Comparative Pharmacology
Head-to-head clinical analysis: LICART versus LIDOCAINE HYDROCHLORIDE.
Peer-Reviewed Evidence
Head-to-head clinical analysis: LICART versus LIDOCAINE HYDROCHLORIDE.
LICART vs LIDOCAINE HYDROCHLORIDE
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Licart is a fibrin sealant containing human fibrinogen and thrombin. When applied, thrombin converts fibrinogen to fibrin, forming a stable clot that mimics the final stage of coagulation. It also contains factor XIII and aprotinin to cross-link fibrin and inhibit fibrinolysis, respectively.
Lidocaine hydrochloride is a sodium channel blocker that inhibits voltage-gated sodium channels in neuronal and cardiac cell membranes, stabilizing the membrane and preventing depolarization, thereby blocking nerve impulses and exerting local anesthetic and antiarrhythmic effects.
Adults: 50 mg orally once daily.
IV: 1-1.5 mg/kg bolus, then 1-4 mg/min continuous infusion. Max: 3 mg/kg (300 mg) loading dose. For ventricular arrhythmias.
None Documented
None Documented
Terminal elimination half-life of 6-8 hours in adults with normal renal function. Prolonged in renal impairment (up to 20-24 hours in ESRD), requiring dose adjustment in CrCl <30 mL/min.
Terminal elimination half-life is 1.5–2 hours in adults. In patients with heart failure, hepatic cirrhosis, or those on CYP-inhibitors, half-life may be prolonged to ≥3 hours; in neonates, up to 3–6 hours.
Primarily renal excretion (80-85% as unchanged drug), with 10-15% biliary/fecal elimination. Less than 5% metabolized to inactive glucuronide conjugate.
Primarily hepatic metabolism (90% CYP3A4, also CYP1A2) to inactive metabolites (monoethylglycinexylidide, glycinexylidide); <10% excreted unchanged in urine. Renal elimination accounts for the majority of metabolite clearance.
Category C
Category A/B
Local Anesthetic
Local Anesthetic / Antiarrhythmic (Class Ib)