose concentration; diabetic patients should be closely monitored for signs of hypoglycemia ... /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
Concurrent use of corticosteroids, glucocorticoid, especially with significant mineralocorticoid activity, prolonged therapeutic corticotropin or sodium-containing medications or foods with anabolic steroids may increase the possibility of edema; in addition, concurrent use of glucocorticoids or corticotropin with anabolic steroids may promote development of severe acne. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
Concurrent use of hepatotoxic medications with anabolic steroids may result in an increased incidence of hepatotoxicity; patients, especially those on prolonged administration or those with a history of liver disease, should be carefully monitored. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
Concurrent use of anabolic steroids with somatrem or somatropin may accelerate epiphyseal maturation. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141

12.1.4 Human Toxicity Excerpts

/CASE REPORTS/ A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae. Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. Although the steroids had been discontinued, the patient's general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement.
Habscheid W et al; Dtsch Med Wochenschr 124 (36): 1029-32 (1999)
/CASE REPORTS/ A report of 2 men (aged 22 and 40 yr) with psychotic episodes following two 8 wk courses of 15 mg/day of methandrostenolone and 10 mg 2 times/day of methyltestosterone, respectively is presented. Both patients responded well to neuroleptics and were able to discontinue these medications permanently after several wk. Neither patient reported any serious psychopathology before the index episode. Both, with no further exposure to steroids, have remained psychiatrically normal during more than 2 yr follow-up. It was concluded that anabolic steroids emerge as a likely causative factor in both cases.
Pope HG, Katz DL; Lancet 1 (Apr 11): 863 (1987)
/CASE REPORTS/ A 19-year-old man with paroxysmal nocturnal hemoglobinuria treated for 3 years with methandienone was admitted to the hospital with hemoperitoneum due to the rupture of an hepatic tumor. Histology revealed that it was a benign liver cell adenoma, with a pathologic appearance and mode of clinical presentation closely resembling those of cases observed to develop in association to contraceptive steroids.
Hernadez-Nieto L et al; Cancer 40 (4): 1761-4 (1977)
/CASE REPORTS/ Two prepubertal girls were treated with Dianabol cream by their family physicians during 6 and 8 months because of an anal exzema. In both of them, growth velocity and bone maturation were accelerated, and there was hypertrophy of the clitoris and deepening of the voice. In one girl, all symptoms with the exception of the deep voice had disappeared six years after the discontinuation of treatment. In the other girl, final evaluation is not yet possible. The two observations show that androgens and anabolic steroids may have a marked systemic action if applied percutaneously. Treatment with these compounds is indicated very rarely in children and should be restricted to pediatric endocrinologists.
Sorgo W et al; Helv Paediatr Acta 37 (4): 401-6 (1982)
/CASE REPORTS/ Chronic abuse of anabolic steroids is widespread. Hypertrophy of skeletal and heart muscle is a well-known effect of chronic anabolic steroid abuse. Structural alterations of blood vessels are new side effects. We report a case of a 32-year-old bodybuilder after long-term use of anabolic steroids who died of cardiac arrest. Coronary angiography and autopsy findings showed especially a hypertrophic heart, structural changes of coronary arteries, intracoronary thrombosis and myocardial infarction, ventricular thrombosis and systemic embolism
Tischer KH et al; Z Kardiol 92 (4): 326-31 (2003)

