Inhibits T lymphocyte activation, binds to the intracellular protein FKBP-12 to form a complex, inhibits calcineurin activity, prevents the dephosphorylation and translocation of NF-AT, inhibits the transcription of multiple genes (such as IL-2, interferon-γ, IL-3, IL-4, IL-5, GM-CSF and TNF-α), inhibits the release of mediators from skin mast cells and basophils, and downregulates the expression of FCΣRI on the surface of Langerhans cells.

Azithromycin is a 15-membered macrolide antibiotic. In vitro tests have shown that azithromycin has antibacterial effects on a variety of common clinical pathogens, including Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms. The mechanism of action is the same as that of erythromycin, mainly binding to the 50S subunit of the bacterial ribosome and inhibiting RNA-dependent protein synthesis.

It is rapidly converted into the antiviral compound penciclovir in the body, which has an inhibitory effect on herpes simplex virus type Ⅰ (HSV-1), herpes simplex virus type Ⅱ (HSV-2) and varicella zoster virus (VZV). It inhibits the activity of HSV-2 polymerase by competing with guanosine triphosphate, thereby selectively inhibiting the synthesis and replication of herpes virus DNA.

External use has anti-inflammatory, anti-allergic, antipruritic and exudation reducing effects

It is a semi-synthetic broad-spectrum bactericidal agent. It has strong antibacterial activity against Mycobacterium tuberculosis in vitro, with a minimum inhibitory concentration (MIC) of 0.12-0.25 mg/L, which is 2-10 times stronger than rifampicin; its anti-tuberculosis infection effect in mice is also better than rifampicin. Mycobacterium leprae and other mycobacteria such as Mycobacterium kansasii and Mycobacterium toad are also sensitive to this product, but Mycobacterium avium is resistant. In addition, this product has high antibacterial activity against most Gram-positive cocci, with a MIC of 0.025 mg/L; it has poor effect on Gram-negative bacteria. Its effect on Chlamydia is similar to that of erythromycin and doxycycline, which is worse than rifampicin; it has poor effect on methicillin-resistant Staphylococcus. According to the results of in vitro tests, Chlamydia, Staphylococcus aureus and Neisseria gonorrhoeae will develop resistance to this product. Combined with doxycycline, it has a synergistic effect on Neisseria gonorrhoeae; combined with isoniazid, its effect on Mycobacterium tuberculosis far exceeds that of rifampicin and isoniazid. Its mechanism of action is the same as that of rifampicin, which is to firmly bind to the subunit of DNA-dependent RNA polymerase, inhibit the synthesis of bacterial RNA, prevent the enzyme from connecting to DNA, thereby blocking the RNA transcription process and stopping the synthesis of DNA and protein. Animal experiments have shown that this product has certain liver toxicity and teratogenic effects on the fetus.