In a comparative study on 189 patients with adjustment disorder with anxiety, one group of patients took 150mg of Stresam daily for 28 days, while the other group took 2mg of Lorazepam (Ativan). The treatment efficiency was similar for both drugs regarding mean HAM-A score. However, more people from etifoxine group responded to the treatment by the day 28 (72% and 56%). The first group also experienced fewer side effects compared to lorazepam group and fewer cases of rebound anxiety. Similar results were obtained in the comparative study of Stresam with Alprazolam (Xanax).
Unlike benzodiazepines, etifoxine appears to produce its anxiolytic effects by activating β2 and β3 subunit containing channels of the GABA A receptor complex (a different binding site than benzodiazepines), and by stimulating the production of GABA(A) active neurosteroids that act in conjunction with etifoxine's direct effects.  This difference in binding means that etifoxine can be used alongside benzodiazepines to potentiate their effects without competing for binding sites;  however, it also means that the effects of etifoxine are not reversed by the benzodiazepine antagonist flumazenil . 
Benzodiazepines may influence neurosteroid metabolism by virtue of their actions on translocator protein (TSPO; "peripheral benzodiazepine receptor").  The pharmacological actions of benzodiazepines at the GABA A receptor are similar to those of neurosteroids . Factors which affect the ability of individual benzodiazepines to alter neurosteroid levels may depend upon whether the individual benzodiazepine drug interacts with TSPO. Some benzodiazepines may also inhibit neurosteroidogenic enzymes reducing neurosteroid synthesis.