Levobupivacaine (DB01002): A Comprehensive Monograph on its Pharmacology, Clinical Utility, and Safety Profile

Executive Summary

Levobupivacaine is a long-acting, small-molecule local anesthetic belonging to the amino-amide class of drugs. It is the pure S-(-)-enantiomer of bupivacaine, a widely used but more cardiotoxic racemic mixture.[1] The primary role of levobupivacaine is to provide local or regional anesthesia and analgesia for a broad spectrum of surgical procedures, obstetric applications, and for postoperative pain management.[1]

The development of levobupivacaine was a targeted effort to create a safer alternative to racemic bupivacaine. Reports in the late 1970s and 1980s linked bupivacaine to severe, and sometimes fatal, cardiotoxicity, particularly with accidental intravascular injection.[4] Subsequent research revealed that this toxicity was stereoselective, residing predominantly with the R-(+)-enantiomer.[5] Consequently, levobupivacaine was isolated and developed to retain the potent and long-lasting anesthetic properties of its parent compound while significantly reducing the risk of cardiovascular and central nervous system (CNS) toxicity.[2] This improved safety margin represents its principal therapeutic advantage and the core rationale for its clinical use.

The mechanism of action of levobupivacaine is consistent with other local anesthetics: it produces a reversible blockade of nerve impulse propagation by inhibiting voltage-gated sodium channels within the neuronal membrane.[1] By binding to the intracellular aspect of these channels, it prevents the influx of sodium ions necessary for depolarization, thereby increasing the threshold for electrical excitation and halting the transmission of pain signals.[1]