It acts on the smooth muscle of the coronary and peripheral blood vessels and the atrioventricular node, inhibits the influx of Ca2 into the cells, shows vasodilation and prolongs the conduction time of the atrioventricular node, and is effective for hypertension, arrhythmia, and angina pectoris. Specifically, it includes: 1. Effect on blood pressure: reduce hypertension, reduce peripheral vascular resistance and myocardial oxygen consumption, increase cardiac output, reduce blood pressure without reducing the blood flow of the brain, coronary arteries, and kidneys, and show a sodium diuretic effect; 2. Effect on arrhythmia: prolong the conduction time, effective refractory period and functional refractory period of the atrioventricular node, and inhibit supraventricular rapid arrhythmia caused by atrial electrical stimulation; 3. Effect on myocardial ischemia: improve the balance of myocardial oxygen supply and demand, dilate the main coronary artery and side branches, increase blood flow to the ischemic part of the myocardium, inhibit coronary artery spasm, protect myocardial function and energy metabolism, and reduce the infarct focus.

By acting on the smooth muscle of the coronary and peripheral blood vessels and the atrioventricular node, inhibiting the influx of Ca2 into the cells, showing vasodilation and prolonging the conduction time of the atrioventricular node, it is effective for hypertension, arrhythmia, and angina pectoris. 1. Effect on blood pressure: It can reduce hypertension under anesthesia or without anesthesia, reduce peripheral vascular resistance and myocardial oxygen consumption while lowering blood pressure, increase cardiac output, and reduce blood pressure without reducing the blood flow of the brain, coronary arteries, and kidneys, and show a sodium diuretic effect. 2. Effect on arrhythmia: Prolong the conduction time, effective refractory period, and functional refractory period of the atrioventricular node, show effects on supraventricular tachyarrhythmia, and inhibit supraventricular tachyarrhythmia caused by atrial electrical stimulation. 3. Effect on myocardial ischemia: Improve the balance of myocardial oxygen supply and demand, dilate the main and side branches of the coronary arteries, increase blood flow in the ischemic part of the myocardium, and inhibit coronary artery spasm; myocardial protection, inhibit excessive influx of Ca2 into cells during myocardial ischemia, maintain cardiac function and myocardial energy metabolism, and reduce the infarct focus.

Pemetrexed is an antifolate preparation with a core pyrrolopyrimidine group in its structure. It inhibits cell replication and thus tumor growth by destroying the normal metabolic process dependent on folate in cells. In vitro studies have shown that pemetrexed can inhibit the activity of thymidylate synthase, dihydrofolate reductase and glycinamide nucleotide formyltransferase, which are enzymes necessary for the synthesis of folate and participate in the bioresynthesis of thymine nucleotides and purine nucleotides. Pemetrexed enters the cell through the carrier carrying folic acid and the folate binding protein transport system on the cell membrane. Once pemetrexed enters the cell, it is converted into polyglutamate under the action of folylpolyglutamate synthetase. Polyglutamate remains in the cell and becomes an inhibitor of thymidylate synthase and glycinamide nucleotide formyltransferase. Polyglutamate is a time-concentration dependent process in tumor cells, while the concentration in normal tissues is very low. The half-life of polyglutamate metabolites in tumor cells is prolonged, thereby prolonging the duration of drug action in tumor cells. Preclinical studies have shown that pemetrexed can inhibit the growth of mesothelioma cell lines (MSTO-211H, NCI-H2052) in vitro. Studies on the mesothelioma cell line MSTO-211H have shown that pemetrexed combined with cisplatin has a synergistic effect.

Extract from the above information