12.1.5 Non-Human Toxicity Excerpts

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The action of different doses and time of metandrostenolone administration on liver morphology and activity of the enzymes of blood serum, liver and pancreatic tissue was studied in experiments on male rats. It was established that metandrostenolone regardless of its dose and time of administration produces changes in enzymatic activity and in morphological characteristics, manifesting in hypertrophy of hepatocytes in modification of the cell size of the reticuloendothelium as well as in the magnitude and amount of nucleoli in the nucleus. The changes also involve impaired rhythmicity of RNA and glycogen synthesis by the liver.
Nesterin MF et al; Farmakol Toksikol 43 (5): 597-601 (1980)
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Daily oral dose of 0.44 mg/animal induced infertility in 50% of female mink. Treatment of females decreased proportion of females in their litters.
Westermarck H et al; Effect of Methandienone on Fur Quality & Reproduction of Mink; Zentralbl Veterinaermed, Reihe a 26(9): 752 (1979)
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The present study compared the effects of chronic exposure to three individual anabolic-androgenic steroids (AASs), stanozolol (0.05-5 mg/kg), 17alpha-methyltestosterone (0.5-5 mg/kg), and methandrostenolone (0.5-5 mg/kg) on the onset of puberty and estrous cyclicity in the rat. Female rats received daily injections of AASs for 30 days (Postnatal Day [PN] 21-51). Rats receiving the highest dose of each of the AASs (5 mg/kg) displayed vaginal opening at a younger age than rats receiving the oil vehicle. The day of first vaginal estrus was delayed in rats receiving stanozolol (5 mg/kg) or 17alpha-methyltestosterone (0.5-5 mg/kg) but not in rats receiving methandrostenolone. At the highest dose (5 mg/kg), each of the AASs reduced the incidence of regular estrous cyclicity during the treatment period. Concurrent administration (on PN21-51) of the androgen receptor antagonist, flutamide (10 mg/kg, twice daily), reversed the effects of 17alpha-methyltestosterone (5 mg/kg) on vaginal opening. Flutamide administration also eliminated the effects of stanozolol (5 mg/kg) and 17alpha-methyltestosterone (5 mg/kg) on the day of first vaginal estrus. In contrast, rats receiving flutamide and methandrostenolone (5 mg/kg) exhibited first vaginal estrus earlier than controls. The present results indicate that chronic exposure to AASs during development has deleterious effects on the female neuroendocrine axis and that these effects appear be mediated via multiple mechanisms.
Clark AS et al; Biol Reprod 68 (2): 465-71(2003)
/GENOTOXICITY/ Metandrostenolone provoked no chromosomal aberrations in bone marrow cells of mice, but induced dominant lethal mutations in sexual cells of males in the stages of early spermatids and spermatocytes. This was established from increased preimplantation lethality weeks 3, 4 and 5 and from postimplantation embryonic lethality weeks 3, 5 and 6 after the experiment was started.
Maganova NB et al; Vopr Pitan (4): 63-5 (1980)

12.1.6 Populations at Special Risk

Anabolic steroids should be used with caution in children and adolescents and only by specialists who are aware of their effects on bone maturation because of possible premature epiphyseal closure, precocious sexual development in males, and virilization in females. The epiphyseal maturation may be accelerated more rapidly than linear growth in children, and the effect may continue for 6 months after the medication has been discontinued. /Anabolic Steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
Anabolic steroids are not recommended for use during pregnancy, since studies in animals have shown that anabolic steroids cause masculinization of the fetus. Risk-benefit must be carefully considered. /Anabolic steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141
Anabolic steroids may decrease blood glucose concentrations; diabetic patients should be closely monitored for signs of hypoglycemia and dosage of hypoglycemic agent adjusted as necessary. /Anabolic steroids/
Thomson.Micromedex. Drug Information for the Health Care Professional. 25th ed. Volume 1. Plus Updates. Content Reviewed by the United States Pharmacopeial Convention, Inc. Greenwood Village, CO. 2005., p. 141

12.2 Ecological Information

12.2.1 Environmental Fate / Exposure Summary

Methandrostenolone's production and use as an anabolic steroid and possible methandrostenolone use as a performance enhancement drug in athletes may result in its release to the environment through various waste streams. If released to air, an estimated vapor pressure of 1.2X10-8 mm Hg at 25 °C indicates methandrostenolone will exist solely in the particulate phase in the atmosphere. Particulate-phase methandrostenolone will be removed from the atmosphere by wet and dry deposition. Methandrostenolone does not absorb light at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight. If released to soil, methandrostenolone is expected to have slight mobility based upon an estimated Koc of 2,100. Volatilization from water or moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 2.2X10-9 atm-cu m/mole. Methandrostenolone is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation data were not available. If released into water, methandrostenolone is expected to adsorb to suspended solids and sediment based upon the estimated Koc. An estimated BCF of 100 suggests the potential for bioconcentration in aquatic organisms is high. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Occupational exposure to methandrostenolone may occur through dermal contact with this compound at workplaces where methandrostenolone is produced or used. Exposure to the drug among the general population may be limited to those taking methandrostenolone (an anabolic steroid). Intentional human exposure may have occurred from possible methandrostenolone use as a performance enhancement drug in athletes. (SRC)

