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1. When used with alcohol or other non-steroidal anti-inflammatory drugs, gastrointestinal side effects increase and there is a risk of ulcers. Long-term use with acetaminophen may increase kidney toxicity. 2. When used with aspirin or other salicylic acid drugs, the efficacy is not enhanced, but the incidence of gastrointestinal adverse reactions and bleeding tendency increases. 3. When used with anticoagulants such as heparin and dicoumarol and platelet aggregation inhibitors, there is an increased risk of bleeding. 4. When used with furosemide, the latter's sodium excretion and hypotensive effects are weakened. 5. When used with verapamil and nifedipine, the blood concentration of this product increases. 6. This product can increase the blood concentration of digoxin.

This product belongs to the sulfonamide broad-spectrum antibacterial drug, which has antibacterial effects on both Gram-positive and Gram-negative bacteria. However, bacterial resistance to this type of drug is common at present. The number of resistant strains in Staphylococcus, gonococci, meningococci, and Enterobacteriaceae has increased. Sulfonamides are also active against the following microorganisms: Chlamydia trachomatis, Nocardia asteroides, Plasmodium falciparum, and Toxoplasma gondii. Sulfonamides are broad-spectrum antibacterial agents, similar in structure to para-aminobenzoic acid (PABA), and can compete with PABA for dihydrofolate synthase in bacteria, thereby preventing PABA from being used as a raw material to synthesize folic acid required by bacteria, 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. The effects of sulfonamides can be antagonized by PABA and its derivatives (procaine, tetracaine). In addition, the presence of pus and tissue decomposition products also has an antagonistic effect because it provides substances necessary for bacterial growth.

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It can form a thin film on the surface of damaged gastric mucosa, thereby resisting the invasion of gastric acid on the mucosa and protecting the gastric mucosa. In addition, it can absorb pepsin and neutralize gastric acid, but the effect is weak.