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NEUROLOGY 1996;46:3S-7S
© 1996 American Academy of Neurology

Pharmacology and pharmacokinetics of fosphenytoin

Thomas R. Browne, MD, Alan R. Kugler, PhD and Michael A. Eldon, PhD

From the Departments of Neurology and Pharmacology, Boston University School of Medicine, and the Neurology Service, Department of Veterans Affairs Medical Center, Boston, MA (Dr. Browne); Department of Pharmacokinetics and Drug Metabolism (Dr. Kugler), and Department of Clinical Pharmacology (Dr. Eldon), Parke-Davis Pharmaceutical Research, Division of Warner-Lambert Co., Ann Arbor, MI.
Supported in part by the United States Department of Veterans Affairs.
Address correspondence and reprint requests to Dr. Thomas R. Browne, Neurology Service (127), Department of Veterans Affairs Medical Center, 150 South Huntington Avenue, Boston, MA 02130.

Abstract.

Fosphenytoin sodium, a phosphate ester prodrug of phenytoin, was developed as a replacement for parenteral phenytoin sodium.Unlike phenytoin, fosphenytoin is freely soluble in aqueous solutions, including standard IV solutions, and is rapidly absorbed by the IM route. Fosphenytoin is metabolized (conversion half-life of 8 to 15 min) to phenytoin by endogenous phosphatases. Therapeutic free (unbound) and total plasma phenytoin concentrations are consistently attained after IM or IV administration of fosphenytoin loading doses. Fosphenytoin has fewer local adverse effects (e.g., pain, burning, and itching at the injection site) after IM or IV administration than parenteral phenytoin. Systemic effects related to the CNS are similar for both preparations, but transient paresthesias are more common with fosphenytoin.

NEUROLOGY 1996;46(Suppl 1): S3-S7