12.2.2 Artificial Pollution Sources

Methandrostenolone's production and use as an anabolic steroid(1) and possible use as a performance enhancement drug in athletes(2) may result in its release to the environment through various waste streams(SRC).
(1) O'Neil MJ, ed; The Merck Index. 13th ed. Whitehouse Station, NJ: Merck and Co., Inc. p. 1064 (2001)
(2) Donahue JL, Lowenthal DT; Am J Ther 7: 365-73 (2000)

12.2.3 Environmental Fate

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 2,100(SRC), determined from a structure estimation method(2), indicates that methandrostenolone is expected to have slight mobility in soil(SRC). Volatilization of methandrostenolone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.2X10-9 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Methandrostenolone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.2X10-8 mm Hg(SRC), determined from a fragment constant method(4). Biodegradation data were not available(SRC, 2005).
(1) Swann RL et al; Res Rev 85: 17-28 (1983)
(2) Meylan WM et al; Environ Sci Technol 26: 1560-67 (1992)
(3) Meylan WM, Howard PH; Environ Toxicol Chem 10: 1283-93 (1991)
(4) Lyman WJ; p. 31 in Environmental Exposure From Chemicals Vol I, Neely WB, Blau GE, eds, Boca Raton, FL: CRC Press (1985)
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 2,100(SRC), determined from a structure estimation method(2), indicates that methandrostenolone is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.2X10-9 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 100(SRC), from an estimated log Kow of 3.5 (6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is high(SRC). Biodegradation data were not available(SRC, 2005).
(1) Swann RL et al; Res Rev 85: 17-28 (1983)
(2) Meylan WM et al; Environ Sci Technol 26: 1560-67 (1992)
(3) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 4-9, 15-1 to 15-29 (1990)
(4) Meylan WM, Howard PH; Environ Toxicol Chem 10: 1283-93 (1991)
(5) Franke C et al; Chemosphere 29: 1501-14 (1994)
(6) Meylan WM, Howard PH; J Pharm Sci 84: 83-92 (1995)
(7) Meylan WM et al; Environ Toxicol Chem 18: 664-72 (1999)
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), methandrostenolone, which has an estimated vapor pressure of 1.2X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase methandrostenolone may be removed from the air by wet and dry deposition(SRC). Methandrostenolone does not absorb light at wavelengths >290 nm(3) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).
(1) Bidleman TF; Environ Sci Technol 22: 361-367 (1988)
(2) Lyman WJ; p. 31 in Environmental Exposure From Chemicals Vol I, Neely WB, Blau GE, eds, Boca Raton, FL: CRC Press (1985)
(3) O'Neil MJ, ed; The Merck Index. 13th ed. Whitehouse Station, NJ: Merck and Co., Inc. p. 1064 (2001)

12.2.4 Environmental Abiotic Degradation

Methandrostenolone is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(1). Methandrostenolone does not absorb light at wavelengths >290 nm(2) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).
(1) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 7-4, 7-5 (1990)
(2) O'Neil MJ, ed; The Merck Index. 13th ed. Whitehouse Station, NJ: Merck and Co., Inc. p. 1064 (2001)

12.2.5 Environmental Bioconcentration

An estimated BCF of 100 was calculated for methandrostenolone(SRC), using an estimated log Kow of 3.5(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is high(SRC), provided the compound is not metabolized by the organism(SRC).
(1) Meylan WM, Howard PH; J Pharm Sci 84: 83-92 (1995)
(2) Meylan WM et al; Environ Toxicol Chem 18: 664-72 (1999)
(3) Franke C et al; Chemosphere 29: 1501-14 (1994)

12.2.6 Soil Adsorption / Mobility

Using a structure estimation method based on molecular connectivity indices(1), the Koc of methandrostenolone can be estimated to be 2,100(SRC). According to a classification scheme(2), this estimated Koc value suggests that methandrostenolone is expected to have slight mobility in soil.
(1) Meylan WM et al; Environ Sci Technol 26: 1560-67 (1992)
(2) Swann RL et al; Res Rev 85: 17-28 (1983)

