This product is a pyrimidine anti-metabolite drug that mainly acts on cells in the S proliferation phase. It interferes with cell proliferation by inhibiting the synthesis of cell DNA. After entering the human body, cytarabine is phosphorylated by kinase and converted into cytarabine triphosphate and cytarabine diphosphate. The former can strongly inhibit the synthesis of DNA polymerase, and the latter can inhibit the conversion of cytidine diphosphate to deoxycytidine diphosphate, thereby inhibiting cell DNA polymerization and synthesis. This product is a cell cycle-specific drug, which is most sensitive to cells in the S proliferation phase, and has a weaker effect on inhibiting RNA and protein synthesis.

The anti-tumor target is microtubules, mainly inhibiting the polymerization of tubulin and affecting the formation of spindle microtubules. It stops mitosis at metaphase. It can also interfere with protein metabolism and inhibit the activity of RNA polymerase, and inhibit the synthesis of cell membrane lipids and the transport of amino acids on the cell membrane. The inhibitory effect on transplanted tumors is greater than that of vinca alkaloids and has a wide anti-tumor spectrum. In addition to being effective against tumor strains sensitive to vinca alkaloids, it also has effects on mouse Ridgeway osteosarcoma, Mecca lymphosarcoma, X-5563 myeloma, etc. There is no cross-resistance between vincristine, vinblastine and vindesine, and vincristine has the strongest neurotoxicity among the three.

In vitro animal tests show that this product is effective against liver cancer BEL-7402, esophageal cancer CaEs-17, laryngeal cancer SMMC-7721, and cervical cancer.

This product is a cyclic non-specific anticancer drug that acts directly on DNA, mainly cross-linking between and within the chains of cell DNA, destroying DNA and inhibiting tumor growth.

It gradually turns into fluorouracil in the body and interferes with and blocks the synthesis of DNA, RNA and protein. After adding uracil, the decomposition of fluorouracil in tumor tissue is inhibited, and the concentration of fluorouracil is relatively increased. In addition, fluorouracil is mainly decomposed in the liver and part of the tumor tissue. After adding uracil, only a small amount of decomposition is found in the tumor tissue, which may also be related to the high amount of phosphorylated products of fluorouracil in the tumor.

It can block the degradation of tegafur and specifically increase the concentration of fluorouracil and its active metabolites in tumor tissues. When it is mixed with tegafur at a ratio of 1:4, it can significantly increase the concentration of fluorouracil in tumor tissues (maximum T/B ratio).