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.

This product is an intermediate in the synthesis of Schisandrae Chinensis A, which can reduce liver damage and alanine aminotransferase (ALT) elevation caused by carbon tetrachloride; inhibit liver microsomal lipid peroxidation caused by carbon tetrachloride, its metabolic conversion to carbon monoxide, and reduce the consumption of reduced coenzyme II and oxygen in the metabolic process, protecting the structure and function of liver cell biomembrane; reduce the increase of liver ALT induced by prednisone, and promote liver regeneration in mice with partial hepatectomy; have a significant induction effect on cytochrome P450 enzyme activity, enhance the detoxification ability of carbon tetrachloride and certain carcinogens; improve protein metabolism in some hepatitis patients, increase albumin and reduce globulin. It has no negative conversion effect on HbsAg and HbeAg, and cannot shrink enlarged liver and spleen.

This product has the function of regulating autonomic nervous system dysfunction and endocrine balance disorders.

Trimethoprim (TMP) is an antibacterial agent, a lipophilic weak base, and its chemical structure belongs to the pyrimethamine class. It has antibacterial activity against Escherichia coli, Klebsiella, Proteus mirabilis, Salmonella, and Shigella, but has no obvious antibacterial effect on Streptococcus pneumoniae, Neisseria gonorrhoeae, and Neisseria meningitidis, and has no effect on Pseudomonas aeruginosa. The mechanism of action of this product is to interfere with bacterial folic acid metabolism. It mainly selectively inhibits the activity of bacterial dihydrofolate reductase, so that dihydrofolate cannot be reduced to tetrahydrofolate, and synthetic folic acid is the main component of nucleic acid biosynthesis. Therefore, this product prevents the synthesis of bacterial nucleic acids and proteins, and the binding of this product to bacterial dihydrofolate reductase is 50,000 to 60,000 times tighter than that to mammalian enzymes. The combination of this product and sulfonamides can double block the bacterial folic acid synthesis metabolism, have a synergistic effect, enhance the antibacterial activity of sulfonamides, and convert the antibacterial effect into a bactericidal effect, reducing the production of drug-resistant strains.

It selectively inhibits succinate dehydrogenase in the muscles of the worm, affects the anaerobic metabolism of the worm muscles, and reduces energy production; it depolarizes the nerve muscles, causing continuous muscle contraction and paralysis; its cholinergic effect is beneficial to the excretion of the worm; it may have an inhibitory effect on the microtubule structure of the worm; it has immune regulation and immune excitation functions.