Background:

Levetiracetam (LEV) is a newly developed antiepileptic drug (AED) with a broad spectrum of ef?cacy against partial and generalized seizures. [1]

The mode of action of LEV seems to be different from other AED. Synaptic vesicle protein 2A which can block calcium release from intraneuronal stores is shown to be the binding site of levetiracetam. Thus, it works against the negative modulators of gamma-aminobutyric acid and glycin-gated currents. Moreover, LEV does not have the ablility to induce cytochrome P450 isoenzyme.[2]

A study has shown that an oral dose of LEV can’t bind to plasma proteins, while no hepatic metabolism was observed. One-third of the metabolized drug was found to be hydrolyzed and the others were excreted unchanged in the urine.[3]

参考文献:
[1] Nabil J. Azar, Patsy Aune. Acute pancreatitis and elevated liver transaminases after rapid titration of oral levetiracetam. Journal of Clinical Neuroscience. June 2014. 21(6): 1053-1054.
[2] Xiao-Qiao Chen, Wei-Na Zhang, Zhi-Xian Yang, Meng Zhao, Fang-Cheng Cai, Shao-Ping Huang, Li Gao, Bao-Dong Pang, Xi Chen, Li-Ping Zou. Efficacy of Levetiracetam in Electrical Status Epilepticus During Sleep of Children: A Multicenter Experience. Pediatric Neurology. March 2014. 50(3): 243-249.
[3] Shahnaz Akhtar Chaudhry, Geert’t Jong, Gideon Koren. The fetal safety of Levetiracetam: A systematic review. Reproductive Toxicology. July 2014. 46: 40-45.