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.

It can significantly inhibit the day and night basal gastric acid secretion, and can also inhibit the gastric acid secretion induced by food, histamine, pentagastrin, caffeine and insulin.

Its antiasthmatic effect is slightly weaker than that of theophylline, and its cardiac stimulant effect is only 1/20 to 1/10 of that of aminophylline. It has less impact on the heart and nervous system, and is especially suitable for asthma patients with tachycardia. It has a direct relaxant effect on respiratory smooth muscle, and its mechanism of action is the same as that of theophylline, which is partly due to the release of endogenous adrenaline and noradrenaline. In addition, it can enhance the contractility of the diaphragm and help improve respiratory function.

This product is first converted into 5-fluoro-2-deoxyuridine nucleotide in the body, which inhibits thymine nucleotide synthetase, blocking the conversion of deoxyuridine nucleotide into deoxythymine nucleotide, thereby inhibiting DNA biosynthesis. In addition, by preventing uracil and orotic acid from incorporating into RNA, the effect of inhibiting RNA synthesis is achieved. This product is a cell cycle-specific drug that mainly inhibits S-phase cells.

It has anti-inflammatory, antipyretic and analgesic effects. Its mechanism of action is to reduce the synthesis of prostaglandins by inhibiting cyclooxygenase. It stops the formation of pain nerve impulses in inflammatory tissues and inhibits inflammatory reactions, including inhibiting the chemotaxis of leukocytes and the release of lysosomal enzymes. As for the antipyretic effect, it acts on the hypothalamic temperature regulation center, causing peripheral vasodilation and sweating, which increases heat dissipation. This central antipyretic effect may also be related to the inhibition of prostaglandin synthesis in the hypothalamus.