Lidocaine Hydrochloride Monohydrate

Lidocaine (Lignocaine) hydrochloride hydrate inhibits sodium channels involving complex voltage and using dependence. Lidocaine hydrochloride hydrate 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 hydrochloride hydrate is an amide derivative and has potential for the research of ventricular arrhythmia.

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].

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].

[1]. Cummins TR, et al. Setting up for the block: the mechanism underlying lidocaine's use-dependent inhibition of sodium channels. J Physiol. 2007 Jul 1;582(Pt 1):11. 

[2]. Sui H, et al. Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145. BMC Cancer. 2019 Mar 15;19(1):233. 

[3]. Li Z, et al. Evaluation of the antinociceptive effects of lidocaine and bupivacaine on the tail nerves of healthy rats. Basic Clin Pharmacol Toxicol. 2013 Jul;113(1):31-6.