To determine whether PPARδ agonists are beneficial in experimental liver fibrosis, mice are treated orally with a PPARδ agonist, KD-3010, or with the well-validated PPARδ agonist GW501516. KD-3010, but not GW501516, shows hepatoprotective and antifibrotic effects in liver fibrosis induced by carbon tetrachloride (CCl₄) or bile duct ligation (BDL). Liver injury is induced by repeated injections of CCl₄, and mice are treated daily with vehicle, the widely used PPARδ agonist GW501516, or the PPARδ agonist KD-3010 by oral gavage. Control oil-injected mice do not show any liver damage. Liver injury consisting of hepatocyte death and inflammation is seen in the vehicle- or GW501516-treated group injected with CCl₄ on H&E-stained liver sections but is markedly reduced in the KD3010-treated group^[1].