The drug has not been found to induce or irreversible inhibit drug metabolizing cytochrome P450 species (Rendic, S., 2002) and is therefore most probably devoid of capacity for ALAS1-induction. Further, levobupivacaine is the S(-)-entiomer of the non-porphyrinogenic drug bupivacaine, and this gives theoretical grounds to classify levobupivacaine as probably not porphyrinogenic. One case of uneventful use reported.

Levobupivacaine is a local anesthetic of the amide type, the S(-)-entiomer of bupivacaine.

Local anaesthtic. Levobupivacaine is equipotent to bupivacaine.

Volume required to obtain uM concentrations when injected intravenously: approximately 4 ml (of levobupivacaine 5 mg/ml).

The pharmacokinetics of levobupivacaine are similar to those of the racemic form, bupivacaine. It is extensively metabolised and excreted as its metabolites mainly in the urine, with smaller amounts appearing in the faeces. 3-Hydroxylevobupivacaine is a major metabolite and its formation is mediated by the cytochrome P450 isoenzyme CYP1A2; the isoenzyme CYP3A4 is also involved in the metabolism of levobupivacaine. Rendic (2002) reports that levobupivacaine is a substrate of CYP3A4 and CYP1A2. Gennery et al (2000) also concludes that metabolism is primarily via cytochrome P450 isoenzymes.

Thunell, S., study to be published: 1 patient exposed without porphyric adverse reaction reported.

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