Chloroquine mainly acts on erythrozoites, and after 48 to 72 hours, the schizonts in the blood are killed. This product is ineffective against the infrared stage of Plasmodium vivax malaria, so it cannot cure Plasmodium vivax malaria. It can cure falciparum malaria. Chloroquine is ineffective against the infrared stage and has no direct effect on gametocytes, so it cannot be used for etiology prevention and interruption of transmission.

It can significantly inhibit the basal gastric acid secretion during the day and night, and can also inhibit the gastric acid secretion induced by food, histamine, pentagastrin, caffeine and insulin.

Amoxicillin is a penicillin antibiotic that has good antibacterial activity against Streptococcus such as Streptococcus pneumoniae and hemolytic Streptococcus, aerobic Gram-positive cocci such as non-penicillinase-producing Staphylococci and Enterococcus faecalis, aerobic Gram-negative bacteria such as Escherichia coli, Proteus mirabilis, Salmonella, Haemophilus influenzae, Neisseria gonorrhoeae, and Helicobacter pylori. Amoxicillin exerts its bactericidal effect by inhibiting the synthesis of bacterial cell walls, which can quickly dissolve and rupture bacteria into spherical bodies.

This product has a broad-spectrum antimicrobial effect in vitro, including aerobic Gram-negative and Gram-positive bacteria, anaerobes, Rickettsia, spirochetes and Chlamydia. It has bactericidal effects on Haemophilus influenzae, Streptococcus pneumoniae and Neisseria meningitidis; it only has antibacterial effects 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, enters bacterial cells by diffusion, and reversibly binds to the 50S subunit of bacterial ribosomes, inhibiting the formation of peptide chains, thereby preventing protein synthesis.

It is a selective β1-adrenergic receptor blocker with no membrane stabilizing effect and endogenous sympathomimetic activity. However, it does not inhibit the bronchodilator effect of isoproterenol. Its mechanism of lowering blood pressure and reducing myocardial oxygen consumption is the same as that of propranolol. Large-scale clinical trials have confirmed that atenolol can reduce the mortality rate of acute myocardial infarction within 0 to 7 days. The therapeutic dose has no significant inhibition on myocardial contractility.