This product acts specifically on the gastric mucosal parietal cells, reducing the activity of H/KATPase in the parietal cells, thereby inhibiting the secretion of gastric acid. Compared with omeprazole and lansoprazole, this product has a weaker inhibitory effect on cytochrome P450-dependent enzymes. No adverse effects were found in either short-term or long-term administration of pantoprazole. This drug is non-carcinogenic, does not impair fertility, and does not induce teratogenesis. After 2.5 years of continuous medication, there were no changes in various experimental parameters of liver enzymology and cholesterol metabolism.

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 folic acid 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 folic acid and participate in the bioresynthesis of thymine nucleotides and purine nucleotides. The half-life of polyglutamic acid 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 has a synergistic effect in combination with cisplatin.

Relaxation of vascular smooth muscle, dilation of arterial terminals, especially veins. Dilation of veins can promote peripheral blood aggregation and reduce venous return to the heart, thereby reducing left ventricular end diastolic pressure and pulmonary capillary wedge pressure. Arteriolar dilation can reduce systemic vascular resistance, arterial systolic pressure and mean arterial pressure, and also dilate coronary arteries. The importance of reducing anterior diastolic pressure, posterior diastolic pressure and coronary diastolic pressure is not clear.

Relax vascular smooth muscle, reduce myocardial oxygen consumption, and increase coronary perfusion. The specific mechanism includes the release of nitric oxide (NO), activation of guanylate cyclase, and increase of cyclic guanosine monophosphate (cGMP) in smooth muscle cells, thereby relaxing vascular smooth muscle, dilating peripheral arteries and veins, and reducing preload and afterload.