This product is a long-acting non-steroidal anti-inflammatory drug that can inhibit the activity of cyclooxygenase and reduce the synthesis of prostaglandins. Animal experiments have shown that the anti-inflammatory and analgesic effects of this product are weaker than indomethacin, but stronger than aspirin.

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 the following bacteria: Haemophilus influenzae, Streptococcus pneumoniae and Neisseria meningitidis. It only has antibacterial effects on the following bacteria: Staphylococcus aureus, Streptococcus pyogenes, Streptococcus viridans, Group B hemolytic Streptococcus, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Salmonella typhi, Salmonella paratyphi, Shigella, Bacteroides fragilis and other anaerobic bacteria. The following bacteria are usually resistant to chloramphenicol: Pseudomonas aeruginosa, Acinetobacter, Enterobacter, Serratia marcescens, indole-positive Proteus, methicillin-resistant Staphylococcus and Enterococcus. This product is an antibacterial agent. Chloramphenicol is fat-soluble and enters bacterial cells by diffusion, and reversibly binds to the 50S subunit of the bacterial ribosome, which blocks the growth of the peptide chain (possibly due to the inhibition of the action of transpeptidase), thereby inhibiting the formation of the peptide chain and preventing protein synthesis.

By inhibiting cyclooxygenase, it selectively inhibits the synthesis of prostaglandins in the hypothalamic temperature regulation center, leading to peripheral vasodilation and sweating to achieve an antipyretic effect; by inhibiting the synthesis and release of prostaglandins, it increases the pain threshold and has an analgesic effect. It is a peripheral analgesic, weaker than aspirin, and is only effective for mild and moderate pain. This product has no obvious anti-inflammatory effect.

By inhibiting cyclooxygenase, it selectively inhibits the synthesis of prostaglandins in the hypothalamic temperature regulation center, leading to peripheral vasodilation and sweating to achieve an antipyretic effect; by inhibiting the synthesis and release of prostaglandins, it increases the pain threshold and has an analgesic effect. It is a peripheral analgesic, weaker than aspirin, and is only effective for mild and moderate pain. This product has no obvious anti-inflammatory effect.

This product is an acetanilide antipyretic analgesic. It inhibits cyclooxygenase and selectively inhibits the synthesis of prostaglandins in the hypothalamic temperature regulation center, leading to peripheral vasodilation and sweating to achieve an antipyretic effect. Its antipyretic effect is similar to that of aspirin. It inhibits the synthesis and release of prostaglandins, etc., increases the pain threshold and has an analgesic effect. It is a peripheral analgesic, weaker than aspirin, and is only effective for mild and moderate pain. This product has no obvious anti-inflammatory effect.

This product is a benzimidazole derivative, which is rapidly metabolized into sulfoxide, sulfone alcohol and 2-amine sulfone alcohol in the body. It selectively and irreversibly inhibits the polymerization of the cytoplasmic microtubule system of the parasite's intestinal wall cells, blocks its absorption of various nutrients and glucose, leads to the depletion of endogenous glycogen in the worm, and inhibits the fumarate reductase system, preventing the production of adenosine triphosphate, making it impossible for the worm to survive and reproduce. It can also cause the degeneration of the cytoplasmic microtubules of the worm's intestinal cells, and bind to its microtubule protein, causing intracellular transport blockage, resulting in the accumulation of Golgi endocrine granules, the gradual dissolution of the cytoplasm, and the complete degeneration of the absorbing cells, causing the death of the worm. It has the effect of completely killing hookworm eggs and whipworm eggs and partially killing ascarid eggs. In addition to killing and expelling various nematodes parasitic in animals, it also has a significant killing and expelling effect on tapeworms and cysticerci.

1. Effect on water and electrolyte excretion: It can increase the excretion of water, sodium, chloride, potassium, calcium, magnesium, phosphorus, etc.; mainly by inhibiting the active reabsorption of NaCl by the thick-walled segment of the renal tubular loop, reducing the osmotic pressure gradient difference of the medullary interstitial fluid, leading to increased excretion of water, Na, and Cl. It promotes the secretion of K by the distal tubules, increases the excretion of Ca2+ and Mg2+, increases uric acid excretion with short-term medication, and may cause hyperuricemia with long-term medication. 2. Effect on hemodynamics: It inhibits the activity of prostaglandin degrading enzymes, increases prostaglandin E2, dilates blood vessels, and increases renal blood flow; it does not affect the glomerular filtration rate, and helps prevent acute renal failure; it dilates the pulmonary capacitance veins, reduces the permeability of pulmonary capillaries, reduces the amount of blood returning to the heart, and reduces the left ventricular end-diastolic pressure, and is suitable for the treatment of acute left heart failure and adult respiratory distress syndrome.