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.

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.

Creatine phosphate plays an important role in the energy metabolism of muscle contraction. It is the chemical energy reserve of myocardial and skeletal muscles and is used for the resynthesis of ATP. The hydrolysis of ATP provides energy for the contraction process of actomyosin. Insufficient energy supply caused by slowed oxidative metabolism is an important factor in the formation and development of myocardial cell damage. Insufficient creatine phosphate levels have important clinical significance in the damage of myocardial contractility and functional recovery ability. In fact, in myocardial injury, there is a close relationship between the amount of high-energy phosphate compounds in cells and the survival and contractile function recovery ability of cells. Therefore, maintaining the level of high-energy phosphate compounds has become the basic principle of various methods to limit myocardial damage, and it is also the basis for cardiac metabolic protection. Animal experiments and human cardiac arrest experiments have shown the role of sodium creatine phosphate and its possibility of protecting the myocardium.

Creatine phosphate plays an important role in the energy metabolism of muscle contraction. It is the chemical energy reserve of myocardial and skeletal muscles and is used for the resynthesis of ATP. The hydrolysis of ATP provides energy for the contraction process of actomyosin. Insufficient energy supply caused by slowed oxidative metabolism is an important factor in the formation and development of myocardial cell damage. Insufficient creatine phosphate levels have important clinical significance in the damage of myocardial contractility and functional recovery ability. In fact, in myocardial injury, there is a close relationship between the amount of high-energy phosphate compounds in cells and the survival and contractile function recovery ability of cells. Therefore, maintaining the level of high-energy phosphate compounds has become the basic principle of various methods to limit myocardial damage, and it is also the basis for cardiac metabolic protection. Animal experiments and human cardiac arrest experiments have shown the role of sodium creatine phosphate and its possibility of protecting the myocardium.