A water-soluble bile acid that steadies protein folding and holds back cell self-destruction. Its dependable effect: abnormal liver and bile-flow markers improve. Single studies suggest better insulin action in obesity and blood-vessel protection after a sugar load. The motor neuron disease claim failed a larger test. Lifespan and vision claims rest on animals. Loose stools usual; long-term safety unmeasured. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Alanine aminotransferase | 10–26 U/L (men), 9–22 U/L (women) | Primary marker of liver cell injury and the outcome most reliably moved |
| Aspartate aminotransferase | 10–26 U/L | Confirms hepatocellular injury and flags non-liver sources |
| Alkaline phosphatase | 70–100 U/L | Defining marker of impaired bile flow and the main efficacy endpoint in cholestatic use |
| Gamma-glutamyl transferase | Below 20 U/L | Most sensitive marker of biliary obstruction and of the compound's biliary action |
| Total bilirubin | 0.4–1.0 mg/dL | Detects impaired bile excretion, the main safety signal for a bile-flow-stimulating agent |
| Fasting insulin | 2–5 µIU/mL | Tracks the insulin-sensitivity effect, the main metabolic outcome |
| Glycated haemoglobin | 4.8–5.3% | Confirms whether improved insulin action translates into better glucose control over months |
| Total serum bile acids | Below 10 µmol/L | Direct safety marker for bile-acid accumulation and the biochemical correlate of itch |
| High-sensitivity C-reactive protein | Below 0.5 mg/L | General marker of systemic inflammation, the pathway the compound is proposed to damp |
| Albumin | 4.2–5.0 g/dL | Measures the liver's synthetic capacity, which rose in the cirrhosis trial |
Cadence: Baseline panel before starting; liver panel at 6–8 weeks, metabolic markers at 12 weeks, both every 3–6 months thereafter, moving to every 6–12 months once values are stable