RESEARCH MONOGRAPH · KDC-MN-389

Oxandrolone

May 9, 2026 Kodiac biolabs Research Revised May 30, 2026 2 min read

Our opinion on this compound

67/100

The mildest 17-alpha-alkylated AAS with surprisingly good clinical burn and wasting data

Oxandrolone is the unusual entry in the 17-alpha-alkylated AAS class. The methyl group at the 17-alpha position confers oral bioavailability (the standard alkylation trick that prevents first-pass conjugation), but oxandrolone is unusually mild on hepatic markers compared to stanozolol or methyltestosterone. Why exactly is still debated; the 2-oxa substitution in the A-ring (which is what 'ox' indicates in the name) seems to shift metabolism away from the more hepatotoxic pathways.

The clinical evidence is actually solid for an AAS. The Demling, Wolfe, and Sheffield-Moore work on severe burn patients showed accelerated lean mass recovery and wound healing at 10 to 20 mg/day. The Hart trials in pediatric burn patients (where it's been used for decades) are some of the better-designed AAS clinical trials in the literature. The Schroeder HIV-wasting work in the 1990s was also clean. Real anabolic effect, modest virilization, mild lipid changes.

What we like for research is that oxandrolone is one of the more interpretable AAS for asking clean anabolism-versus-androgenicity questions. The myotrophic-to-androgenic ratio (the Hershberger assay number, though that assay has its own limitations) is high. Affinity at AR is moderate, but the binding doesnt fully account for the in vivo profile, so there's likely some non-genomic or tissue-distribution story we don't fully understand.

What we don't like is the hepatic safety profile, even though it's mild for the class. 17-alpha-alkylation is still an alkylation, and the literature has plenty of case reports of cholestasis and peliosis in patients on chronic oxandrolone. The Sheffield-Moore work used short courses precisely to avoid this.

The clinical pediatric use in Turner syndrome growth retardation is the other interesting indication, with FDA approval in that space dating back decades, more cautious than enthusiastic but documented.

Sourcing for research is regulated, oxandrolone is Schedule III in the US and equivalent elsewhere. Pharmaceutical reference standards are available, HPLC purity reliable. The black-market and athletic supplement adulteration problem is very real, so trust matters more here than for most compounds.

Evidence: 78
Mechanism: 80
Reliability: 78
Safety: 55
Sourcing: 55
Value: 55
Signal: 70
Staying power: 65

Plain-language summary Intrigue 55 / 100

Oxandrolone (Anavar, Oxandrin) is a synthetic anabolic steroid developed by Searle in 1962. The 17-alpha-alkylation makes it orally active by blocking liver breakdown, and the 2-oxa substitution shifts the profile toward anabolic (muscle-building) over androgenic (masculinizing) effects in standard assays. FDA-approved for severe weight loss after surgery, trauma, infection, or chronic illness, plus bone pain in osteoporosis. Burn recovery is the cleanest clinical use case, where AAS protocols have solid evidence. HIV wasting is another approved indication. In the gym world it is one of the most commonly diverted oral AAS because users perceive a relatively favorable side-effect profile. Schedule III. Hepatotoxic at high doses owing to the alkylation. Reference 17-alpha-alkylated oral AAS. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

17-alpha-alkylated oral anabolic steroid

A 17-alpha-alkylated synthetic anabolic steroid; clinically used in burn recovery and HIV wasting; widely used in non-medical AAS contexts.

Abstract

Oxandrolone (17-beta-hydroxy-17-alpha-methyl-2-oxa-5-alpha-androstan-3-one; CAS 53-39-4; molecular formula C19H30O3; molecular weight 306.44) is a 17-alpha-alkylated synthetic anabolic-androgenic steroid (AAS) developed by Searle in 1962 and approved by the FDA (Anavar, Oxandrin) for severe weight loss following surgery, trauma, infection, or chronic illness; for relief of bone pain in osteoporosis; and for compensation of catabolic states. Mechanism: AR agonism (lower than testosterone but with relatively higher anabolic-to-androgenic ratio in the Hershberger assay). The 2-oxa substitution and 17-alpha alkylation produce oral activity (resistance to first-pass hepatic metabolism) and a more anabolic profile relative to androgenic. Plasma half-life is approximately 9 hours. Schedule III in the US under the CSA. Used in burn recovery (where AAS clinical use is well-established) and in HIV wasting; the most commonly diverted oral AAS for non-medical bodybuilding owing to a perceived favorable side effect profile. Used as a reference 17-alpha-alkylated oral AAS in research.

Mechanism of action

17-alpha-alkylated oral anabolic-androgenic steroid; AR agonism with relatively favorable anabolic-to-androgenic ratio. Hepatotoxic at high doses owing to alkylation.

Reported research dose ranges

Reported research dose ranges vary across the published literature.

References

Wolfe RR, et al. Effects of oxandrolone on whole body protein synthesis. J Clin Endocrinol Metab 1995.
Berger JR, et al. Oxandrolone in AIDS-wasting myopathy. AIDS 1996.
Murad MH, et al. Drug-induced hepatotoxicity. Clin Liver Dis 2011.

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KDC-MN-389

The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

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Oxandrolone

Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

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Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

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