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| Trade names | Winstrol, Stromba, others[1] | ||
| Other names | Androstanazol; Androstanazole; Stanazol; WIN-14833; NSC-43193; NSC-233046; 17α-Methyl-2'H-5α-androst-2-eno[3,2-c]pyrazol-17β-ol; 17α-Methylpyrazolo[4',3':2,3]-5α-androstan-17β-ol | ||
| AHFS/Drugs.com | Multum Consumer Information | ||
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| Routes of administration | By mouth,intramuscular injection (veterinary)[2] | ||
| Drug class | Androgen;Anabolic steroid | ||
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| Pharmacokinetic data | |||
| Bioavailability | High[4] | ||
| Metabolism | Liver[6] | ||
| Eliminationhalf-life | Oral: 9 hours[5] IMTooltip Intramuscular injection: 24 hours (aq. susp.)[5][2] | ||
| Duration of action | IM: >1 week[6] | ||
| Excretion | Urine: 84%[citation needed] | ||
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| ECHA InfoCard | 100.030.801 | ||
| Chemical and physical data | |||
| Formula | C21H32N2O | ||
| Molar mass | 328.500 g·mol−1 | ||
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Stanozolol (abbrev.Stz), sold under many brand names, is asynthetic androgen andanabolic steroid (AAS) medication derived fromdihydrotestosterone (DHT). It is used to treathereditary angioedema.[7][1][8] It was developed by American pharmaceutical companySterling-Winthrop in 1962, and has been approved by the U.S.Food and Drug Administration for human use, though it is no longer marketed in the United States.[8][9] It is also used inveterinary medicine.[1][8] Stanozolol has mostly been discontinued, and remains available in only a few countries.[1][8] It is givenby mouth in humans or byinjection into muscle in animals.[8]
Unlike most AAS, stanozolol is notesterified and is sold as anaqueous suspension, or in oral tablet form.[8] The drug has a high oralbioavailability, due to a C17α alkylation which allows the hormone to survive first-passliver metabolism when ingested.[10][8] It is because of this that stanozolol is also sold intablet form.[8]
Stanozolol is one of the AAS commonly used asperformance-enhancing drugs and is banned from use insports competition under the auspices of theWorld Anti-Doping Agency (WADA). It is an anabolic steroid that is known to have a diuretic effect. Additionally, stanozolol has been highly restricted in UShorse racing.[11][12][13]
Stanozolol has been used with some success to treat venous insufficiency. It stimulates blood fibrinolysis and has been evaluated for the treatment of the more advanced skin changes in venous disease such as lipodermatosclerosis. Several randomized trials noted improvement in the area of lipodermatosclerosis, reduced skin thickness, and possibly faster ulcer healing rates with stanozolol.[14][15] It is also being studied to treat hereditary angioedema, osteoporosis, and skeletal muscle injury.[16][17]
Stanozolol is used forphysique- and performance-enhancing purposes bycompetitiveathletes,bodybuilders, andpowerlifters.[8]
Side effects of stanozolol includevirilization (masculinization),hepatotoxicity,[8]cardiovascular disease, andhypertension.
| Medication | Ratioa |
|---|---|
| Testosterone | ~1:1 |
| Androstanolone (DHT) | ~1:1 |
| Methyltestosterone | ~1:1 |
| Methandriol | ~1:1 |
| Fluoxymesterone | 1:1–1:15 |
| Metandienone | 1:1–1:8 |
| Drostanolone | 1:3–1:4 |
| Metenolone | 1:2–1:3 |
| Oxymetholone | 1:2–1:9 |
| Oxandrolone | 1:13–1:3 |
| Stanozolol | 1:1–1:3 |
| Nandrolone | 1:3–1:16 |
| Ethylestrenol | 1:2–1:19 |
| Norethandrolone | 1:1–1:2 |
| Notes: In rodents.Footnotes:a = Ratio of androgenic to anabolic activity.Sources: See template. | |
As an AAS, stanozolol is anagonist of theandrogen receptor (AR), similarly toandrogens liketestosterone and DHT.[8][18] Itsaffinity for the androgen receptor is about 22% of that ofdihydrotestosterone.[19] Stanozolol is not asubstrate for5α-reductase as it is already 5α-reduced, and so is not potentiated in so-called "androgenic" tissues like theskin,hair follicles, andprostate gland.[8][18] This results in a greater ratio ofanabolic toandrogenic activity compared totestosterone.[8][18] In addition, due to its 5α-reduced nature, stanozolol is non-aromatizable, and hence has no propensity for producingestrogenic effects such asgynecomastia orfluid retention.[8][18] Stanozolol also does not possess anyprogestogenic activity of significance.[8][18] Because of the presence of its 17α-methyl group, themetabolism of stanozolol issterically hindered, resulting in it beingorally active, although alsohepatotoxic.[8][18]
In addition to classical AR signaling,in-vitro work with mesenchymal stem-cell micromass cultures shows that stanozolol:
Pharmacological blockade of either PR (mifepristone) or COX-2 (indomethacin) abolishes these effects, confirming that stanozolol’s osteochondral activity requires simultaneous PR signaling and PGE₂-driven crosstalk with the BMP2 pathway.[20]
Additionally, stanozolol has been shown to exert activity via estrogen receptor alpha (ERα) in vivo. In a rat model of GnRH agonist-induced growth plate suppression, stanozolol restored chondrocyte proliferation via ERα activation, indicating selective estrogen receptor-mediated effects in growth plate cartilage.[21]
