AKR-001 has been engineered to mimic the biological activity of fibroblast growth factor 21 (FGF21), which regulates multiple metabolic pathways and cellular processes. By delivering sustained signaling through FGF21’s receptors, AKR-001 has the potential to address NASH, by reducing liver fat, inflammation and fibrosis.
Current investigational NASH therapies are classified as either metabolic, or anti-inflammatory/fibrotic. AKR-001 is both. AKR-001 redirects calories away from the liver, restores lipid metabolism in the liver to a healthy state and protects against hepatocyte stress and death. It also directly suppresses downstream inflammation and fibrosis.
Results from our ongoing Phase 2a BALANCED clinical trial are beginning to show AKR-001’s potential to be a cornerstone in NASH treatment. We reported the results of the primary endpoint and multiple secondary endpoints at week 12. All three dose groups treated with AKR-001 saw highly statistically significant absolute reductions in liver fat (12-15%, compared to 0% for placebo), relative reductions in liver fat (63-72%, compared to 0% for placebo) and reduction in the liver enzyme ALT (24-32 U/L, compared to 6U/L for placebo).