Acetylhydroxyamine is a competitive inhibitor of urease. It has an amide group with a similar structure to urea. It forms a chelate with urease in the body, inhibiting the activity of the enzyme. Urease is a biochemical inducer of urinary tract stones. When its activity is inhibited, urea decomposition decreases, urinary ammonia concentration decreases, and pH value decreases, thereby dissolving urinary stones and preventing the formation of infectious urinary tract stones. Animal experiments have shown that this product can cause teratogenesis and bone marrow suppression.

It is a sulfonamide diuretic that works by inhibiting the reabsorption of water and electrolytes in the dilution segment of the distal renal tubular cortex. The mechanism of blood pressure reduction is unknown, but possible mechanisms include regulating calcium influx into vascular smooth muscle cells; stimulating the synthesis of prostaglandins PGE2 and prostaglandins PGI2; and reducing vascular hypersensitivity to vasopressors, thereby inhibiting vasoconstriction. This product has little or no effect on cardiac output, heart rate and rhythm when lowering blood pressure. Long-term use of this product rarely affects glomerular filtration rate or renal blood flow. This drug does not affect the metabolism of blood lipids and carbohydrates.

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 binding 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.