Unlike benzodiazepines,<unk>  may produce its anxiolytic effects through a dual mechanism, by directly binding to GABAA receptors and (purportedly, exact binding site undetermined) to the mitochondrial translocator protein (TSPO), resulting in increases in endogenous neurosteroids. At GABAA receptors<unk>  binds at the α+β− interface and preferentially potentiates α2β3γ2 and α3β3γ2 receptor types. This direct allosteric potentiation can only be observed at relatively high concentrations (starting at > 1 micromolar) and is perhaps not physiologically relevant at normal human doses. This is different from benzodiazepines and<unk>  can be used alongside benzodiazepines to potentiate their effects without competing for binding sites; however, it also means that the direct effects of<unk>  are not reversed by the benzodiazepine antagonist flumazenil.<unk>  stimulates the biosynthesis of endogenous neurosteroids, for example: allopregnanolone (3-alpha,5-alpha THP), a nanomolar potentiator of GABA activity.
Etifoxine
Quinine
Ipriflavone
Tuberculinic acid
Trenbolone hexahydrobenzylcarbonate
Artemether
Milbemycin oxime
Dimetacrine