This product is an antiviral drug. It has an inhibitory effect on herpes simplex virus, varicella zoster virus, cytomegalovirus, etc. in vitro. It inhibits viral replication by interfering with viral DNA polymerase and binding to the growing DNA chain, causing the extension of the DNA chain to be interrupted. This product has a special affinity for viruses, but has low toxicity to mammalian host cells.

This product is a hypoglycemic drug. (1) It stimulates the pancreatic islet b cells to secrete insulin, provided that the pancreatic islet b cells still have a certain ability to synthesize and secrete insulin; (2) It inhibits hepatic glycogenolysis and gluconeogenesis by increasing portal vein insulin levels or acting directly on the liver, thereby reducing the generation and output of glucose by the liver; (3) It may also increase the sensitivity of extrapancreatic tissues to insulin and the utilization of sugar (possibly mainly through post-receptor effects). Therefore, the overall effect is to reduce fasting blood sugar and postprandial blood sugar.

Candesartan cilexetil is rapidly hydrolyzed into active metabolites in the body, candesartan, which is a selective angiotensin II receptor (AT1) antagonist. It antagonizes the vasoconstriction of angiotensin II by binding to the AT1 receptor of vascular smooth muscle, thereby reducing peripheral vascular resistance. It is also believed that candesartan can exert a certain antihypertensive effect by inhibiting the secretion of aldosterone by the adrenal glands. Candesartan does not inhibit kininase II and does not affect the degradation of bradykinin.

Candesartan cilexetil is rapidly hydrolyzed into active metabolites in the body, candesartan, which is a selective angiotensin II receptor (AT1) antagonist. It antagonizes the vasoconstriction of angiotensin II by binding to the AT1 receptor of vascular smooth muscle, thereby reducing peripheral vascular resistance. It is also believed that candesartan can exert a certain antihypertensive effect by inhibiting the secretion of aldosterone by the adrenal glands. Candesartan does not inhibit kininase II and does not affect the degradation of bradykinin.

1. 5-HT3 receptor antagonism: In the 5-hydroxytryptamine-induced guinea pig isolated colon contraction experiment and rat and ferret heart rate slowing reflex (Bezold-Jarisch reflex) experiment, it showed 5-HT3 receptor antagonism. 2. Anti-malignant tumor drug-induced vomiting inhibition: The vomiting of ferrets induced by cisplatin was inhibited by giving this product before or after the initial vomiting. Cisplatin and other anti-malignant tumor drugs can free 5-hydroxytryptamine from the chromaffin cells in the digestive tract, and 5-hydroxytryptamine binds to the 5-HT3 receptors present in the gastrointestinal mucosa and the vagus nerve endings.