Stanozolol has highoralbioavailability, due to the presence of itsC17α alkyl group and the resistance togastrointestinal andlivermetabolism that it results in.[4][22][23] The medication has very lowaffinity for human serumsex hormone-binding globulin (SHBG), about 5% of that of testosterone and 1% of that of DHT.[24] Stanozolol ismetabolized in theliver, ultimately becomingglucuronide andsulfateconjugates.[6] Itsbiological half-life is reported to be 9 hours whentaken by mouth and 24 hours when given byintramuscular injection in the form of anaqueous suspension.[5][2] It is said to have aduration of action of one week or more via intramuscular injection.[6]
Stanozolol, also known as 17α-methyl-2'H-androst-2-eno[3,2-c]pyrazol-17β-ol, is asynthetic17α-alkylatedandrostanesteroid and aderivative of5α-dihydrotestosterone (DHT) with amethyl group at the C17α position and apyrazolering attached to the A ring of the steroid nucleus.[7]
Variouschemical syntheses of stanozolol have been published.[25]
Stanozolol is subject to extensive hepatic biotransformation by a variety of enzymatic pathways. The primary metabolites are unique to stanozolol and are detectable in the urine for up to 10 days after a single 5–10 mg oral dose. Methods for detection in urine specimens usually involve gas chromatography-mass spectrometry or liquid chromatography-mass spectrometry.[26][27][28]
In 1962, Stanozolol was brought to market in the US byWinthrop under the tradename "Winstrol" and in Europe by Winthrop's partner,Bayer, under the name "Stromba".[29]
Also in 1962, theKefauver Harris Amendment was passed, amending theFederal Food, Drug, and Cosmetic Act to require drug manufacturers to provide proof of the effectiveness of their drugs before approval.[30] The FDA implemented itsDrug Efficacy Study Implementation (DESI) program to study and regulate drugs, including stanozolol, that had been introduced prior to the amendment. The DESI program was intended to classify all pre-1962 drugs that were already on the market as effective, ineffective, or needing further study.[31] The FDA enlisted theNational Research Council of theNational Academy of Sciences to evaluate publications on relevant drugs under the DESI program.[32]
In June 1970 the FDA announced its conclusions on the effectiveness of certain AAS, including stanozolol, based on the NAS/NRC reports made under DESI. The drugs were classified as probably effective as adjunctive therapy in the treatment of senile and postmenopausalosteoporosis but only as an adjunct, and inpituitary dwarfism (with a specific caveat for dwarfism, "until growth hormone is more available"), and as lacking substantial evidence of effectiveness for several other indications. Specifically, the FDA found a lack of efficacy for stanozolol as "an adjunct to promote body tissue-building processes and to reverse tissue-depleting processes in such conditions as malignant diseases and chronic nonmalignant diseases; debility in elderly patients, and other emaciating diseases; gastrointestinal disorders resulting in alterations of normal metabolism; use during pre-operative and postoperative periods in undernourished patients and poor-risk surgical cases due to traumatism; use in infants, children, and adolescents who do not reach an adequate weight; supportive treatment to help restore or maintain a favorable metabolic balance, as in postsurgical, postinfectious, and convalescent patients; of value in pre- operative patients who have lost tissue from a disease process or who have associated symptoms, such as anorexia; retention and utilization of calcium; surgical applications; gastrointestinal disease, malnourished adults, and chronic illness; pediatric nutritional problems; prostatic carcinoma; and endocrine deficiencies."[33] The FDA gave Sterling six months to stop marketing stanozolol for the indications for which there was no evidence for efficacy, and one year to submit further data for the two indications for which it found probable efficacy.[33]
In August and September 1970, Sterling submitted more data; the data was not sufficient but the FDA allowed the drug to continue to be marketed, since there was an unmet need for drugs for osteoporosis and pituitary dwarfism, but Sterling was required to submit more data.[34]
In 1980 the FDA removed the dwarfism indication from the label for stanozolol sincehuman growth hormone drugs had come on the market, and mandated that the label for stanozolol and other steroids say: "As adjunctive therapy in senile and postmenopausal osteoporosis. AAS are without value as primary therapy but may be of value as adjunctive therapy. Equal or greater consideration should be given to diet, calcium balance, physiotherapy, and good general health promoting measures." and gave Sterling a timeline to submit further data for other indications it wanted for the drug.[35] Sterling submitted data to the FDA intended to support the effectiveness of Winstrol for postmenopausal osteoporosis andaplastic anemia in December, 1980 and August 1983 respectively. The FDA's Endocrinologic and Metabolic Drugs Advisory Committee considered the data submitted for osteoporosis in two meetings held 1981 and the data foraplastic anemia in 1983.[34]
