This product is a blood volume expander. Its volume expansion effect and blood dilution effect depend on the molecular weight, degree of substitution, substitution mode and drug concentration, as well as the dosage and infusion rate. After healthy volunteers infused 500ml of this product within 30 minutes, their volume expansion effect was 100% of the infusion volume of this product, and this 100% volume effect can be stably maintained for 4-6 hours.

This product is a blood volume expander. Its volume expansion effect and blood dilution effect depend on the molecular weight, degree of substitution, substitution mode and drug concentration, as well as the dosage and infusion rate. After healthy volunteers infused 500ml of this product within 30 minutes, their volume expansion effect was 100% of the infusion volume of this product, and this 100% volume effect can be stably maintained for 4-6 hours.

Cell cycle specific antimetabolite drugs, mainly act on tumor cells in the DNA synthesis phase (S phase), can prevent the progression from G1 phase to S phase; inhibit ribonucleotide reductase, reduce the amount of deoxynucleotides; dFdCTP competes with dCTP to bind to the DNA chain, resulting in cessation of DNA chain synthesis, DNA breakage and cell death. It has anticancer activity against a variety of mouse tumors, and the mode of administration affects its activity and toxicity.

Cell cycle specific antimetabolites mainly act on tumor cells in the DNA synthesis phase (S phase), preventing the progression from G1 phase to S phase. Active products dFdCDP and dFdCTP are generated through intracellular metabolism, inhibiting ribonucleotide reductase, deoxycytidine deaminase, etc., interfering with DNA synthesis and repair, leading to DNA chain cessation and breakage, and ultimately causing cell death. It has significant anticancer activity against a variety of human and mouse tumors, and its effect is closely related to the method of administration.

Cell cycle-specific anti-metabolite drugs mainly act on tumor cells in the DNA synthesis phase (S phase), preventing the progression from the G1 phase to the S phase; inhibiting ribonucleotide reductase, reducing the amount of deoxynucleotides, and interfering with DNA synthesis and repair; their active metabolites dFdCDP and dFdCTP inhibit related enzymes through different mechanisms and embed into the DNA chain, leading to DNA breakage and cell death.

Rosuvastatin is a selective, competitive HMG-CoA reductase inhibitor that increases the number of liver LDL receptors on the cell surface, enhances the uptake and catabolism of LDL, and inhibits liver VLDL synthesis, thereby reducing the total number of VLDL and LDL particles. For patients with multiple hypercholesterolemia and mixed dyslipidemia, rosuvastatin can reduce total cholesterol, LDL-C, ApoB, non-HDL-C levels, and can also reduce TG and increase HDL-C levels.

Rosuvastatin is a selective, competitive HMG-CoA reductase inhibitor that increases the number of liver LDL receptors on the cell surface, enhances the uptake and catabolism of LDL, inhibits liver VLDL synthesis, and reduces the total number of VLDL and LDL particles. For patients with multiple hypercholesterolemia, rosuvastatin can reduce total cholesterol, LDL-C, ApoB, non-HDL-C levels, and can also reduce TG and increase HDL-C levels.