Most orally administered anabolic steroids function by having an alkylated 17α-carbon atom, which prevents first-pass metabolism by the liver.[5] This approach however results in the AAS having hepatotoxicity.[5] Quinbolone is not 17α-alkylated; instead it has increased oral bioavailability due to its cyclopentenyl ether group.[citation needed] After ingestion, the inactive quinbolone is transformed into boldenone.[1]
Quinbolone itself has very few androgenic effects, and most of what it does have are a result of its conversion to boldenone and its metabolites.[1][6][additional citation(s) needed] Because of high doses necessary for androgenic effects, cost and inconvenience meant that quinbolone never proved to be commercially successful, and its clinical applications were fulfilled by alternative, more effective, AAS.[citation needed] Its illicit usage in bodybuilding and athletics likewise proved limited, though drug tests are still used to detect its metabolites as it remains a banned substance for most competitive sports.[5]
Quinbolone, via boldenone, can be transformed into estrogens, and hence may have some estrogenic activity.[6]
Quinbolone can be prepared from testosterone. Dehydrogenation using DDQ forms boldenone. Reaction with 1,1-dimethoxycyclopentane followed by heating to eliminatemethanol gives quinbolone.
Quinbolone was described as early as 1962.[7] It was marketed in Italy by Parke-Davis.[3]
References
^ abcdGalletti F, Gardi R (July 1971). "Metabolism of 1-dehydroandrostanes in man. I. Metabolism of 17 -hydroxyandrosta-1,4-dien-3-one, 17 -cyclopent-1'-enyloxyandrosta-1,4-dien-3-one (quinbolone) and androsta-1,4-diene-3,17-dione (1)". Steroids. 18 (1): 39–50. doi:10.1016/s0039-128x(71)80169-1. PMID5098537.
