This product is an antagonist of angiotensin II (Ang II) receptor AT1. It inhibits vasoconstriction and the release of aldosterone by selectively blocking the binding of Ang II to AT1 receptor, thus producing a hypotensive effect.

It inhibits bacterial protein synthesis by hindering the bacterial transpeptidation process. It has antibacterial effects on a variety of Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms, including but not limited to Staphylococcus aureus, Streptococcus pyogenes, Pneumococcus, Haemophilus influenzae, Moraxella catarrhalis, Treponema pallidum, Neisseria gonorrhoeae, Chlamydia trachomatis, etc. The mechanism of action is the same as that of erythromycin, mainly binding to the 50S subunit of the bacterial ribosome to inhibit RNA-dependent protein synthesis.

Carvedilol has both (1) and non-selective (2) receptor blocking effects within the therapeutic dose range, and has no intrinsic sympathomimetic activity. This product blocks the (1) receptors on the postsynaptic membrane, thereby dilating blood vessels and reducing peripheral vascular resistance; it blocks the (2) receptors, inhibits the secretion of renin by the kidneys, blocks the renin-angiotensin-aldosterone system, and produces a hypotensive effect. Carvedilol lowers blood pressure rapidly and can maintain its hypotensive effect for a long time. It has no effect on left ventricular ejection fraction, cardiac function, renal function, renal blood perfusion, peripheral blood flow, plasma electrolytes and blood lipid levels, does not affect the heart rate or slightly slows it down, and rarely produces water and sodium retention.

It is rapidly converted into penciclovir in the body and has an inhibitory effect on HSV-1, HSV-2 and VZV. It is phosphorylated into penciclovir triphosphate by viral thymidine kinase, which selectively inhibits the synthesis and replication of herpes virus DNA.

It is rapidly converted into penciclovir in the body and has inhibitory effects on HSV-1, HSV-2 and VZV. It is phosphorylated into penciclovir triphosphate by viral thymidine kinase, selectively inhibiting the synthesis and replication of herpes virus DNA.