The γ-aminobutyric acid aminotransferase (GABA-AT) is the enzyme responsible for GABA degradation in the brain. When the GABA levels fall to low, seizure can result. L-β-Chloroalanine hydroxamate is a time-dependent inactivator of GABA-AT, able to cross the blood-brain barrier and to delay the onset of drug-induced seizure. The mechanism of inactivation involves the buffer-catalyzed conversion of L-β-chloroalanine hydroxamate to cycloserine.