This product belongs to Class Ib antiarrhythmic drugs, inhibits the permeability of cell membrane to Na, but does not promote K outflow. It can slow down the conduction of various parts of the cardiac conduction system, reduce membrane reactivity, increase the excitation threshold, prolong the effective adaptation period of the atrium, atrioventricular node, His-Purkinje system (Purkinjes fibers) and ventricle, and block the forward and reverse conduction of the bypass pathway.

It has strong analgesic, local anesthesia, cooling, antipyretic, anti-inflammatory and detumescent effects. Compared with pethidine, it has comparable analgesic effects, but takes a little longer to take effect, and lasts longer; its analgesic effect is 7 times that of the antipyretic analgesic aminopyrine.

Extract from the above information

It is a non-addictive analgesic with strong analgesic, local anesthesia, cooling, antipyretic, anti-inflammatory and detumescent effects. Compared with pethidine, it has the same analgesic effect, but takes a little longer to take effect and lasts longer. Its analgesic effect is 7 times that of the antipyretic analgesic aminopyrine.

Anti-epileptic effect. It may be related to the increase in the concentration of inhibitory neurotransmitter γ-aminobutyric acid (GABA) in the brain. Generally, the increase in GABA is achieved by reducing metabolism or reabsorption. In addition, valproic acid acts on the postsynaptic receptor site to simulate or enhance the inhibitory effect of GABA. Its effect on the nerve membrane has not yet been fully elucidated. It may directly act on the membrane activity related to potassium conduction.