Oxandrolone

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Oxandrolone
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Clinical data
Pregnancy
category
  • X
Routes of
administration
Oral
ATC code
Legal status
Legal status
  • Prescription only (US)
Pharmacokinetic data
Bioavailability97%
MetabolismHepatic
Elimination half-life9 hour
ExcretionUrinary:90%; Fecal:6%
Identifiers
CAS Number
PubChem CID
DrugBank
E number{{#property:P628}}
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Chemical and physical data
FormulaC19H30O3
Molar mass306.44 g/mol

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Oxandrolone (Oxandrin) is an anabolic steroid created by Searle Laboratories under the trademark Anavar, and introduced into the US in 1964. It is taken orally, and unlike other steroids delivered in this manner, most of which are Class II steroids, the majority of its effects are due to reaction with the androgen receptor. In sufficient dosage, Oxandrolone is highly likely to bind well with the receptor, and is therefore a Class I steroid, while having few other side-effects.

As opposed to most other anabolic steroids Oxandrolone has two major advantages: First of all it does not aromatize (convert to estrogen which causes gynecomastia - breast tissue) and it does not significantly influence on low dosages (10mg) body's normal testosterone production (HPTA axis). When dosages are high (this goes for any anabolic steroid) then your body feels that it has enough testosterone and it reduces the production of LH (luteinizing hormone) which no longer stimulates Leydig cells in testicles to produce testosterone therefore causing testicular atrophy (shrinking). Post Cycle Therapy (PCT) is of course needed for high dosages (40-50mg) of this synthetic derivative of testosterone because as the dosage increases the influence on HPTA is bigger. Lack of PCT will of course lead to protein catabolism until body's normal testosterone secretion is back to normal.

The drug was prescribed for a number of medical disorders causing involuntary weight loss, in order to promote muscle regrowth. It had also been shown to be partially successful in treating cases of osteoporosis. However, in part due to bad publicity from its abuses by bodybuilders, Oxandrolone was discontinued by Searle Laboratories in 1989. It was picked up by Bio-Technology General Corporation, now Savient Pharmaceuticals, Inc. who, following successful clinical trials in 1995, released it under the tradename Oxandrin.

It was approved for orphan drug status by the Food and Drug Administration (FDA) in treating alcoholic hepatitis, Turner's syndrome, and weight loss caused by HIV. In addition, the drug has shown positive results in treating anaemia and hereditary angioedema. In a randomized, double-blind study, patients with 40% total body surface area burns were selected to receive standard burn care plus Oxandrolone, or without Oxandrolone. Those treated with Oxandrolone showed improve body composition, preserved muscle mass and reduced hospital stay time. [1] Other studies however have shown links between prolonged use of the drug and problems of liver toxicity similar to those found with other 17α-alkylated steroids. Even in small dosages, many users reported gastro-intestinal problems such as bloating, nausea, skin rash and itching (hives), black, tarry stools or light-colored stools, depression, unusual bleeding, unusual swelling, yellowing of the eyes or skin, and diarrhoea.

In rare cases, serious and even fatal cases of liver problems have developed during treatment with oxandrolone. Oxandrolone may increase the amount of low density lipoprotein (LDL; 'bad cholesterol') and decrease the amount of high density lipoprotein (HDL; 'good cholesterol') in the blood. This may increase the risk of developing heart disease. Oxandrolone may damage the liver or increase LDL without causing symptoms. It is important to have regular laboratory tests to be sure that the liver is working properly and that LDL has not increased. Oxandrolone may also decrease fertility in men.

Before the Controlled Substances Act was passed to restrict the production, sale, and usage of anabolic steroids, Oxandrolone's characteristics lent itself well towards use by female athletes. Its specificity targeting the androgen receptor meant that, unlike many other steroids, it had not been reported to cause stunted growth in younger users (because it doesn't convert to estrogen, thats the reason women typically don't grow as tall as men -- they have more estrogen) and at typical dosage rarely caused noticeable masculinising effects outside of stimulating muscle growth. It is not easily metabolised into DHT or estrogen. As such, a typical dose of 20-30 mg provided elevated androgen levels for up to eight hours. To increase effectiveness, bodybuilders typically "stacked" the drug with others such as Testosterone, further enhancing body mass gain.

Besides the obvious health risks (liver and coronary), the biggest problem with Oxandrolone (and with any anabolic steroid) is of course abuse and addiction without the supervision of a physician. Addiction rate for steroids is so high that the U.S. Controlled Substances Act considers anabolic steroids a Schedule III drug therefore even possession is a felony. Abuse being one major problem most bodybuilders consider a normal dose for a novice being 20-30mg's per day when in fact 10 mg is more then enough for someone who never had used. Higher dosages not only lead to AR (Androgen Receptor) damage and HPTA suppression but also damages the liver being a 17α-alkylated. It is specially made 17α-alkylated because if it would not be then the liver would consider it a toxin and would destroy it.

Since Searle stopped production, biggest sellers are La Pharma Italy and British Dragon Thailand. It is considered by the medical community the safest of all steroids in terms of side effects.

Further reading

References

  • "The Effects of Oxandrolone and Exercise on Muscle Mass and Function in Children With Severe Burns". Pediatrics. 119. 2006.
  • "Oxandrolone induced lean mass gain during recovery from severe burns is maintained after discontinuation of the anabolic steroid". Burns. 8. 2003.
  1. Shriners Burns Hospital for Children. The Effect of Oxandrolone On the Endocrinologic, Inflammatory and Hypermetabolic Responses During the Acute Phase Postburn. 2006. [1]

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