It can inhibit viral DNA and RNA polymerase, thereby inhibiting viral reproduction. On human embryonic kidney cells, 1% concentration has a significant inhibitory effect on DNA viruses (adenovirus, herpes virus) and RNA viruses (echovirus), and has an inhibitory effect on all stages of the viral proliferation cycle. It has no direct effect on free viral particles.

Diclofenac 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 into prostaglandins. At the same time, it can also promote the combination of arachidonic acid with triglycerides (triacylglycerols), reduce the concentration of free arachidonic acid in cells, and indirectly inhibit the synthesis of leukotrienes. Diclofenac is a stronger non-steroidal anti-inflammatory drug, and its inhibitory effect on prostaglandin synthesis is stronger than that of aspirin and indomethacin.

Rifampicin is a semi-synthetic broad-spectrum antibacterial drug of the rifamycin class, which has antibacterial activity against a variety of pathogenic microorganisms. The drug has a significant bactericidal effect on Mycobacterium tuberculosis and some non-tuberculous mycobacteria (including Mycobacterium leprae, etc.) both inside and outside the host cells. Rifampicin has a good antibacterial effect on aerobic Gram-positive bacteria, including enzyme-producing strains of Staphylococcus aureus and methicillin-resistant strains, Streptococcus pneumoniae, other Streptococcus, Enterococcus, Listeria, Bacillus anthracis, Clostridium perfringens, Corynebacterium diphtheriae, anaerobic cocci, etc. It also has a high degree of antibacterial activity against aerobic Gram-negative bacteria such as Neisseria meningitidis, Haemophilus influenzae, and Neisseria gonorrhoeae. Rifampicin also has a good effect on Legionella, and has an inhibitory effect on pathogens such as Chlamydia trachomatis, lymphogranuloma venereum, and psittacosis.