• Metabolism: Relatively little biotransformation, only 5% is metabolized by cytochrome P450 CYP2E1 to hexafluoroisopropanol (HFIP) with release of inorganic fluoride and CO2. No other metabolic pathways have been identified for sevoflurane. Route of Elimination: The low solubility of sevoflurane facilitates rapid elimination via the lungs. In vivo metabolism studies suggest that approximately 5% of the sevoflurane dose may be metabolized. Up to 3.5% of the sevoflurane dose appears in the urine as inorganic fluoride. Half Life: 15-23 hours
• Uses/Sources: Used for induction and maintenance of general anesthesia in adult and pediatric patients for inpatient and outpatient surgery.
• Treatment: In the event of overdosage, or what may appear to be overdosage, the following action should be taken: discontinue administration of sevoflurane, maintain a patent airway, initiate assisted or controlled ventilation with oxygen, and maintain adequate cardiovascular function. (L1712)
• Route of Exposure: Rapidly absorbed into circulation via the lungs, however solubility in the blood is low.

• Carcinogenicity: No indication of carcinogenicity to humans (not listed by IARC).
• Toxicity: LD50: 10.8 g/kg (Rat) (A308) LC50: 49881 ppm/hr (Inhalation, Rat) (A308)

Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor.