ATC Group: A05AX Other drugs for bile therapy

The World Health Organization's ATC classification organizes medical drugs based on therapeutic properties, chemical composition, and anatomy. It helps make essential medicines readily available globally and is widely used in the pharmaceutical industry.

Position of A05AX in the ATC hierarchy

Level Code Title
1 A Alimentary tract and metabolism
2 A05 Bile and liver therapy
3 A05A Bile therapy
4 A05AX Other drugs for bile therapy

Group A05AX contents

Code Title
A05AX01 Piprozolin
A05AX02 Hymecromone
A05AX03 Cyclobutyrol
A05AX04
A05AX05
A05AX06
A05AX07

Active ingredients in A05AX

Active Ingredient

Hymecromone is an inhibitor of hyaluronic acid synthesis and has a spasmolytic effect on extrahepatic bile ducts. Hymecromone is an approved prescription drug used for treating biliary spasm. This action takes place through a musculotropic mechanism, without atropinic effects. Increased choleresis is also observed without excitation of gall bladder contraction.

Maralixibat is a minimally absorbed, reversible, potent, selective inhibitor of the ileal bile acid transporter (IBAT). Maralixibat acts locally in the distal ileum to decrease the reuptake of bile acids and increase the clearance of bile acids through the colon, reducing the concentration of bile acids in the serum.

Odevixibat is a reversible, potent, selective inhibitor of the ileal bile acid transporter (IBAT). Odevixibat acts locally in the distal ileum to decrease the reuptake of bile acids and increase the clearance of bile acids through the colon, reducing the concentration of bile acids in the serum. The extent of reduction of serum bile acids does not correlate with systemic PK.

Seladelpar is a peroxisome proliferator-activated receptor delta (PPARδ) agonist, or delpar. PPARδ is a nuclear receptor expressed in the liver and other tissues. PPARδ activation reduces bile acid synthesis in the liver through Fibroblast Growth Factor 21 (FGF21)-dependent downregulation of CYP7A1, the key enzyme for the synthesis of bile acids from cholesterol and by decreasing cholesterol synthesis and absorption. These actions result in lower bile acid exposure in the liver and reduced circulating bile acid levels.

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