Troxerutin

The pharmacodynamic effects of HR have been demonstrated in different in vitro and in vivo studies. At the cellular level the capability of HR to protect the vascular wall from the oxidative attack of activated blood cells and its affinity to the endothelium of capillaries and venoles could be shown.

In studies in healthy individuals or in patients suffering from CVI the following pharmacodynamic effects of HR could be demonstrated:

• reduction of the capillary permeability
• restoration of the veno-arteriolar reflex
• increase of the venous refilling time
• increase of the transcutaneous oxygen tension.

All these effects are compatible with the primary effect of HR being on the microvascular endothelium, with a resultant diminution of oedema.

The standardised mixture of HR consists of mono-HR, di-HR, tri-HR, and tetra-HR, which differ in the number of their hydroxyethyl substituents.

Absorption

After oral administration of ¹⁴C-HR, peak plasma levels are detected after 2-9 hours.

Distribution

The plasma level declines progressively until 40 hours, after which the decline is very slow. This observation and the results obtained after i.v. application, indicate that HR may be distributed to tissues (especially the endothelium of vessels), from which it is progressively and slowly released back into the circulation.

Plasma protein binding is 27-29%.

Biotransformation

The main metabolic pathway of HR after oral administration is hepatic Oglucuronidation.

Elimination

HR and its metabolites are excreted by both the biliar and the renal route. Excretion via the renal pathway is complete after 48 hours. The mean terminal half-life of the main constituent of HR, the tri-HR, is 18.3 hours with a range of 13.5 to 25.7 hours.

Non-clinical data reveal no special hazard for humans based on conventional studies of acute dose toxicity, repeated dose toxicity, genotoxicity and toxicity to reproduction.