The structure of cyclocreatine is fairly flat (planar), which aids in passive diffusion across membranes. It has been used with success in an animal study, where mice suffered from a SLC6A8 (creatine transporter at the blood brain barrier) deficiency, which is not responsive to standard creatine supplementation.  This study failed to report increases in creatine stores in the brain, but noted a reduction of mental retardation associated with increased cyclocreatine and phosphorylated cyclocreatine storages.  As demonstrated by this animal study and previous ones, cyclocreatine is bioactive after oral ingestion   and may merely be a creatine mimetic, able to phosphorylate ADP via the creatine kinase system. 
When tested in vitro , 7-keto appears to activate the beta subset of the estrogen receptor (ERβ) with an EC 50 around 500μM which is partially blocked by exemestane (aromatase inhibitor or AI); there was no apparent activity on the classical subset (ERα) and parent DHEA and DHEAS were eqipotent.  As activity was hindered with an AI and there was efficacy in HepG2 cells but not Hep293 (expressing  and not expressing  aromatase, respectively) it is though that 7-oxo can be metabolized into an estrogen. 
It is also important for the reader to know and understand that excessive doses of anabolic steroids are absolutely unnecessary for the preservation of muscle during T3 use. A total weekly anabolic steroid use of 300 – 500mg per week (any anabolic steroid) should be more than sufficient for the preservation of muscle and the retention of nitrogen during the use of higher T3 doses. Stronger anabolic steroids such as Trenbolone or Winstrol will stave off muscle loss from T3 at only 200mg per week. The use of excessive anabolic steroid doses merely for the purpose of muscle preservation during T3 use is completely unnecessary.