This product is a macrolide antibiotic, which has inhibitory effects on Gram-positive bacteria such as Staphylococcus aureus, Streptococcus, and Pneumococcus, as well as some Gram-negative bacteria such as Haemophilus influenzae, Bordetella pertussis, Neisseria gonorrhoeae, Legionella pneumophila, and some anaerobic bacteria such as Bacteroides fragilis, Streptococcus peptostreptococcus, and Propionibacterium acnes. In addition, it also has inhibitory effects on mycoplasma. The characteristics of this product are that its antibacterial activity in vitro is similar to that of erythromycin, but its antibacterial activity in vivo against some bacteria such as Staphylococcus aureus, Streptococcus, and Haemophilus influenzae is stronger than that of erythromycin. There is cross-resistance between this product and erythromycin. The mechanism of action of this product is to inhibit the association of the 50S subunit of the nuclear protein and inhibit protein synthesis to produce an antibacterial effect.

It is an H2 receptor blocker that can inhibit basal gastric acid and gastrin-stimulated gastric acid secretion, and reduce the activity of gastric acid and pepsin.

In the acidic environment of the stomach, it forms a diffuse protective layer covering the mucosal surface, preventing gastric acid, enzymes and food from invading the mucosa. It has the effects of reducing pepsin activity, increasing mucin secretion, promoting the release of prostaglandins from the mucosa, and enhancing the defense of the gastric mucosa. In addition, it also has a certain killing effect on Helicobacter pylori and can promote the healing of lesions.

This product belongs to Class III antiarrhythmic drugs. The main electrophysiological effect is to prolong the action potential and effective refractory period of various myocardial tissues, which is conducive to eliminating reentrant excitement. At the same time, it has mild non-competitive α and β adrenergic receptor blocking and mild Class I and IV antiarrhythmic properties. Reduce the automaticity of the sinus node. It has no effect on the resting membrane potential and action potential height. The inhibition of forward conduction of the atrioventricular bypass pathway is greater than the reverse. Due to excessive prolongation of repolarization, the electrocardiogram after oral administration has a prolonged QT interval and T wave changes, which can slow down the heart rate by 15~20% and prolong the PR and Q-T intervals by about 10%. It has a direct dilation effect on the coronary arteries and peripheral blood vessels. It can affect thyroid hormone metabolism.

This product belongs to the class Ic (i.e., directly acting on the cell membrane) antiarrhythmic drug. The experimental results of isolated animal myocardium indicate that 0.5-1ug/min can reduce the depolarization effect during contraction, thereby prolonging conduction, slightly prolonging the duration of action potential and the effective refractory period, and can increase the threshold potential of myocardial cells, significantly reducing the spontaneous excitability of the myocardium. It acts on both the atrium and ventricle (mainly affecting the Purkinje fibers, with a smaller effect on the myocardium), and also on the formation and conduction of excitement. Clinical data show that the therapeutic dose (300mg orally and 30mg intravenously) can reduce the irritability of the myocardium, the effect is long-lasting, PQ and QRS are increased, and the effective refractory period of the atrium and atrioventricular node is prolonged. It has an antagonistic effect on various types of experimental arrhythmias.

This product belongs to the class Ic (i.e., directly acting on the cell membrane) antiarrhythmic drug. The experimental results of isolated animal myocardium indicate that 0.5-1ug/min can reduce the depolarization effect during contraction, thereby prolonging conduction, slightly prolonging the duration of action potential and the effective refractory period, and can increase the threshold potential of myocardial cells, significantly reducing the spontaneous excitability of the myocardium. It acts on both the atrium and ventricle (mainly affecting the Purkinje fibers, with a smaller effect on the myocardium), and also on the formation and conduction of excitement. Clinical data show that the therapeutic dose (300mg orally and 30mg intravenously) can reduce the irritability of the myocardium, the effect is long-lasting, PQ and QRS are increased, and the effective refractory period of the atrium and atrioventricular node is prolonged. It has an antagonistic effect on various types of experimental arrhythmias.