Phenytoin pharmacokinetics

Phenytoin pharmacokinetics refers to the absorption, distribution, metabolism, and excretion (ADME) of the antiepileptic drug phenytoin. It is characterized by non-linear, saturable elimination kinetics (Michaelis-Menten kinetics), primarily mediated by the hepatic enzymes Cytochrome P450 2C9 (CYP2C9) and 2C19 (CYP2C19) [StatPearls: Phenytoin]. Because the metabolic pathway becomes saturated at therapeutic concentrations, small dose increases can lead to disproportionately large increases in plasma levels, creating a high risk for toxicity [PubMed: PMC3001218]. Phenytoin is also highly protein-bound to albumin, and its pharmacokinetics can be significantly altered by conditions that change protein levels or by drugs that compete for binding sites [NIH: LiverTox]. Clinically, this necessitates therapeutic drug monitoring to maintain levels within the narrow therapeutic window of 10-20 mcg/mL. This entry is classified as incorrect as a target because it describes a pharmacological process rather than a specific molecular entity like a receptor or enzyme. Understanding these parameters is essential for avoiding adverse effects such as ataxia, nystagmus, and severe cutaneous reactions [PubChem: Phenytoin].

Other names

Phenytoin ADMEPhenytoin metabolismPhenytoin elimination kinetics

Not applicable as this is a pharmacokinetic process; however, the drug phenytoin acts by stabilizing the inactive state of voltage-gated sodium channels (PubChem: Phenytoin).