Basic introduction of telmisartan


Telmisartan (telmisartan), chemical name is 4 '-[4-methyl -6-(1-methyl -1H-benzimidazol-2-yl)-2-propyl -1H-benzimidazol-1-ylmethyl] biphenyl -2-carboxylic acid, molecular formula C33H30N4O2, white or white crystalline powder, odorless, tasteless. Dissolved in chloroform, slightly soluble in dichloromethane or dimethylformamide, slightly soluble in methanol, very slightly soluble in ethanol, almost insoluble in water, soluble in 1mol/L sodium hydroxide solution, very slightly soluble in 0.1mol/L hydrochloric acid solution.
Non-peptide angiotensin II receptor antagonist, selective, difficult to reverse the blockade of ATI receptor, and no effect on other receptor systems. For mild to moderate hypertension. Telmisartan is a new antihypertensive drug and a specific angiotensin II receptor (AT type I) antagonist for the treatment of essential hypertension. The surrogate angiotensin II receptor binds with high affinity to the AT I receptor subtype (known site of action of ANGIOTENSIN II). Telmisartan does not have any site agonist effect at the AT I receptor site, and selectively binds to the AT I receptor, and the binding effect is lasting. No affinity for other receptors, including AT2 and other less characteristic AT receptors. The function of these other receptors is unknown, and the possible receptor overstimulation effect due to the increase in angiotensin II levels caused by telmisartan is also unknown. Telmisartan does not inhibit human plasma renin, nor does it block ion channels. It does not inhibit angiotensin-converting enzyme II, which can also degrade the adverse reactions caused by the enhanced action of bradykinin. The administration of 80mg of telmisartan in humans almost completely inhibits the increase in blood pressure caused by angiotensin II. The inhibitory effect lasted for 24 hours and was still measurable at 48 hours. The antihypertensive effect was gradually obvious within 3 hours after the first dose. The maximum antihypertensive effect is obtained 4 weeks after the start of treatment and can be maintained during long-term treatment. If treatment is abruptly interrupted, blood pressure gradually returns to pre-treatment levels after a few days without rebound hypertension. In a clinical trial that directly compared two hypertension drugs, the incidence of dry cough was significantly lower in the treatment group than in the angiotensin-converting enzyme inhibitor group.