Fasiglifam (TAK-875) was developed as a treatment for type 2 diabetes. It works by stimulating the G protein-coupled receptor GPR40, which is found in pancreatic beta cells. Activation of this receptor enhances glucose-dependent insulin secretion, meaning it helps the body release more insulin only when blood sugar levels are high. This mechanism reduces the risk of hypoglycemia, a common side effect with other diabetes medications. The compound showed promising results in clinical trials by significantly lowering HbA1c levels, a key marker of long-term blood glucose control. It was considered a potential alternative for patients who do not achieve adequate control with existing therapies like metformin or sulfonylureas. However, development was discontinued due to safety concerns, particularly liver toxicity observed in some patients during long-term use. Despite its efficacy, the risk of hepatotoxicity outweighed the benefits, leading to the termination of its clinical development.