All About Oxandrolone

Nelson Vergel

Thread starter #2

Oxandrolone is characterized by a modification in the basic structure of testosterone to include a substitution of an oxygen atom in place of the methylene group at the C2 position in the steroid ring, this molecule has a 17α-alkylated group at the C17 position that prevents deactivation of this steroid by hepatic first-pass metabolism - allowing for oral administration. Given these alterations, oxandrolone also shows resistance to hepatic metabolism further enhancing action [20]. While mild elevations in hepatic transaminases have been noted [45], oxandrolone is not known for significant hepatic side effects such as cholestasis, peliosis hepatis, hepatic adenomas, and hepatocellular carcinomas. Minor adverse events have been noted in clinical trials on oxandrolone including alterations in cholesterol levels [20].

Similar to nandrolone, oxandrolone has marked anabolic activity, with a myotrophic/androgenic ratio of 10:1 [46]. It has shown clinical efficacy in acute catabolic disorders such as severe burn injuries, after extensive surgery, and severe trauma. There have also been positive clinical outcomes in chronic catabolic disorders such as the treatment of HIV/AIDS-associated wasting [47], neuromuscular diseases such as Duchenne muscular dystrophy [48], amyotrophic lateral sclerosis [45], and COPD [49]. Oxandrolone is also used to offset the protein catabolism associated with long-term corticosteroid use and relief of the bone pain accompanying osteoporosis [20].

As with nandrolone, the reproductive effects of oxandrolone are not well studied. Several case reports note reversible steroid-induced azoospermia with oxandrolone use in combination with other AAS [50, 51]. Caution should be employed in all men of reproductive age given known effects on the LH/FSH axis and the potential resultant effects on spermatogenesis.

Source: Wu, C. & Kovac, J.R. Curr Urol Rep (2016) 17: 72.

Nelson Vergel

Thread starter #3

Oxandrolone was first described in 1962. It was developed into a medicine several years later by pharmaceutical giant G.D. Searle & Co. (now Pfizer), which sold it in the United States and the Netherlands under the Anavar trade name. Searle also sold/licensed the drug under different trade names including Lonavar (Argentina, Australia), Lipidex (Brazil), Antitriol (Spain), Anatrophill (France), and Protivar. Oxandrolone was designed to be an extremely mild oral anabolic, one that could even be used safely by women and children. In this regard Searle seems to have succeeded, as Anavar has shown a high degree of therapeutic success and tolerability in men, women, and children alike. During its early years, Anavar had been offered for a number of therapeutic applications, including the promotion of lean tissue growth during catabolic illness, the promotion of lean tissue growth following surgery, trauma, infection, or prolonged corticosteroid administration, or the support of bone density in patients with osteoporosis.

By the 1980's, the FDA had slightly refined the approved applications of Anavar to include the promotion of weight gain following surgery, chronic infection, trauma, or weight loss without definite pathophysiologic reason. In spite of its ongoing track record of safety, Searle decided to voluntarily discontinue the sale of Anavar on July 1, 1989. Lagging sales and growing public concern about the athletic use of anabolic steroids appeared to be at the root of this decision. With the Anavar brand off the market, oxandrolone had completely vanished from U.S. pharmacies. Soon after, oxandrolone products in international markets (often sold by or under license from Searle) began to disappear as well, as the leading global manufacturer of the drug continued its withdrawal from the anabolic steroid business. For several years during the early 1990's, it looked as if Anavar might be on its way out of commerce for good.

It would be approximately six years before oxandrolone tablets would be back on the U.S. market. The product returned to pharmacy shelves in December 1995, this time under the Oxandrin name by Bio-Technology General Corp. (BTG). BTG would continue selling it for the FDA approved uses involving lean mass preservation, but had also been granted orphan-drug status for the treatment of AIDS wasting, alcoholic hepatitis, Turner's syndrome in girls, and constitutional delay of growth and puberty in boys. Orphan drug status gave BTG a 7-year monopoly on the drug for these new uses, allowing them to protect a very high selling price. Many patients were outraged to learn that the drug would cost them (at wholesale price) between $3.75 and $30 per day, which was many times more costly than Anavar had been just several years back. The release of a 10 mg tablet from BTG several years later did little to reduce the relative cost of the drug.

