Pharmacological action All calcitonin has similar structure, and it is a single chain composed of 32 amino acids, and the arrangement order of 7 amino acids with a ring-shaped N- terminal varies with species. Because salmon calcitonin has high affinity with receptor binding site, it has better effect and longer action time than mammalian calcitonin. Salmon calcitonin inhibits osteoclast activity through its specific receptor. When the bone absorption rate increases, such as osteoporosis, it can obviously reduce the bone conversion to normal level. It has been proved that salmon calcitonin has analgesic effect on animal models and humans, which may be the result of direct action on the central nervous system. A single dose of this product can produce obvious clinical biological effects in human body. After medication, the urinary excretion of calcium, phosphorus and sodium (by reducing renal tubular reabsorption) increased, and the urinary hydroxyproline excretion decreased significantly. Long-term parenteral use of this product can significantly reduce bone turnover markers such as collagen pyridine crosslinking and bone alkaline phosphate isoenzyme. Calcitonin inhibits the secretion of stomach and pancreas. Because of these characteristics, this product is beneficial to the treatment of acute pancreatitis. Pre-clinical safety data have been studied on routine long-term toxicity, reproductive effects, mutagenicity and carcinogenicity in experimental animals. In toxicity test, it was found that the slight effect of salmon calcitonin was caused by its pharmacological action. This product has no embryotoxicity, teratogenic and mutagenic potential risks. Toxicity and carcinogenicity studies show that the incidence of pituitary adenoma will increase when rats are exposed to salmon calcitonin at a lower dose than clinical dose. However, further pre-clinical studies, especially the carcinogenicity studies in mice, found that the induction of pituitary adenoma was specific to mice. The drug dose given to mice in this experiment was about 760 times greater than the conventional dose of 50IU. At present, no adverse reactions related to pituitary adenoma have been found in patients. Therefore, there is sufficient evidence that the induction of pituitary adenoma is mouse-specific, and there is no correlation between pituitary adenoma and clinical application of this product.