This product is a phenothiazine antipsychotic, and its mechanism of action is mainly related to its blocking of dopamine receptors (DA2) in the mesolimbic system and mesocortical pathways. It has a blocking effect on dopamine (DA1) receptors, 5-hydroxytryptamine receptors, M-type acetylcholine receptors, and α-adrenaline receptors, and has a wide range of effects. In addition, this product can inhibit the dopamine receptors in the medulla oblongata emetic chemoreceptor area at low doses, and directly inhibit the vomiting center at high doses, producing a strong antiemetic effect. It inhibits the body temperature regulation center and lowers the body temperature. The body temperature can change with changes in the external environment. It blocks the action of peripheral α-adrenaline receptors, dilates blood vessels, causes a drop in blood pressure, and also has a certain effect on the endocrine system.

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.

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.

The antipsychotic effect is mainly related to its blocking of dopamine receptors (DA2) in the mesolimbic system and mesocortical pathways related to emotional thinking, while blocking the alpha-adrenaline receptors in the reticular formation ascending activation system is related to the sedative and tranquilizing effect. This product has a strong antiemetic effect and a weak sedative effect.

1. It is a non-selective competitive inhibitor of adrenergic β-receptor blockers, blocking β1 and β2 receptors on the heart, reducing the contractile force and contractile speed of the heart, while inhibiting the contraction of vascular smooth muscle, reducing myocardial oxygen consumption, and restoring the oxygen supply and demand relationship of ischemic myocardium to a low level of balance, which can be used to treat angina pectoris. 2. It inhibits the adrenergic excitement of cardiac pacemaker potentials and is used to treat arrhythmias. 3. It can be used to treat hypertension by blocking central and adrenergic neurons, inhibiting renin release and reducing cardiac output. 4. It competitively antagonizes the effects of isoproterenol and norepinephrine, blocks β2 receptors, and reduces the release of plasma-related hormones.