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.

By blocking the membrane transport of calcium ions in myocardial and vascular smooth muscle, inhibiting the influx of calcium ions into cells, it causes a decrease in myocardial contractility and vasodilation. Animal experiments have shown that by reducing myocardial contractility and peripheral vascular resistance, myocardial oxygen consumption is reduced; by dilating coronary vessels and developing collateral circulation, the oxygen supply to myocardial ischemic sites is increased; by inhibiting the consumption of high-energy phosphate compounds, the ability to resist hypoxia is enhanced.

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 bacterial cells by diffusion, reversibly binds to the 50S subunit of bacterial ribosomes, inhibits the formation of peptide chains, and thus prevents protein synthesis.

It has anti-thrombotic effect. It inhibits platelet aggregation and release, inhibits adenosine uptake, increases cyclic adenosine monophosphate (cAMP) in platelets, inhibits phosphodiesterase (PDE), strengthens the increase in cGMP concentration caused by endothelial relaxing factor (EDRF), inhibits the formation of thromboxane A2 (TXA2), enhances the effect of endogenous PGI2, and has a vasodilating effect.

This product 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.