Aspartic acid has a strong affinity for cells and can be used as a carrier to facilitate the entry of potassium ions and magnesium ions into the cytoplasm and mitochondria to maintain the normal excitability and stability of the internal environment of cells such as nerve tissue, myocardium, and smooth muscle. It transports electrolytes to the myocardium, promotes myocyte depolarization, maintains myocardial contractility, and reduces myocardial oxygen consumption. It has a protective effect on the myocardium when hypoxia is caused by coronary circulation disorders. Aspartic acid participates in the ornithine cycle and promotes urea production.

Aspartic acid has a strong affinity for cells and can be used as a carrier to facilitate the entry of potassium ions and magnesium ions into the cytoplasm and mitochondria to maintain the normal excitability and stability of the internal environment of cells such as nerve tissue, myocardium, and smooth muscle. It transports electrolytes to the myocardium, promotes myocyte depolarization, maintains myocardial contractility, and reduces myocardial oxygen consumption. It has a protective effect on the myocardium when hypoxia is caused by coronary circulation disorders. Aspartic acid participates in the ornithine cycle and promotes urea production.

It is a ribonucleotide reductase inhibitor. Its mechanism of action is to inhibit nucleoside diphosphate reductase, prevent nucleotides from being reduced to deoxynucleotides, thereby inhibiting the synthesis of deoxyribonucleic acid, without interfering with the synthesis of ribonucleic acid or protein. It is a cell cycle-specific drug, more sensitive to differentiated and proliferated cells, with lower toxicity, and faster oral absorption. The plasma concentration reaches the highest level after 2 hours and disappears after 6 hours.

Anti-angina drug. It has the effect of antagonizing adrenaline, norepinephrine and vasopressin, can reduce vascular resistance, increase coronary and circulatory blood flow, promote myocardial metabolism and myocardial energy production. At the same time, it can reduce myocardial oxygen consumption, thereby improving the balance of myocardial oxygen supply and demand. It can also increase tolerance to cardiac glycosides. By preserving the energy metabolism in ischemic cells and preventing the decrease of intracellular ATP levels, it ensures the perfect function of ion pumps and normal transmembrane sodium-potassium pump transport while maintaining the stability of the intracellular environment, reduces intracellular acidosis and prevents the accumulation of sodium and calcium in myocardial cells, protects cell contraction function and limits cell lysis and endothelial damage caused by oxygen free radicals.

This product is a sulfonamide antibacterial drug. After decomposition, the 5-aminosalicylic acid produced will complex with the intestinal wall connective tissue and stay in the intestinal wall tissue for a long time to play an antibacterial, anti-inflammatory and immunosuppressive role, such as reducing Escherichia coli and Clostridium, while inhibiting the synthesis of prostaglandins and other inflammatory mediators leukotrienes. Sulfapyridine produced by the decomposition of this product shows a weak antibacterial effect on intestinal flora.

Produced by the decomposition of sulfasalazine, it shows a weak antibacterial effect on intestinal flora.

Extract from the above information