12.2.7 Volatilization from Water / Soil

The Henry's Law constant for methandrostenolone is estimated as 2.2X10-9 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that methandrostenolone is expected to be essentially nonvolatile from moist soil (SRC) and water surfaces(2). Methandrostenolone is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.2X10-8 mm Hg(SRC), determined from a fragment constant method(3).
(1) Meylan WM, Howard PH; Environ Toxicol Chem 10: 1283-93 (1991)
(2) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 15-1 to 15-29 (1990)
(3) Lyman WJ; p. 31 in Environmental Exposure From Chemicals Vol I, Neely WB, Blau GE, eds, Boca Raton, FL: CRC Press (1985)

12.2.8 Probable Routes of Human Exposure

Occupational exposure to methandrostenolone may occur through dermal contact with this compound at workplaces where methandrostenolone is produced or used(SRC). Exposure to the drug among the general population may be limited to those taking methandrostenolone (an anabolic steroid)(SRC). Intentional human exposure may have occurred from methandrostenolone use as a possible performance enhancement drug in athletes(1).
(1) Donahue JL, Lowenthal DT; Am J Ther 7: 365-73 (2000)

13 Associated Disorders and Diseases

14 Literature

14.1 Consolidated References

14.2 NLM Curated PubMed Citations

14.3 Springer Nature References

14.4 Thieme References

14.5 Chemical Co-Occurrences in Literature

14.6 Chemical-Gene Co-Occurrences in Literature

14.7 Chemical-Disease Co-Occurrences in Literature

15 Patents

15.1 Depositor-Supplied Patent Identifiers

15.2 WIPO PATENTSCOPE

15.3 Chemical Co-Occurrences in Patents

15.4 Chemical-Disease Co-Occurrences in Patents

15.5 Chemical-Gene Co-Occurrences in Patents

16 Interactions and Pathways

16.1 Chemical-Target Interactions

17 Biological Test Results

17.1 BioAssay Results

18 Classification

18.1 MeSH Tree

18.2 NCI Thesaurus Tree

18.3 ChEBI Ontology

18.4 LIPID MAPS Classification

18.5 KEGG: ATC

18.6 KEGG: Target-based Classification of Drugs

18.7 KEGG: Drug Groups

18.8 WHO ATC Classification System

18.9 ChemIDplus

18.10 UN GHS Classification

18.11 EPA CPDat Classification

18.12 NORMAN Suspect List Exchange Classification

18.13 EPA DSSTox Classification

18.14 MolGenie Organic Chemistry Ontology

19 Information Sources

  1. CAS Common Chemistry
    LICENSE
    The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc/4.0/
  2. ChemIDplus
    ChemIDplus Chemical Information Classification
    https://pubchem.ncbi.nlm.nih.gov/source/ChemIDplus
  3. DrugBank
    LICENSE
    Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode)
    https://www.drugbank.ca/legal/terms_of_use
  4. DTP/NCI
    LICENSE
    Unless otherwise indicated, all text within NCI products is free of copyright and may be reused without our permission. Credit the National Cancer Institute as the source.
    https://www.cancer.gov/policies/copyright-reuse
  5. EPA DSSTox
    CompTox Chemicals Dashboard Chemical Lists
    https://comptox.epa.gov/dashboard/chemical-lists/
  6. European Chemicals Agency (ECHA)
    LICENSE
    Use of the information, documents and data from the ECHA website is subject to the terms and conditions of this Legal Notice, and subject to other binding limitations provided for under applicable law, the information, documents and data made available on the ECHA website may be reproduced, distributed and/or used, totally or in part, for non-commercial purposes provided that ECHA is acknowledged as the source: "Source: European Chemicals Agency, http://echa.europa.eu/". Such acknowledgement must be included in each copy of the material. ECHA permits and encourages organisations and individuals to create links to the ECHA website under the following cumulative conditions: Links can only be made to webpages that provide a link to the Legal Notice page.
    https://echa.europa.eu/web/guest/legal-notice
  7. FDA Global Substance Registration System (GSRS)
