Lidocaine (Lignocaine) inhibits sodium channels involving complex voltage and using dependence^[1]. Lidocaine decreases growth, migration and invasion of gastric carcinoma cells via up-regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways. Lidocaine is an amide derivative commonly used to anesthetize. Lidocaine is a drug to treat ventricular arrhythmia and an effective tumor-inhibitor^[2]. IC50 & Target: sodium channels^[1], MEK/ERK, NF-κB^[2] In Vitro: Lidocaine (Lignocaine) (10 nM; 48 hours) decreases significantly cell proliferation^[2].
Lidocaine (1-10 nM; 24-72 hours) inhibits cell viability and achieves the most suppressing effects at the concentration of 10 nM and treatment time 48 hours^[2].
Lidocaine (10 nM; 48 hours) increases significantly the apoptotic cell rate^[2].
Lidocaine (10 nM; 48 hours) down-regulates Cyclin D1 and up-regulates p21 expression significantly^[2].
In Vivo: Lidocaine (Lignocaine) causes completely reversible tail nerve block in rats. Mechanical nociception block produced by lidocaine has slower onset and faster recovery compared with thermal nociception block^[3].