Broad-spectrum antiviral drug. It has the effect of inhibiting the growth of multiple viruses such as respiratory syncytial virus, influenza virus, hepatitis A virus, adenovirus, etc. in vitro, and its mechanism is not fully understood. After entering the virus-infected cells, the drug is rapidly phosphorylated, and its product acts as a competitive inhibitor of viral synthase, inhibiting inosine monophosphate dehydrogenase, influenza virus RNA polymerase and mRNA guanosine transferase, thereby causing a decrease in intracellular guanosine triphosphate, impairing viral RNA and protein synthesis, and inhibiting viral replication and transmission. It may also have an immune effect and neutralizing antibody effect on respiratory syncytial virus.

Disinfectant and antiseptic with antibacterial effect

Clearing away heat and purging fire and cooling blood and relieving pain

When applied externally, it can promote local blood circulation and has anti-inflammatory, antipruritic and analgesic effects.

When applied externally, it can promote local blood circulation and has anti-inflammatory, antipruritic and analgesic effects.

It has anti-inflammatory, antipyretic and analgesic effects. Its mechanism of action is to reduce the synthesis of prostaglandins by inhibiting cyclooxygenase. It stops the formation of pain nerve impulses in inflammatory tissues and inhibits inflammatory reactions, including inhibiting the chemotaxis of leukocytes and the release of lysosomal enzymes. As for the antipyretic effect, it acts on the hypothalamic temperature regulation center, causing peripheral vasodilation and sweating, which increases heat dissipation. This central antipyretic effect may also be related to the inhibition of prostaglandin synthesis in the hypothalamus.

It has a broad-spectrum antimicrobial effect in vitro, including aerobic Gram-negative and Gram-positive bacteria, anaerobes, Rickettsia, spirochetes and Chlamydia. It has a bactericidal effect on Haemophilus influenzae, Streptococcus pneumoniae and Neisseria meningitidis; it only has an antibacterial effect on anaerobic bacteria such as Staphylococcus aureus, Streptococcus pyogenes, Streptococcus viridans, Group B hemolytic Streptococcus, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Salmonella typhi, Salmonella paratyphi, Shigella, Bacteroides fragilis, etc. Pseudomonas aeruginosa, Acinetobacter, Enterobacter, Serratia marcescens, indole-positive Proteus, methicillin-resistant Staphylococcus and Enterococcus are usually resistant to chloramphenicol. Chloramphenicol is fat-soluble and enters the bacterial cell by diffusion, reversibly binds to the 50S subunit of the bacterial ribosome, inhibits the action of transpeptidase, prevents the formation of peptide chains, and thus prevents protein synthesis.

Vitamin B12 is converted into methylcobalamin and coenzyme B12 in the body to become active. Methylcobalamin participates in folic acid metabolism. When it is deficient, it hinders the recycling of tetrahydrofolate, thereby hindering the synthesis of thymidine deoxynucleotides, blocking DNA synthesis, and stagnating the maturation and division of blood cells, leading to megaloblastic anemia. Coenzyme B12 promotes the conversion of methylmalonyl coenzyme A, an intermediate product of fat metabolism, into succinyl coenzyme A to participate in the tricarboxylic acid cycle. When it is deficient in the human body, it causes increased excretion of methylmalonic acid and abnormal fatty acid metabolism. At the same time, it affects the synthesis of myelin lipids and the maintenance of the normal function of sheathed nerve fibers, resulting in clinical symptoms of nerve damage.