This product is an opioid receptor antagonist, which has almost no pharmacological activity itself, but can competitively antagonize various opioid receptors and has a strong affinity for m receptors. It completely or partially corrects the central inhibitory effects of opioids, such as respiratory depression, sedation and hypotension; it has a wake-promoting effect on animals with acute ethanol poisoning; it is a pure opioid receptor antagonist and does not cause respiratory depression, psychotomimetic reactions or miotic reactions; there is no drug resistance, nor physiological or mental dependence; it antagonizes the effects of opioids by competing for the same receptor sites.

This product is a proton pump inhibitor for gastric parietal cells. It is relatively stable under neutral and weakly acidic conditions and rapidly activated under strongly acidic conditions. Its pH-dependent activation characteristics make it more selective for H and K-ATPase. This product can specifically inhibit the H and K-ATPase on the secretory microtubules and tubular vesicles in the cytoplasm of the parietal cell apical membrane, causing irreversible inhibition of the enzyme, thereby effectively inhibiting the secretion of gastric acid. Since H and K-ATPase are the last process of acid secretion in parietal cells, this product has a strong acid-suppressing ability. It can not only non-competitively inhibit gastric acid secretion caused by gastrin, histamine, and choline, but also inhibit part of the basal gastric acid secretion that is not affected by choline or H2 receptor blockers. When used in combination with other drugs, this product has the advantage of small drug interactions. This product is metabolized through the I system of the cytochrome P450 enzyme system in hepatocytes, and can also be metabolized through the II system. When used with other drugs that are metabolized by the P450 enzyme system, the metabolic pathway of this product can be carried out through the II enzyme system, making it less likely to have competitive effects on the drug-metabolizing enzyme system, reducing the interaction between drugs in the body. No mutagenic, carcinogenic or teratogenic effects.

This product acts specifically on the gastric mucosal parietal cells, reducing the activity of H/KATPase in the parietal cells, thereby inhibiting the secretion of gastric acid. Compared with omeprazole and lansoprazole, this product has a weaker inhibitory effect on cytochrome P450-dependent enzymes. No adverse effects were found in either short-term or long-term administration of pantoprazole. This drug is non-carcinogenic, does not impair fertility, and does not induce teratogenesis. After 2.5 years of continuous medication, there were no changes in various experimental parameters of liver enzymology and cholesterol metabolism.

It can reduce the level of DHBV-DNA in the serum of ducks infected with hepatitis B virus (DHBV) and has a protective effect on toxic liver damage in mice caused by CCL4 and galactosamine

Non-digitalis cardiotonic agents have positive inotropic effects, can enhance myocardial contractility, improve myocardial pump function, have vasodilatory effects, can reduce myocardial oxygen consumption; improve myocardial cell metabolism, protect ischemic and hypoxic myocardium; can improve sinoatrial node P cell function.

Cyclic adenosine meglumine is a non-digitalis cardiotonic agent with positive inotropic effect. It can enhance myocardial contractility, improve myocardial pump function, dilate blood vessels, and reduce myocardial oxygen consumption. It can improve myocardial cell metabolism and protect ischemic and hypoxic myocardium. It can improve the function of sinoatrial node P cells.