Chemically,<unk>  is a derivative of the neurotransmitter γ-aminobutyric acid (GABA). It is believed to work by activating (or agonizing) GABA receptors, specifically the GABAB receptors. Its beneficial effects in spasticity result from its actions in the brain and spinal cord. Pharmacodynamics<unk>  produces its effects by activating the GABAB receptor, similar to the drug phenibut which also activates this receptor and shares some of its effects.<unk>  is postulated to block mono-and-polysynaptic reflexes by acting as an inhibitory ligand, inhibiting the release of excitatory neurotransmitters. However,<unk>  does not have significant affinity for the GHB receptor, and has no known abuse potential. The modulation of the GABAB receptor is what produces<unk> 's range of therapeutic properties. Similarly to phenibut (β-phenyl-GABA), as well as pregabalin (β-isobutyl-GABA), which are close analogues of<unk> ,<unk>  (β-(4-chlorophenyl)-GABA) has been found to block α2δ subunit-containing voltage-gated calcium channels (VGCCs). However, it is weaker relative to phenibut in this action (Ki = 23 and 39 μM for R- and S-phenibut and 156 μM for<unk> . Moreover,<unk>  is in the range of 100-fold more potent by weight as an agonist of the GABAB receptor in comparison to phenibut, and in accordance, is used at far lower relative dosages. As such, the actions of<unk>  on α2δ subunit-containing VGCCs are likely not clinically-relevant. Pharmacokinetics The drug is rapidly absorbed after oral administration and is widely distributed throughout the body. Biotransformation is low: the drug is predominantly excreted unchanged by the kidneys. The half-life of<unk>  is roughly 2–4 hours; it therefore needs to be administered frequently throughout the day to control spasticity appropriately.
Baclofen
Spasmofen
Topiramate
Belinostat
Selegiline
Zonisamide
Felbamate
Rimonabant