Henan Life Pharmaceutical Co., Ltd.

This product is a medium-acting sulfonamide. It has antibacterial effects on non-enzyme-producing Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, Escherichia coli, Klebsiella, Salmonella, Shigella and other Enterobacteriaceae, gonococci, meningococci, Haemophilus influenzae. In addition, it also has antimicrobial activity against Chlamydia trachomatis, Nocardia asteroides, Plasmodium and Toxoplasma in vitro. The antibacterial activity of this product is the same as that of sulfamethoxazole. However, in recent years, bacterial resistance to this product has increased, especially Streptococcus, Neisseria and Enterobacteriaceae. Sulfonamides are broad-spectrum antibacterial agents. This product is similar in structure to para-aminobenzoic acid (PABA), and can compete with PABA on dihydrofolate synthase in bacteria, thereby preventing PABA from being used as a raw material to synthesize folic acid required by bacteria, and reducing the amount of metabolically active tetrahydrofolate, which is an essential substance for bacteria to synthesize purine, thymidine and deoxyribonucleic acid (DNA), thereby inhibiting the growth and reproduction of bacteria.

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 has a broad-spectrum antimicrobial effect in vitro, including aerobic Gram-negative and Gram-positive bacteria, anaerobes, Rickettsia, spirochetes and Chlamydia. It has a bactericidal effect on Haemophilus influenzae, Streptococcus pneumoniae and Neisseria meningitidis; it has an antibacterial effect on 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. It diffuses into bacterial cells and reversibly binds to the 50S subunit of the bacterial ribosome, inhibiting the formation of peptide chains and thus preventing protein synthesis.

Diclofenac is a non-steroidal anti-inflammatory analgesic derived from phenylacetic acid. Its mechanism of action is to inhibit the activity of cyclooxygenase, thereby blocking the conversion of arachidonic acid into prostaglandins. At the same time, it can also promote the combination of arachidonic acid with triglycerides (triacylglycerols), reduce the concentration of free arachidonic acid in cells, and indirectly inhibit the synthesis of leukotrienes. Diclofenac is a stronger non-steroidal anti-inflammatory drug, and its inhibitory effect on prostaglandin synthesis is stronger than that of aspirin and indomethacin.