It significantly enhances the immune function of T cells, macrophages, and NK cells, induces killer cells, LAK cells, and activates tumor-infiltrating lymphocytes (TIL), and synergistically enhances immune function with other cytokines, promotes the localization of tumors and infection lesions, and has significant immune enhancement and anti-tumor effects. Common side effects during treatment include fever, chills, fatigue, nausea, mild loss of appetite, etc. Rare side effects include local reactions, rashes, decreased blood pressure, water retention, elevated transaminases, etc. Most of the above side effects are mild and easily tolerated, and can be relieved on their own after stopping the drug.

It significantly enhances the immune function of T cells, macrophages, and NK cells, induces killer cells, LAK cells, and activates tumor-infiltrating lymphocytes (TIL), and synergizes with other cytokines to enhance immune function, promote the localization of tumors and infection lesions, and has significant immune enhancement and anti-tumor effects. Common side effects during treatment include fever, chills, fatigue, nausea, mild loss of appetite, etc., and rare side effects include local reactions, rashes, decreased blood pressure, water retention, and increased transaminase. Most of the above side effects are mild and easily tolerated, and can be relieved on their own after stopping the drug.

It has a significant effect of increasing the number of peripheral blood leukocytes in normal rabbits. The peak of the leukocyte count occurs on the 4th day after the first administration, which is 72% higher than before the administration, which is better than the leukocyte-raising drug shark liver alcohol. It has a significant effect of increasing leukocytes in rabbits with leukopenia caused by cobalt 60-gamma ray and deep X-ray irradiation. It also has a preventive effect on leukopenia when administered two days before irradiation. It can also prevent leukopenia in mice caused by mitomycin C. It has a synergistic inhibitory effect on the solid type of Ehrlich carcinoma when used in combination with cyclophosphamide, and the toxicity of leukopenia caused by cyclophosphamide is significantly reduced.

This product is a new type of anti-microtubule drug. It promotes tubulin polymerization, inhibits depolymerization, maintains tubulin stability, and inhibits cell mitosis. In vitro experiments have shown that paclitaxel has a significant radiosensitization effect, which may be to stop cells in the G2 and M phases that are sensitive to radiotherapy. Paclitaxel is a mitotic inhibitor or spindle poison. It has a different mechanism of action from the commonly used chemotherapy drugs. It induces and promotes the assembly of microtubules. Paclitaxel has the effect of polymerizing and stabilizing microtubules, causing rapidly dividing tumor cells to be firmly fixed in the mitotic stage, blocking the replication of cancer cells and causing them to die.

This product is a prodrug of acyclovir. It is rapidly absorbed after oral administration and quickly converted into acyclovir in the body. Its antiviral effect is exerted by acyclovir. After acyclovir enters the herpes infected cells, it competes with deoxynucleoside for viral thymidine kinase or cellular kinase. The drug is phosphorylated into activated acyclosine triphosphate, which competes with deoxyguanine triphosphate for viral DNA polymerase as a substrate for viral replication, thereby inhibiting viral DNA synthesis and showing antiviral effect. The antiviral activity of this product in vivo is better than that of acyclovir, and the therapeutic index for herpes simplex virus type I and type II is 42.91% and 30.13% higher than that of acyclovir, respectively. It also has a high efficacy against varicella zoster virus and has very low toxicity to mammalian host cells.