In the mid 1980s, the neuroactive steroids 3α,5α-tetrahydroprogesterone or allopregnanolone (3α,5α-THP) and 3α,5α- tetrahydrodeoxycorticosterone (3α,5α-THDOC) were shown to modulate neuronal excitability via their interaction with GABA A receptors. The steroids 3α,5α-THP and 3α,5α-THDOC were able to enhance the GABA-elicited Cl − current.  In addition, these steroids might enhance the binding of muscimol and benzodiazepines to GABA A receptors.  Structure- activity studies (SAR) showed that the 3alpha-OH group is essential for the anesthetic actions of these steroids,  they also have an optimally-placed hydrogen bond accepting group on the β face of the steroid at the C-17 position. The four steroid rings form a rigid framework for positioning these hydrogen groups in three-dimensional space.  Analogues 5 and 6 (Figure 10) are weak modulators of GABA A receptor function because the flexible side chains in these analogues do not have the conformations required for high biological activity. 
The pharmacological actions of benzodiazepines at the GABA A receptor are similar to those of neurosteroids . Neuroactive steroids are positive allosteric modulators of the GABA A receptor, enhancing GABA function and in turn have effects on mood and other functions. Many benzodiazepines ( diazepam , medazepam , estazolam , temazepam , flunitrazepam and nitrazepam) potently inhibit the enzymes involved in the metabolism of neurosteroids. The tetrahydroxazole ring that cloxazolam and oxazolam have decreases the inhibitory potency of benzodiazepines on neurosteroids. Thus there could be subtle differences between cloxazolam and other benzodiazepines.  However, because the parent prodrugs of cloxazolam and oxazolam were tested rather than the active metabolites, this is purely speculative.