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.

The second-generation sulfonylurea hypoglycemic drug acts selectively on pancreatic beta cells, promotes insulin secretion, and enhances the effect of glucose intake, thereby inhibiting liver glucose production and output; it reduces platelet aggregation and adhesion, and helps prevent and treat diabetic microangiopathy.

This product belongs to the 4-nitrogen steroid hormone compound, which is a specific type II 5α-reductase competitive inhibitor, inhibiting the conversion of peripheral testosterone into dihydrotestosterone, and reducing the level of dihydrotestosterone in blood, prostate, skin and other tissues. By reducing the level of dihydrotestosterone in blood and prostate tissue, it inhibits prostate hyperplasia and improves the related clinical symptoms of benign prostatic hyperplasia.

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.

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.