Gut-restricted LXR activation provides a novel therapeutic avenue for treating Intestinal Failure-Associated Liver Disease (IFALD) without the systemic side effects of hepatic steatosis.
The amide analog WUSTL0717 demonstrates exceptional intestinal retention, specifically targeting LXR target genes in the gut rather than the liver.
Hepatoprotection is achieved through the upregulation of portal venous Apolipoprotein A1 (ApoA1) and phospholipids, reinforcing the protective role of gut-derived HDL.
Preclinical models show that local LXR agonism not only prevents liver fibrosis but also improves nutrient absorption and promotes weight recovery in SBS patients.
Background
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