It inhibits bacterial protein synthesis by hindering the bacterial transpeptidation process. It has antibacterial effects on a variety of Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms. The mechanism of action is the same as that of erythromycin, mainly binding to the 50S subunit of the bacterial ribosome to inhibit RNA-dependent 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.

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It has strong anti-inflammatory, liver cell membrane protection and liver function improvement effects. It can reduce the increase of serum alanine aminotransferase and aspartate aminotransferase caused by carbon tetrachloride, thioacetamide and D-galactosamine, significantly reduce the morphological damage of D-galactosamine to the liver and improve the chronic damage of immune factors to the liver morphology.

1. It can obviously inhibit the synthesis of thromboxane A2 (TXA2), counteract the platelet aggregation caused by arachidonic acid (AA), and has a stronger and faster antiplatelet aggregation effect than aspirin (ASP). 2. It can enhance the fibrinolytic activity and promote the dissolution of thrombus. 3. It can reduce the specific viscosity of whole blood and plasma, and accelerate the electrophoresis of red blood cells. 4. It can relax the vascular smooth muscle, dilate the artery, and increase the blood flow of the coronary artery and cerebral artery. 5. It can improve the ability to resist hypoxia. 6. It can strongly scavenge free radicals. 7. It can inhibit the inflammatory exudation of capillaries.