Racecadotril is an enkephalinase inhibitor. Enkephalinase can degrade enkephalins. This product can selectively and reversibly inhibit enkephalinase, thereby protecting endogenous enkephalins from degradation, prolonging the physiological activity of endogenous enkephalins in the digestive tract, and reducing excessive secretion of water and electrolytes. Oral racecadotril acts on peripheral enkephalinase, does not affect the enkephalinase activity of the central nervous system, and has no significant effect on gastrointestinal motility and intestinal basal secretion.

This product has a broad-spectrum antibacterial effect and strong antibacterial effect. It has strong antibacterial activity against most Enterobacteriaceae, such as Escherichia coli, Klebsiella, Proteus, Salmonella, Shigella, and Gram-negative bacteria such as Haemophilus influenzae, Legionella pneumophila, and Neisseria gonorrhoeae; it also has antibacterial effects on Gram-positive bacteria such as Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, and Mycoplasma pneumoniae and Chlamydia pneumoniae, but has poor effects on anaerobic bacteria and enterococci. Its mechanism of action is to inhibit the activity of bacterial DNA gyrase, prevent the synthesis and replication of bacterial DNA, and cause bacterial death.

It has strong anti-inflammatory, liver cell membrane protection and liver function improvement effects. It can reduce the increase of serum alanine aminotransferase and aspartate aminotransferase caused by carbon tetrachloride, thioacetamide and D-galactosamine, reduce the morphological damage of D-galactosamine to the liver and improve the chronic damage of immune factors to the liver morphology.

This product is an anti-trichomonal and anti-anaerobic drug, which has an inhibitory or killing effect on Trichomonas and most anaerobic bacteria.

This product is a prodrug of acyclovir. It is rapidly absorbed after oral administration and quickly converted into acyclovir in the body. Its antiviral effect is exerted by acyclovir. After acyclovir enters the herpes infected cells, it competes with deoxynucleoside for viral thymidine kinase or cellular kinase. The drug is phosphorylated into activated acyclosine triphosphate, which competes with deoxyguanine triphosphate for viral DNA polymerase as a substrate for viral replication, thereby inhibiting viral DNA synthesis and showing antiviral effect. The antiviral activity of this product in vivo is better than that of acyclovir, and the therapeutic index for herpes simplex virus type I and type II is 42.91% and 30.13% higher than that of acyclovir, respectively. It also has a high efficacy against varicella zoster virus and has very low toxicity to mammalian host cells.