Quinbolone (Anabolicum Vister) is an anabolic steroid with weak androgenic effects. It was developed by Parke-Davis in an attempt to create a viable orally-administered anabolic steroid with little or no liver toxicity. The drug is atypical in that steroid molecules are usually only given officially distinct names when there is a permanent structural difference between the parent molecule and itself. Quinbolone, however, differs from its parent molecule (boldenone) solely by the addition of an easily removed cyclopentenyl ether group. Most orally administered anabolic steroids function by having an alkylated 17α-carbon atom, which prevents first-pass metabolism by the liver. This approach does, however, give the drug a high hepatotoxicity. Quinbolone is not 17α-alkylated; instead it has increased oral bioavailability due to its cyclopentenyl ether group. This allows the drug to be fully dissolved in an oil base, which is then absorbed into the lymphatic system via the large intestine, from which it travels into the blood. Once there the ester group detaches and the relatively inactive quinbolone becomes boldenone, which then reacts with the androgen receptor of any muscles it comes into contact with. 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. This, combined with its unusual route of absorption, provides the drug with highly variable results, meaning that large quantities of the drug (100-200 mg per day) must be taken in order to maintain high enough concentrations in the blood for noticeable and consistent effects. The cost and inconvenience of this meant that quinbolone never proved commercially successful, and its clinical applications were fulfilled by alternative, more effective, steroids. 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.