In April 1984, the FDA announced that the data was not sufficient, and withdrew the marketing authority for stanozolol for senile and postmenopausal osteoporosis and for raising hemoglobin levels in aplastic anemia.[34][36]
In 1988, Sterling was acquired byEastman Kodak for $5.1 billion and in 1994 Kodak sold the drug business of Sterling toSanofi for $1.675 billion.[37][38]
Sanofi had stanozolol manufactured in the US bySearle, which stopped making the drug in October 2002.[39] Even with no drug in production, Sanofi sold the stanozolol business toOvation Pharmaceuticals in 2003, along with the two other drugs.[40] At that time, the drug had not been discontinued and was considered a treatment forhereditary angioedema.[40] In March 2009, Lundbeck purchased Ovation[41]
In 2010, Lundbeck withdrew stanozolol from the market in the US; as of 2014 no other company is marketing stanozolol as a pharmaceutical drug in the US but it can be obtained via acompounding pharmacy.[42][43][44][45]
Pfizer had marketed stanozolol as a veterinary drug; in 2013 Pfizer spun off its veterinary business toZoetis[46] and in 2014 Pfizer transferred the authorizations to market injectable and tablet forms of stanozolol as a veterinary drug to Zoetis.[47][48]
It is used in veterinary medicine as an adjunct in the management of wasting diseases, to stimulate theformation of red blood cells, arouse appetite, and promote weight gain, but the evidence for these uses is weak. It is used as a performance-enhancing drug in race horses. Its side effects include weight gain, water retention, anddifficulty eliminating nitrogen-based waste products and it is toxic to the liver, especially in cats. Because it may promote the growth of tumors, it is contraindicated in dogs with enlarged prostates.[49]: 730–371
Stanozolol and other AAS were commonly used to treathereditary angioedema attacks, until several drugs were brought to market specifically for treatment of that disease, the first in 2009:Cinryze,Berinert,ecallantide (Kalbitor),icatibant (Firazyr) andRuconest.[44][45] Stanozolol is still used long-term to reduce the frequency of severity of attacks.[50]
Stanozolol is thegeneric name of stanozolol inEnglish,German,French, andJapanese and itsINNTooltip International Nonproprietary Name,USANTooltip United States Adopted Name,USPTooltip United States Pharmacopeia,BANTooltip British Approved Name,DCFTooltip Dénomination Commune Française, andJANTooltip Japanese Accepted Name, whilestanozololum is its name inLatin,stanozololo is its name inItalian and itsDCITTooltip Denominazione Comune Italiana, andestanozolol is its name inSpanish.[7][51][1]Androstanazole,androstanazol,stanazol,stanazolol, andestanazolol are unofficial synonyms of stanozolol.[7][1] It is also known by its former developmental code nameWIN-14833.[7][1][51]
Brand names under which stanozolol is or has been marketed include Anaysynth, Menabol, Neurabol Caps., Stanabolic (veterinary), Stanazol (veterinary), Stanol, Stanozolol, Stanztab, Stargate (veterinary), Stromba, Strombaject, Sungate (veterinary), Tevabolin, Winstrol, Winstrol Depot, and Winstrol-V (veterinary).[7][1]
 | The examples and perspective in this sectiondeal primarily with the United States and do not represent aworldwide view of the subject. You mayimprove this section, discuss the issue on thetalk page, or create a new section, as appropriate.(January 2012) (Learn how and when to remove this message) |
In theUnited States, like other AAS, stanozolol is classified as acontrolled substance under federal regulation; they were included asSchedule III controlled substances under theAnabolic Steroids Control Act of 1990 which was passed as part of theCrime Control Act of 1990.[52]: 30
Stanozolol and other synthetic steroids were first banned by theInternational Olympic Committee and theInternational Association of Athletics Federations in 1974, after methods to detect them had been developed.[53]: 716 There are many known cases ofdoping in sports with stanozolol byprofessionalathletes. Stanozolol is especially widely used by the athletes frompost-Soviet countries.[citation needed] As of 2015, it is banned byWorld Anti-Doping Agency[54] andUnited States Anti-Doping Agency.[55]
Stanozolol has been investigated in the treatment of a number ofdermatological conditions includingurticaria,hereditary angioedema,Raynaud's phenomenon,cryofibrinogenemia, andlipodermatosclerosis.[56]
The oral form is marketed for human use whereas an aqueous suspension for injection is used in the veterinary field.
This case is important as stanozolol misuse is relatively common, due to its high oral bioavailability and perceived safety profile compared with other parenteral AAS.
Androgenic compounds rendered resistant to gastrointestinal and liver metabolism by containing an alkyl group at the C17α position, such as stanozolol, are orally active.
Testosterone has low oral bioavailability with only about half of an oral dose available after hepatic first-pass metabolism. Some analogues of testosterone (e.g., methyltestosterone, fluoxymesterone, oxandrolone, and stanozolol) resist such metabolism, so they can be given orally in smaller doses.
