It can be converted into PEG2, PGI2, and PGF2a, and has obvious lipid-lowering and anti-platelet aggregation effects; it has obvious cholesterol-lowering effects, and its efficacy is 163 times that of linoleic acid; it can participate in the synthesis and balance of prostaglandins; it can significantly inhibit platelet aggregation and the synthesis of thromboxane A2 (TXA2) by platelets, thereby changing the TXA2/PGI2 ratio, and has the effect of preventing and treating thrombotic cardiovascular diseases; it has a stimulating effect on brown adipose tissue, promotes the activity of brown fatty acid mitochondria, consumes excess calories and achieves a certain weight loss effect.

This product is a broad-spectrum antifungal drug. It inhibits the biosynthesis of ergosterol by interfering with the activity of cytochrome P450, damages fungal cells and changes their permeability, inhibits the biosynthesis of triglycerides and phospholipids, causes the accumulation of hydrogen peroxide in cells, leads to cell submicrostructure degeneration and cell necrosis. For Candida albicans, it can inhibit the process of transformation from spores to invasive hyphae.

It has the anti-inflammatory, anti-allergic and vasoconstrictive effects of topical glucocorticoids.

It has antibacterial effects on bacteria such as Staphylococcus (methicillin-sensitive strains) and Corynebacterium.

This product belongs to the adrenal cortex hormone class, with anti-inflammatory, anti-allergic, antipruritic and anti-exudative effects. This product acts quickly and has a strong capillary contraction effect. Its anti-inflammatory effect is 112.5 times that of hydrocortisone, 2.3 times that of betamethasone sodium phosphate, and 18.7 times that of fluocinolone. The systemic adverse reactions are 3 times that of fluocinolone, with no sodium retention effect, and have a certain effect of promoting sodium and potassium excretion.

This product is a synthetic nucleoside antiviral drug that can be selectively phosphorylated by the virus's thymidine kinase and converted into a monophosphate, which is then converted into a diphosphate and a triphosphate by the action of cellular enzymes. Acyclovir triphosphate can interfere with DNA polymerase, especially herpes virus DNA enzyme, thereby inhibiting the replication of viral DNA. In vivo and in vitro experiments have shown that acyclovir has an inhibitory effect on herpes simplex virus type Ⅰ (HSV-1), type Ⅱ (HSV-2) and varicella-zoster virus (VZV). Cell culture results show that this product has the strongest effect on inhibiting HSV-1 virus, followed by HSV-2 and VZV virus.