This product is a fluorinated nucleoside analog of the antiviral drug Vidarabine. It has an anti-tumor mechanism similar to Ara-C, but is not deaminated and inactivated by adenosine deaminase. After ingestion, it is rapidly dephosphorylated to generate 2-fluoroarabinoadenosine (F-Ara-A), which is phosphorylated in the cell to become F-Ara-ATP with anti-tumor activity. It can inhibit DNA polymerase, DNA primase, DNA helicase and ribonucleotide reductase, and can also be incorporated into tumor cell DNA and RNA chains to stop chain extension and inhibit DNA and RNA synthesis. However, its precise mechanism needs to be further clarified. This product can inhibit the growth of many human tumors, such as non-Hodgkin's lymphoma, leukemia, breast cancer, non-small cell lung cancer and ovarian tumors in tissue culture and tumor animal models, and it also has the effect of enhancing the activity of many anti-tumor drugs in vitro. This product can be used in combination with gallium nitrate, cytarabine, mitoxantrone or Ara-C plus cisplatin to enhance the killing effect on tumor cells.

Acipimox is a derivative of nicotinic acid, which can inhibit the decomposition of adipose tissue, reduce the release of free fatty acids from adipose tissue, thereby reducing the synthesis of triglycerides (TG) in the liver, and by inhibiting the synthesis of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL), the concentration of triglycerides (TG) and total cholesterol (TC) in the blood decreases. This product can also inhibit the activity of liver lipase and reduce the decomposition of high-density lipoprotein (HDL).

This product is a proton pump inhibitor of gastric parietal cells. It can specifically inhibit the secretory microtubules and tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. Since H, K-ATPase is the last process of acid secretion of parietal cells, this product has a strong acid inhibition ability. It can not only non-competitively inhibit gastric acid secretion caused by gastrin, histamine, choline and food stimulation of the vagus nerve, but also inhibit part of the basic gastric acid secretion that is not affected by choline or H2 receptor blockers. It also has a strong and lasting inhibitory effect on gastric acid secretion caused by dibutyl cyclic adenosine monophosphate (DCAMP) stimulation that cannot be inhibited by H2 receptor antagonists. This product also has an inhibitory effect on pepsin secretion and changes in gastric mucosal blood flow.

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