Ursofalk Mechanism of Action

Pharmacology: Pharmacodynamics: Small amounts of ursodeoxycholic acid occur naturally in human bile.
After oral administration, it reduces cholesterol saturation of the bile by inhibiting cholesterol absorption in the intestine and decreasing cholesterol secretion into the bile. Presumably as a result of dispersion of the cholesterol and formation of liquid crystals, a gradual dissolution of cholesterol gallstones occurs.
According to current knowledge, the effects of ursodeoxycholic acid in hepatic and cholestatic diseases are thought to be due to a relative exchange of lipophilic, detergent-like, toxic bile acids for the hydrophilic, cytoprotective, non-toxic ursodeoxycholic acid, together with an improvement in the secretory capacity of the hepatocytes, as well as to immune-regulatory processes.
Pharmacokinetics: Orally administered ursodeoxycholic acid is rapidly absorbed in the jejunum and upper ileum through passive transport and in the terminal ileum through active transport. The rate of absorption is generally 60 - 80 %. After absorption, the bile acid undergoes almost complete hepatic conjugation with the amino acids glycine and taurine and is then excreted with the bile. First-pass clearance through the liver is up to 60 %.Under the influence of intestinal bacteria, there is partial degradation to 7-keto-lithocholic acid and lithocholic acid. Lithocholic acid is hepatotoxic and causes liver parenchyma damage in a number of animal species. In humans, only very small amounts are absorbed which are sulphated in the liver and thus detoxified, before being excreted in the bile and ultimately in the faeces.
The biological half-life of ursodeoxycholic acid is 3.5 - 5.8 days.