This product is a synthetic antibacterial anti-tuberculosis drug. It has strong activity against bacteria in the growth and reproduction stage, and has almost no effect on bacteria in the dormant stage. It has high antibacterial activity against various types of mycobacteria. There is no cross-resistance between Mycobacterium tuberculosis and this product and other drugs. It may inhibit the metabolism of sensitive bacteria, inhibit RNA synthesis, and interfere with the protein metabolism of Mycobacterium tuberculosis, thereby causing bacterial death. In large doses, it can cause cleft palate, brain exposure, and spinal deformity in mouse experiments; it can cause mild cervical deformity in rat experiments; it can cause cyclops, short limbs, and cleft palate in rabbit experiments.

This product is a broad-spectrum antibacterial drug in the semi-synthetic rifamycin class. Its mechanism of action is to inhibit the activity of ribonucleic acid polymerase in bacteria, thereby affecting the synthesis of ribonucleic acid and protein metabolism, resulting in the cessation of bacterial growth and reproduction to achieve a bactericidal effect. Sensitive bacteria include Staphylococcus aureus (including penicillin-resistant and neomycin-resistant strains), Mycobacterium tuberculosis, Streptococcus pyogenes, Pneumococcus, Gonorrhea, Escherichia coli, Meningococcus, Haemophilus influenzae, Legionella, etc.

It has a good antibacterial effect on human tuberculosis bacteria, and its bactericidal effect is strongest at pH 5-5.5. It is currently the best bactericidal drug for tuberculosis bacteria that grow slowly in phagocytes in an acidic environment. The antibacterial concentration in vivo is 12.5 mu; g/ml, and 50 mu; g/ml can kill tuberculosis bacteria. The concentration that inhibits tuberculosis bacteria inside cells is 10 times lower than that outside cells, and it has almost no antibacterial effect in neutral and alkaline environments. The mechanism of action may be related to pyrazinoic acid. After pyrazinamide penetrates into phagocytes and enters the tuberculosis bacteria, the amidase in the bacteria removes the amide group and converts it into pyrazinoic acid to exert an antibacterial effect. In addition, because pyrazinamide is similar to nicotinamide in chemical structure, it interferes with dehydrogenase by replacing nicotinamide, prevents dehydrogenation, and hinders the use of oxygen by tuberculosis bacteria, which affects the normal metabolism of bacteria and causes death.