CSPC OUYI Pharmaceutical Co., Ltd.

It achieves antibacterial effect by inhibiting the activity of bacterial DNA gyrase and hindering bacterial replication. It has the characteristics of broad antibacterial spectrum and strong antibacterial effect, and has good antibacterial effect on most Enterobacteriaceae, some Gram-positive bacteria, Legionella, Mycoplasma, Chlamydia, etc., but has poor effect on anaerobic bacteria and enterococci.

This product is an intermediate in the synthesis of Schisandrae Chinensis A, which can reduce liver damage and alanine aminotransferase (ALT) elevation caused by carbon tetrachloride; it has an inhibitory effect on liver microsomal lipid peroxidation caused by carbon tetrachloride and the conversion of carbon tetrachloride into carbon monoxide, and reduces the consumption of reduced coenzyme II and oxygen in the process of carbon tetrachloride metabolism, thereby protecting the structure and function of liver cell biomembrane; it can reduce the increase of liver ALT induced by prednisone, and promote liver regeneration in mice with partial hepatectomy; it has a significant induction effect on cytochrome P450 enzyme activity, thereby enhancing the detoxification ability of carbon tetrachloride and certain carcinogens; it has an effect on improving protein metabolism in some hepatitis patients, increasing albumin and reducing globulin. It has no negative conversion effect on HbsAg and HbeAg, and cannot shrink the enlarged liver and spleen.

Dihydropyridine calcium antagonists can selectively inhibit the transmembrane transport of calcium ions into myocardial cells and smooth muscle cells, and inhibit the release of calcium ions from intracellular pools without changing the plasma calcium ion concentration. Pharmacological effects include: 1. It can simultaneously dilate the coronary arteries in the normal blood supply area and the ischemic area, antagonize spontaneous or ergonovine-induced coronary artery spasm, increase the delivery of myocardial oxygen in patients with coronary artery spasm, and relieve and prevent coronary artery spasm; 2. It can inhibit myocardial contraction, reduce myocardial metabolism, and reduce myocardial oxygen consumption; 3. It can dilate peripheral resistance vessels, reduce peripheral resistance, reduce systolic and diastolic blood pressure, and reduce cardiac afterload; 4. It can delay the sinus node function and atrioventricular conduction of the isolated heart; electrophysiological studies of whole animals and humans have not found that this product has the effect of delaying atrioventricular conduction, prolonging the recovery time of the sinus node, and slowing down the sinus node rate.

Synthetic nucleoside antiviral drugs, have inhibitory effects on herpes simplex virus type 1 (HSV-1), HSV-2 and varicella-zoster virus (VZV). It is converted into acyclovir monophosphate by virus-encoded thymidine kinase and further metabolized into triphosphate, thus terminating herpes virus DNA replication.

Synthetic nucleoside antiviral drugs have inhibitory effects on herpes simplex virus type I (HSV-1), type H (HSV-2) and varicella-zoster virus (VZV) in vivo and in vitro. Cell culture results show that this product has the strongest inhibitory effect on HSV-1 virus, followed by HSV-2 and VZV virus. Because this product has affinity for thymidine kinase (TK) encoded by HSV and VZV, it has a highly selective inhibitory effect. This type of viral enzyme converts acyclovir into acyclovir monophosphate, a nucleoside analog. The monophosphate is further converted into diphosphate by guanylate kinase in the cell, and then converted into triphosphate by multiple enzymes in the cell. In vitro, acyclovir triphosphate stops herpes virus DNA replication.