This product is an anti-thyroid drug. Its mechanism of action is to inhibit thyroid peroxidase, thereby hindering the oxidation of iodide absorbed into the thyroid gland and the coupling of tyrosine, and hindering the synthesis of thyroxine (T4) and triiodothyronine (T3). Animal experiments have observed that it can inhibit the synthesis of antibodies by B lymphocytes, reduce the level of thyroid stimulating antibodies in the blood circulation, and restore the function of inhibitory T cells to normal.

Pemetrexed is an antifolate preparation with a core pyrrolopyrimidine group in its structure. It inhibits cell replication and thus tumor growth by destroying the normal metabolic process dependent on folic acid in cells. In vitro studies have shown that pemetrexed can inhibit the activity of thymidylate synthase, dihydrofolate reductase and glycinamide nucleotide formyltransferase, which are enzymes necessary for the synthesis of folic acid and participate in the bioresynthesis of thymine nucleotides and purine nucleotides. The half-life of polyglutamic acid metabolites in tumor cells is prolonged, thereby prolonging the duration of drug action in tumor cells. Preclinical studies have shown that pemetrexed can inhibit the growth of mesothelioma cell lines (MSTO-211H, NCI-H2052) in vitro. Studies on the mesothelioma cell line MSTO-211H have shown that pemetrexed has a synergistic effect in combination with cisplatin.

This product is an enzyme-lowering drug for the treatment of hepatitis created in my country. It is an intermediate in the synthesis of Schisandra chinensis C. Oral administration of 150~200 mg/kg of this product to mice can reduce liver damage and elevated alanine aminotransferase (ALT) caused by carbon tetrachloride. It has an inhibitory effect on liver microsomal lipid peroxidation caused by carbon tetrachloride and the metabolic conversion of carbon tetrachloride into carbon monoxide, and reduces the consumption of reduced coenzyme II and oxygen during carbon tetrachloride metabolism, thereby protecting the structure and function of liver cell biomembranes. This product can also reduce the elevated liver ALT induced by prednisone and promote liver regeneration in mice with partial hepatectomy. The enzyme-lowering effect of this product does not directly inhibit serum and liver ALT activity, nor does it accelerate the inactivation of ALT in the blood. It may be a reflection of reduced liver tissue damage.

This product is a kind of enzyme-lowering drug for the treatment of hepatitis created in my country. It can reduce liver damage and alanine aminotransferase (ALT) elevation caused by carbon tetrachloride, inhibit liver microsomal lipid peroxidation caused by carbon tetrachloride and its metabolic conversion into carbon monoxide, reduce the consumption of reduced coenzyme II and oxygen in the metabolic process, and protect the structure and function of liver cell biomembrane. It can also reduce the increase of liver ALT induced by prednisone and promote liver regeneration in mice with partial hepatectomy. Its enzyme-lowering effect may be a reflection of the reduction of liver tissue damage.

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