Chengdu Brilliant Pharmaceutical Co., Ltd.

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.

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. 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.

This product is an amide local anesthetic, which has a biphasic effect of excitation and inhibition on the central nervous system; at low doses, analgesia and drowsiness occur, and the pain threshold is increased; at high doses, the effect or toxicity is enhanced; at sub-toxic blood concentrations, it has an anticonvulsant effect; at high blood concentrations, it may induce convulsions. At low doses, it promotes the outflow of K in myocardial cells, reduces myocardial autonomy, and has an anti-ventricular arrhythmia effect; at therapeutic doses, it has no significant effect on myocardial electrical activity, atrioventricular conduction and contraction; at high blood concentrations, it can slow down the heart conduction velocity, cause atrioventricular conduction block, inhibit myocardial contractility and reduce cardiac output.

This product is a mucus regulator, which mainly acts on the secretion of bronchial glands, increasing the secretion of low-viscosity salivary mucin and reducing the production of high-viscosity fucoxomucin, thereby reducing the viscosity of sputum and making it easier to cough up. It takes effect quickly after oral administration, and obvious therapeutic effects can be seen within 4 hours of taking it.

Animal experiments have shown that this product can reduce the increase of serum AST and ALT in the animal acute liver injury model caused by TAA (thioacetamide) and CCl4 (carbon tetrachloride), and inhibit the accumulation of triglycerides caused by chronic liver injury model; it can promote liver glycogen synthesis, inhibit the increase of cholesterol, and help the recovery of serum albumin/globulin ratio.