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.

Azithromycin is a 15-membered macrolide antibiotic. In vitro tests have shown that azithromycin has antibacterial effects on a variety of common pathogens in clinical practice, including Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms. The mechanism of action is the same as that of erythromycin, which mainly binds to the 50S subunit of the bacterial ribosome and inhibits RNA-dependent protein synthesis.

In vitro tests of this product have a destructive or inhibitory effect on the morphology or proliferation of cell lines such as liver cancer, esophageal cancer, laryngeal cancer, lung cancer, and cervical cancer. In vivo tests have a certain inhibitory effect on mouse Ehrlich ascites carcinoma, sarcoma-180 and solid liver cancer. It can increase the respiratory control rate and lysosomal enzyme activity of mitochondria in H22 mouse ascites liver cancer cells, interfere with cancer cell division, block in the M phase, and affect its cycle speed. This product can destroy the skeleton of cancer cells (microfilaments, microtubules), affect the ultrastructure of cancer cells, and cause damage to mitochondria, microvilli and plasma membranes. It can inhibit DNA synthesis of cancer cells, but it does not inhibit normal bone marrow cells, and can increase white blood cells.