Quinolone antibiotics are broad-spectrum antibiotics with good antibacterial effects on Gram-positive and Gram-negative bacteria, mycoplasmas, chlamydia, Legionella, and anaerobic bacteria including Bacteroides fragilis and Mycobacterium. They exert their bactericidal effects by inhibiting bacterial DNA gyrase.

Quinolone antibiotics have good antibacterial effects on Gram-positive and Gram-negative bacteria, mycoplasma, chlamydia, Legionella, anaerobic bacteria including Bacteroides fragilis and Mycobacterium. They have a bactericidal effect by inhibiting the action of bacterial DNA gyrase.

This product is an anti-deoxyribonucleic acid (DNA) virus drug. Its pharmacological action is to bind to the viral deoxyribonucleic acid polymerase, reduce its activity and inhibit DNA synthesis. After entering the cell, adenosine monophosphate is phosphorylated to generate adenosine diphosphate (Ara-ADP) and adenosine triphosphate (Ara-ATP). The antiviral activity is mainly caused by adenosine triphosphate (Ara-ATP). Ara-ATP and deoxyadenosine triphosphate (dATP) compete to bind to viral DNAP, thereby inhibiting the activity of the enzyme and the synthesis of viral DNA. At the same time, it inhibits the activity of viral nucleotide reductase and inhibits the synthesis of viral DNA. It can also inhibit the activity of viral DNA terminal deoxynucleotidyl transferase, so that Ara-A penetrates into the viral DNA and connects to the end of the DNA chain 3prime;-OH position, inhibiting the continued synthesis of viral DNA.

This product is an anti-deoxyribonucleic acid (DNA) virus drug. Its pharmacological action is to bind to the viral deoxyribonucleic acid polymerase, reduce its activity and inhibit DNA synthesis. After entering the cell, adenosine monophosphate is phosphorylated to generate adenosine diphosphate (Ara-ADP) and adenosine triphosphate (Ara-ATP). The antiviral activity is mainly caused by adenosine triphosphate (Ara-ATP). Ara-ATP and deoxyadenosine triphosphate (dATP) compete to bind to viral DNAP, thereby inhibiting the activity of the enzyme and the synthesis of viral DNA. At the same time, it inhibits the activity of viral nucleotide reductase and inhibits the synthesis of viral DNA. It can also inhibit the activity of viral DNA terminal deoxynucleotidyl transferase, so that Ara-A penetrates into the viral DNA and connects to the end of the DNA chain 3prime;-OH position, inhibiting the continued synthesis of viral DNA.

Antiviral drug. It has an inhibitory effect on herpes simplex virus, varicella zoster virus, cytomegalovirus, etc. in vitro. After entering the cells infected by herpes virus, this product competes with deoxynucleoside for viral thymidine kinase or cell kinase, and the drug is phosphorylated into activated acyclovir triphosphate, and then inhibits viral replication in two ways: ① Interfering with viral DNA polymerase and inhibiting viral replication; ② Under the action of DNA polymerase, it binds to the growing DNA chain, causing the extension of the DNA chain to be interrupted. This product has a special affinity for viruses, but has low toxicity to mammalian host cells.