This product is a 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 the pancreatic beta cells to secrete insulin, but the prerequisite is that the pancreatic beta cells still have a certain function of synthesizing and secreting insulin. Its mechanism is to specifically bind to the sulfonylurea receptors on the beta cell membrane, thereby closing the K channel, causing changes in membrane potential, opening the Ca2 channel, and increasing the 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).

Acipimox is a derivative of nicotinic acid, which can inhibit the decomposition of adipose tissue, reduce the release of free fatty acids from adipose tissue, thereby reducing the synthesis of triglycerides (TG) in the liver, and by inhibiting the synthesis of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL), the concentration of triglycerides (TG) and total cholesterol (TC) in the blood decreases. This product can also inhibit the activity of liver lipase and reduce the decomposition of high-density lipoprotein (HDL).

Telmisartan is a specific angiotensin II receptor (ATⅠ type) antagonist. Telmisartan replaces angiotensin II receptors and binds to ATⅠ receptor subtypes (known angiotensin II action sites) with high affinity. Telmisartan has no agonist effect at any site on the ATⅠ receptor site. Telmisartan selectively binds to ATⅠ receptors and the binding effect is long-lasting. Telmisartan has no affinity for other receptors (including AT2 and other AT receptors with fewer characteristics). The functions of the above other receptors are not yet known, and the excessive receptor stimulation effect that may be caused by the increase in angiotensin II levels caused by telmisartan is also unknown. Telmisartan does not inhibit human plasma renin or block ion channels. Telmisartan does not inhibit angiotensin converting enzyme II, which can also degrade bradykinin and cause adverse reactions. In humans, administration of 80 mg of telmisartan can almost completely inhibit the increase in blood pressure caused by angiotensin II. The inhibitory effect lasts for 24 hours and can still be measured after 48 hours. The antihypertensive effect gradually becomes apparent within 3 hours after the first dose of telmisartan. The maximum antihypertensive effect can be achieved 4 weeks after the start of treatment and can be maintained in long-term treatment. If telmisartan treatment is suddenly interrupted, blood pressure gradually returns to pre-treatment levels after a few days without rebound hypertension. In a clinical trial directly comparing two antihypertensive drugs, the incidence of dry cough in the telmisartan treatment group was significantly lower than that in the angiotensin-converting enzyme inhibitor treatment group.

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This product is one of the new fluorinated pyrimidine drugs. As a precursor drug of fluorouracil (5-FU), it is converted into free 5-FU by pyrimidine nucleoside phosphorylase in the body after taking it, thereby exerting its anti-tumor effect. It affects DNA and RNA synthesis respectively, mainly acting in the S phase, and also affects cells in other proliferation phases.