It has a significant bactericidal effect on Mycobacterium tuberculosis and some non-tuberculous mycobacteria (including Mycobacterium leprae, etc.) both inside and outside the host cells.

Anti-tuberculosis drugs are a combination of rifampicin, isoniazid and pyrazinamide. Rifampicin has a significant bactericidal effect on Mycobacterium tuberculosis and some non-tuberculous mycobacteria (including Mycobacterium leprae) both inside and outside the host cells.

Anti-tuberculosis drugs are a combination of rifampicin, isoniazid and pyrazinamide. Rifampicin has a significant bactericidal effect on Mycobacterium tuberculosis and some non-tuberculous mycobacteria (including Mycobacterium leprae) both inside and outside the host cells.

It 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 firmly binds to the beta subunit of the DNA-dependent RNA polymerase, inhibiting the synthesis of bacterial RNA and preventing the enzyme from connecting to DNA, thereby blocking the RNA transcription process and stopping the synthesis of DNA and protein.

It has a highly selective bactericidal effect on all types of Mycobacterium tuberculosis, with a strong effect on Mycobacterium tuberculosis in the growth and reproduction stage, and a weaker and slower effect on Mycobacterium tuberculosis in the dormant stage. Its mechanism of action may be to inhibit the synthesis of mycolic acid in sensitive bacteria and cause cell wall rupture.

It has dopamine D2 receptor antagonist activity and acetylcholinesterase inhibitory activity, and exerts gastrointestinal motility through the synergistic effect of the two. In addition, due to its antagonistic effect on dopamine D2 receptor activity, it also has a certain anti-vomiting effect.

1. Increase the sensitivity of peripheral tissues to insulin and increase insulin-mediated glucose utilization; 2. Increase the utilization of glucose by non-insulin-dependent tissues, such as the brain, blood cells, renal medulla, intestines, skin, etc.; 3. Inhibit hepatic gluconeogenesis and reduce hepatic glucose output; 4. Inhibit the uptake of glucose by intestinal wall cells; 5. Inhibit the biosynthesis and storage of cholesterol and reduce blood triglyceride and total cholesterol levels.

This drug belongs to Class 2A, i.e., a β1-receptor blocker without partial agonist activity (cardioselective β-receptor blocker). It has a selective blocking effect on β1-receptors, no PAA (partial agonist activity), and no membrane stabilizing effect. Its effect of blocking β-receptors is about the same as that of propranolol, and its selectivity for β1-receptors is slightly inferior to that of atenolol. The effects of metoprolol on the heart, such as slowing heart rate, inhibiting cardiac contractility, reducing automaticity, and delaying atrioventricular conduction time, are similar to those of propranolol and atenolol. Its effect of reducing elevated blood pressure and heart rate during exercise testing is also similar to that of propranolol and atenolol. Its contraction effect on vascular and bronchial smooth muscle is weaker than that of propranolol, so its effect on the respiratory tract is also smaller, but it is still stronger than that of atenolol. Metoprolol can also reduce plasma renin activity.