As a drug, gabapentin was formerly considered as a structural analogue of the inhibitory neurotransmitter γ-aminobutyric acid (GABA). However, preliminary studies proposed that gabapentin did not bind to either GABA-A or GABA-B receptors, nor was it transform metabolically into GABA.
GBP also prevents voltage-dependent sodium currents. GBP is properly absorbed subsequent to the oral administration. GBP is not metabolized in human beings. It does not induce hepatic microsomal enzymes. It has no plasma protein binding and no interfaces with other drugs. GBP is more than 95% excreted unchanged in urine.
The anticonvulsant effect can be obtained fairly quickly. A three times in a day (TID) schedule has been advocated, but in patients in whom the drug has a long half-life, two times in a day (BID) administration perhaps is adequate. Pediatric subjects aged > 1 month and < 5 years attained ~ 30% less exposures than that experienced in those aged ≥ 5 years.
Nevertheless, in renally compromised patients, the half-life may be considerably longer. Since gabapentin is not bound to plasma proteins, there is no competition with other extremely protein-bound medications, for example phenytoin.
As well, the lack of hepatic metabolism or induction/inhibition of hepatic drug metabolizing enzyme systems (cytochrome P450) or uridinediphosphoglucuronyl transferase isozymes by gabapentin abolishes interactions with other hepatically cleared medications, for instance older AEDs. Adverse effects were commonly mild in intensity and included somnolence, dizziness, ataxia, nystagmus, diplopia, and tremor.