Where it comes from
- Made in
- Liver above all; some from fat, muscle and pancreas
- Sent out by
- Prolonged fasting, a protein-poor diet, fructose and alcohol, and cold; it rises in obesity and fatty liver disease
- Acts on
- Fat tissue (adiponectin, fat burning)
- Hypothalamus (sweet and alcohol preference)
- Liver
- Brown fat
What it does
- Shifts the body to burning fat during fasting
- Curbs the appetite for sugar and alcohol in mice and in human genetic studies; in people a sugar load raises it within hours 1
- Protects the liver against fat and injury; levels rise as the disease worsens
In medicine
- No approved medicine. Pegozafermin, a long-acting analogue, improved fibrosis in 26 to 27 percent of patients against 7 percent on placebo over 24 weeks in a 219-patient phase 2b trial 2
- Efruxifermin did the same in its own phase 2b trial, and both have moved into phase 3 for metabolic liver disease 3
Beyond the body’s own use
- FGF21 variants shape how much sugar and alcohol people like, one of the clearest diet-related signals in human genetics 1
- Fibroblast growth factors are named as a class on the World Anti-Doping Agency’s Prohibited List and banned at all times, in and out of competition 4
- Nothing containing FGF21 is approved; the analogues exist only inside trials, and what they have shown is less liver scarring rather than weight loss 2
Sources
- Søberg et al., FGF21 is a sugar-induced hormone associated with sweet intake and preference in humans, Cell Metabolism 2017
- Loomba et al., Randomised controlled trial of the FGF21 analogue pegozafermin in NASH, New England Journal of Medicine 2023
- Harrison et al., Once-weekly efruxifermin versus placebo in non-alcoholic steatohepatitis (HARMONY), Lancet Gastroenterology and Hepatology 2023
- World Anti-Doping Agency, Prohibited List 2026
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.