Racemic phenibut (beta-phenyl-gamma-aminobutyric acid or 4-amino-3-phenylbutyric acid) is a neuropsychotropic drug that was discovered and introduced into clinical practice in Russia in the 1960s. In pharmacological tests of locomotor activity, antidepressant and pain effects, S-phenibut was inactive. In contrast, R-phenibut turned out to be two times more potent than racemic phenibut in most of the tests. Racemic phenibut and R-phenibut demonstrated an affinity for GABAB receptors, in contrast, S-phenibut was not able to bind receptors. Pharmacological activity of racemic phenibut relies on R-phenibut and this correlates to the binding affinity of enantiomers of phenibut to the GABAB receptor. Both S- and R-phenibut bind to the α2-δ subunit of voltage-dependent calcium channels and exert gabapentin-like anti-nociceptive effects. In addition S-isomer was found to be a substrate of gamma-aminobutyric acid aminotransferase, however, the R-isomer is a competitive inhibitor.

Hecogenin acetate is the acetylated form of Hecogenin, a naturally occurring sapogenin present in the leaves of plants from the Agave genus. It has been found to have antinociceptive activity in mice and has also been investigated as an anti-cancer agent in vitro. Hecogenin appears to exert its anticancer influence by modulating the ERK1/2 signal cascade and activates opioid receptors to influence nocioception.