Related medicinesLuspaterceptSotaterceptGaretosmab
Where it comes from
- Made in
- Granulosa cells, pituitary, placenta, bone marrow, macrophages and many injured tissues
- Sent out by
- In the follicle and the pituitary by the cycle; everywhere else by inflammation and injury
- Acts on
- Pituitary (FSH synthesis)
- Follicles
- Immune cells
- Red cell precursors
- Fibroblasts
What it does
- Stimulates FSH; inhibin and follistatin are the brakes on it
- An early signal of inflammation; in animals it rises within an hour of endotoxin
- Activin signals restrain the late stages of red cell maturation, which is what the activin traps relieve
- In fibrodysplasia ossificans progressiva, the mutant receptor reads activin A as a command to make bone 3
In medicine
- Luspatercept, a trap for activin-family ligands, was approved in November 2019 for the anaemia of beta-thalassaemia and in 2020 for lower-risk myelodysplastic syndromes 1
- Sotatercept, a similar trap, was approved in March 2024 for pulmonary arterial hypertension 2
- Garetosmab, an antibody against activin A, cut new bone in fibrodysplasia ossificans progressiva in a phase 3 trial of 63 adults: 19 new lesions on placebo against one and two on the two doses over 56 weeks 3. It was approved in the United States in August 2026 4
Beyond the body’s own use
- Blocking activin is being tested for muscle wasting and cancer cachexia, on the argument that the traps which relieve anaemia also take the brake off muscle; no such use is approved
- Activin A is a research marker in heart failure and pre-eclampsia, and rises within an hour of an inflammatory insult in animals, which is why it is also studied as an early sepsis signal
Sources
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.