Oxandrolone is an amazing compound. It is amazing how expensive the clinics have priced it. I've seen $15 per 50mg pressed tab from a US compounding pharmacy.
one thing that many athletes are unaware is that Oxandrolone causes lactic acid buildup in the muscle and so therefore if you cycle (bike) or do something repetitive in nature, you'll burn out quicker = no good.

Nelson Vergel

Thread starter #8
one thing that many athletes are unaware is that Oxandrolone causes lactic acid buildup in the muscle and so therefore if you cycle (bike) or do something repetitive in nature, you'll burn out quicker = no good.
I have seen nothing that supports your comment. Do you any references?
I have seen nothing that supports your comment. Do you any references?
If you collectively get enough athletes together that take Oxandrolone (Anavar) it is very common to hear about painful cramps, pumps, lactic acid buildup, however you want to describe it especially in the legs. No scientific studies supporting it that I am aware of. I've experienced it myself. It was also mentioned to me by a very high level athletic coach who coaches everyone from cyclists to Olympians.

Nelson Vergel

Thread starter #10
Oxandrolone lowers estradiol since it is a DHT analog. It can cause tendon and body aches due to this issue.
"Oxandrolone is a synthetic androstane steroid and a 17α-alkylated derivative of DHT.[28][29][4] It is also known as 2-oxa-17α-methyl-5α-dihydrotestosterone (2-oxa-17α-methyl-DHT) or as 2-oxa-17α-methyl-5α-androstan-17β-ol-3-one, and is DHT with a methyl group at the C17α position and the C2 carbon replaced with an oxygen atom.[28][29][4] "

The effect of estrogen on tendon and ligament metabolism and function

J Clin Endocrinol Metab. 2002 Apr;87(4):1467-72.
The effects of transdermal dihydrotestosterone in the aging male: a prospective, randomized, double blind study.

The objective of the study was to investigate the effects of dihydrotestosterone (DHT) gel on general well-being, sexual function, and the prostate in aging men. A total of 120 men participated in this randomized, placebo-controlled study (60 DHT and 60 placebo). All subjects had nocturnal penile tumescence once per week or less, andropause symptoms, and a serum T level of 15 nmol/liter or less and/or a serum SHBG level greater than 30 nmol/liter. The mean age was 58 yr (range, 50-70 yr). Of these subjects, 114 men completed the study. DHT was administered transdermally for 6 months, and the dose varied from 125-250 mg/d. General well-being symptoms and sexual function were evaluated using a questionnaire, and prostate symptoms were evaluated using the International Prostate Symptoms Score, transrectal ultrasonography, and assay of serum prostate-specific antigen. Early morning erections improved transiently in the DHT group at 3 months of treatment (P < 0.003), and the ability to maintain erection improved in the DHT group compared with the placebo group (P < 0.04). No significant changes were observed in general well-being between the placebo and the DHT group. Serum concentrations of LH, FSH, E2, T, and SHBG decreased significantly during DHT treatment. Treatment with DHT did not affect liver function or the lipid profile. Hemoglobin concentrations increased from 146.0 +/- 8.2 to 154.8 +/- 11.4 g/liter, and hematocrit from 43.5 +/- 2.5% to 45.8 +/- 3.4% (P < 0.001). Prostate weight and prostate-specific antigen levels did not change during the treatment. No major adverse events were observed. Transdermal administration of DHT improves sexual function and may be a useful alternative for androgen replacement. As estrogens are thought to play a role in the pathogenesis of prostate hyperplasia, DHT may be beneficial, compared with aromatizing androgens, in the treatment of aging men.