Irbesartan is a potent, orally active, selective angiotensin-II receptor (AT1 subtype) antagonist. It should block all AT1 receptor-mediated effects of angiotensin-II, regardless of the source or synthetic pathway of angiotensin-II. Its selective antagonism of the angiotensin-II receptor (AT1) results in an increase in plasma renin and angiotensin-II levels and a decrease in plasma aldosterone levels. Serum potassium is not significantly affected when irbesartan is administered alone at the recommended dose to patients without electrolyte disturbances. Irbesartan does not inhibit angiotensin-converting enzyme (ACE or kinase II), which generates angiotensin-II, nor does it degrade bradykinin to inactive metabolites. Irbesartan does not require metabolic activation for its activity.

This product is a brain metabolism improving drug, which is a cyclic derivative of r-aminobutyric acid. It has the effect of resisting brain function damage caused by physical and chemical factors. It can promote ATP in the brain, promote acetylcholine synthesis and positively enhance the conduction of nerve excitement, and has the effect of promoting brain metabolism. It can resist brain function damage caused by physical and chemical factors. It has an improving effect on retrograde hyperactivity caused by hypoxia. It can enhance memory and improve learning ability.

This product is a second-generation sulfonylurea antidiabetic drug, which is effective for most patients with type 2 diabetes. It can reduce fasting and postprandial blood sugar and reduce glycosylated hemoglobin (HbAlc) by 1% to 2%. The main function of this type of drug is to stimulate pancreatic b cells to secrete insulin, but the prerequisite is that pancreatic b cells still have a certain function of synthesizing and secreting insulin. Its mechanism is to specifically bind to the sulfonylurea receptor on the b cell membrane, thereby closing the K channel, causing changes in membrane potential, opening the Ca2 channel, and increasing intracellular Ca2, which promotes insulin secretion. In addition, there are extra-pancreatic effects, including improving the insulin resistance of peripheral tissues (such as liver, muscle, and fat).

Antiviral drug. It has an inhibitory effect on herpes simplex virus, varicella zoster virus, cytomegalovirus, etc. in vitro. After entering the cells infected by herpes virus, it competes with deoxynucleoside for viral thymidine kinase or cell kinase, and the drug is phosphorylated into activated acyclovir triphosphate, which inhibits viral replication by interfering with viral DNA polymerase and binding to the growing DNA chain to cause DNA chain extension interruption. It has a special affinity for viruses, but has low toxicity to mammalian host cells.

It achieves its antibacterial effect by inhibiting the activity of bacterial DNA gyrase and hindering bacterial replication. It has good antibacterial effects on most Enterobacteriaceae, some Gram-positive bacteria, Legionella, Mycoplasma, Chlamydia, etc., but has poor effects on anaerobic bacteria and enterococci.