Oral acetanilide antipyretic analgesics may produce antipyretic and analgesic effects mainly by inhibiting the synthesis of prostaglandins.

Adrenergic drugs can constrict the blood vessels in the nasal mucosa and relieve symptoms of nasal congestion and runny nose.

Long-acting tricyclic antihistamines can relieve nasal or non-nasal symptoms of seasonal allergic rhinitis by selectively antagonizing peripheral H1 receptors.

By increasing urine pH and the excretion of citrate, it reduces urine calcium ion concentration and reduces the calcium salt saturation in urine that can form stones. The increase in pH can increase the solubility of uric acid and cystine stones. It has an improvement effect on acidic urine and has a dose-dependent effect in preventing acidic urine. It can inhibit the formation of calcium oxalate crystals and reduce the formation of crystal particles in the renal parenchyma, and has a good stone prevention effect.

Oral administration of urolate increases urine pH and citrate excretion, and decreases urine calcium concentration. This urolate-induced change makes the salts in the urine more susceptible to crystallization. The resulting decrease in calcium concentration can reduce the saturation of urine calcium salts that can form stones. The increase in pH can increase the solubility of uric acid and cystine stones.

It has a broad-spectrum antiviral effect. Its antiviral mechanism is mainly through the binding of interferon to interferon receptors on the surface of target cells, inducing multiple antiviral proteins such as 2-5(A) synthetase, protein kinase PKR, MX protein in target cells, preventing the synthesis of viral proteins, inhibiting the replication and transcription of viral nucleic acids. It also has multiple immune regulatory effects, which can increase macrophage activity and enhance the specific cytotoxicity of lymphocytes to target cells, promote and maintain the body's immune surveillance, immune protection and immune self-stabilization functions.

This product is a third-generation sulfonylurea long-acting antidiabetic drug. Its mechanism of action is to bind to the sulfonylurea receptors on the surface of pancreatic β-cells, promote the closure of KATP channels, cause cell membrane depolarization, open voltage-dependent calcium channels, and promote the release of insulin due to the influx of Ca2+, and inhibit the synthesis of glucose in the liver. In addition, glimepiride can also increase the uptake of cardiac glucose through non-insulin-dependent pathways, which may be due to the increased expression of two proteins, glucose transporter 1 and 4. Since the effect of glimepiride on cardiovascular KATP channels is weaker than that of glibenclamide, gliclazide and glipizide, there are few cardiovascular adverse reactions.