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  8. Hazardous Substances Data Bank (HSDB)
  9. Human Metabolome Database (HMDB)
    LICENSE
    HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications.
    http://www.hmdb.ca/citing
  10. ChEBI
  11. Open Targets
    LICENSE
    Datasets generated by the Open Targets Platform are freely available for download.
    https://platform-docs.opentargets.org/licence
  12. ChEMBL
    LICENSE
    Access to the web interface of ChEMBL is made under the EBI's Terms of Use (http://www.ebi.ac.uk/Information/termsofuse.html). The ChEMBL data is made available on a Creative Commons Attribution-Share Alike 3.0 Unported License (http://creativecommons.org/licenses/by-sa/3.0/).
    http://www.ebi.ac.uk/Information/termsofuse.html
  13. Comparative Toxicogenomics Database (CTD)
    LICENSE
    It is to be used only for research and educational purposes. Any reproduction or use for commercial purpose is prohibited without the prior express written permission of NC State University.
    http://ctdbase.org/about/legal.jsp
  14. EPA Chemical and Products Database (CPDat)
  15. Japan Chemical Substance Dictionary (Nikkaji)
  16. KEGG
    LICENSE
    Academic users may freely use the KEGG website. Non-academic use of KEGG generally requires a commercial license
    https://www.kegg.jp/kegg/legal.html
    Anatomical Therapeutic Chemical (ATC) classification
    http://www.genome.jp/kegg-bin/get_htext?br08303.keg
    Target-based classification of drugs
    http://www.genome.jp/kegg-bin/get_htext?br08310.keg
  17. LIPID MAPS
    Lipid Classification
    https://www.lipidmaps.org/
  18. MassBank Europe
  19. Metabolomics Workbench
  20. NCI Thesaurus (NCIt)
    LICENSE
    Unless otherwise indicated, all text within NCI products is free of copyright and may be reused without our permission. Credit the National Cancer Institute as the source.
    https://www.cancer.gov/policies/copyright-reuse
  21. NIST Mass Spectrometry Data Center
    LICENSE
    Data covered by the Standard Reference Data Act of 1968 as amended.
    https://www.nist.gov/srd/public-law
    Androsta-1,4-dien-3-one, 17-hydroxy-17-methyl-, (17.alpha.)-
    http://www.nist.gov/srd/nist1a.cfm
  22. SpectraBase
    METANDIENONE;17-BETA-HYDROXY-17-ALPHA-METHYL-ANDROSTA-1,4-DIEN-3-ONE
    https://spectrabase.com/spectrum/Bbiqxp9wlHU
    17beta-Hydroxy-17-methylandrosta-1,4-dien-3-one
    https://spectrabase.com/spectrum/5l2PcBA1lxH
  23. NORMAN Suspect List Exchange
    LICENSE
    Data: CC-BY 4.0; Code (hosted by ECI, LCSB): Artistic-2.0
    https://creativecommons.org/licenses/by/4.0/
    Methandrostenolone
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  24. Springer Nature
  25. SpringerMaterials
    (8R,10R,13S,17S)-17-Hydroxy-10,13,17-trimethyl-6,7,8,9,10,11,12,13,14,15,16,17-dodecahydro-cyclopenta[a]phenanthren-3-one
    https://materials.springer.com/substanceprofile/docs/smsid_rksyoppwzsdjyomv
  26. The Cambridge Structural Database
  27. Thieme Chemistry
    LICENSE
    The Thieme Chemistry contribution within PubChem is provided under a CC-BY-NC-ND 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc-nd/4.0/
  28. WHO Anatomical Therapeutic Chemical (ATC) Classification
    LICENSE
    Use of all or parts of the material requires reference to the WHO Collaborating Centre for Drug Statistics Methodology. Copying and distribution for commercial purposes is not allowed. Changing or manipulating the material is not allowed.
    https://www.whocc.no/copyright_disclaimer/
  29. Wikidata
  30. Wikipedia
  31. Medical Subject Headings (MeSH)
    LICENSE
    Works produced by the U.S. government are not subject to copyright protection in the United States. Any such works found on National Library of Medicine (NLM) Web sites may be freely used or reproduced without permission in the U.S.
    https://www.nlm.nih.gov/copyright.html
  32. PubChem
  33. GHS Classification (UNECE)
  34. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
  35. PATENTSCOPE (WIPO)
  36. NCBI
CONTENTS