Ropivacaine differs structurally from the bupivacaine only in the in the substitution of a propyl group for the N-butyl group. Sharing the structural metabolic prerequisites of the non-porphyrogenic drug bupivacaine gives theoretical grounds to classify ropivacaine as probably not porphyrinogenic.

Ropivacaine is a local anesthetic of the amide type. Ropivacaine is exclusively the S-(-)-enantiomer (Ekström, G. & Gunnarsson, U.B., 1996). Ropivacaine differs from bupivacaine only in the 1-substituent on the ring-nitrogen, i.e. propyl versus butyl.

Local anaesthetic.

Volume required to reach uM concentrations when injected intravenously: approximately 1.5 ml (of ropivacaine 10mg/ml).

Ropivacaine is extensively metabolised in the liver, predominantly mediated by CYP1A2; the isoenzyme CYP3A4 plays a minor role in the metabolism of ropivacaine. Ropivacaine is a ligand to CYP 3A4 and may in therapeutic use reach the hepatocyte µM levels needed for activation the nuclear receptors that trigger transcription of the ALAS1 gene. However, the drug is not found to be an inducer or irreversible inhibitor of drug metabolizing cytochrome P450 species (Rendic, 2002) and is therefore most probably devoid of capacity for ALAS1-induction. CYP1A2 is the most important isozyme for the metabolism of ropivacaine. A potent inhibitor of CYP3A4 causes a minor decrease in clearance of ropivacaine, which should be of no clinical relevance (Arlander, E., Ekström, G. et al, 1998) (Ekström, G. & Gunnarsson, U.B., 1996). Ropivacaine is an inhibitor of CYP2D6, but this does not seem to be of major clinical importance (Wink J., Veering B.T. et al, 2008). Rendic (2002) reports that ropivacaine is a substrate of CYP3A4 CYP1A1, CYP1A2, CYP2B6 and 2D6.

None.