It is effective against herpes simplex virus (HSV) type I and II, and secondarily against varicella-zoster virus, but less effective against Epstein-Barr virus and cytomegalovirus. Acyclovir is effective against herpes simplex virus type I and II and varicella-zoster virus because it can be phosphorylated into acyclovir monophosphate by virus-encoded thymidine kinase (TK), which then forms acyclovir diphosphate and triphosphate through the catalysis of cellular enzymes. Acyclovir triphosphate is a strong inhibitor of herpes simplex virus DNA polymerase. It binds to the enzyme as a substrate of viral DNA polymerase and is incorporated into viral DNA, thereby terminating the synthesis of viral DNA.

This product is a glucocorticoid drug. It has anti-inflammatory and anti-allergic effects.

This product belongs to the aminoglycoside antibiotics. The antibacterial spectrum is similar to that of gentamicin. It has antibacterial effects on Gram-negative bacteria such as Escherichia coli, aerogenes, Klebsiella, Proteus mirabilis, some indole-positive Proteus, Pseudomonas aeruginosa, some Neisseria, some non-pigmented Serratia and Shigella; the antibacterial effect of this product on Pseudomonas aeruginosa is 3 to 5 times stronger than that of gentamicin, and Pseudomonas aeruginosa that is moderately sensitive to gentamicin is highly sensitive to this product. Among Gram-positive bacteria, Staphylococcus aureus (including β-lactamase-producing strains) is sensitive to this product; Streptococci (including Streptococcus pyogenes, Pneumococcus, Streptococcus faecalis, etc.) are all resistant to this product. Anaerobic bacteria (Bacteroides), Mycobacterium tuberculosis, Rickettsia, viruses and fungi are also resistant to this product. The mechanism of action of this product is to bind to the 30S subunit of the bacterial ribosome and inhibit the synthesis of bacterial proteins.

It has a selective effect on cerebral blood vessels, improving the oxygen supply to the brain by increasing cerebral blood flow.

Diclofenac sodium is a non-steroidal anti-inflammatory analgesic derived from phenylacetic acid. Its mechanism of action is to inhibit the activity of cyclooxygenase, thereby blocking the conversion of arachidonic acid to prostaglandins. At the same time, it can also promote the combination of arachidonic acid with triglycerides, reduce the concentration of free arachidonic acid in cells, and indirectly inhibit the synthesis of leukotrienes. Animal experiments have confirmed that prostaglandins are one of the mediators of intraocular inflammation, which can lead to the collapse of the blood-aqueous barrier, vasodilation, increased vascular permeability, leukocyte chemotaxis, non-cholinergic mechanism pupil constriction, etc. Diclofenac sodium is a stronger non-steroidal anti-inflammatory drug. Its inhibitory effect on prostaglandin synthesis is stronger than that of aspirin and indomethacin. Diclofenac sodium eye drops have a strong inhibitory effect on the destruction of the blood-aqueous barrier caused by mechanical, chemical, biological and other stimuli.