Where it comes from
- Made in
- Wherever both chains are made at once: ovary, pituitary, placenta
- Sent out by
- With activins A and B
- Acts on
- Pituitary
- Follicles
What it does
- Stimulates FSH like the other activins, and follistatin neutralises it as it does them 1
- In cell work it switches on the bone morphogenetic protein branch, SMAD1/5, far more strongly than activin A does, which is the one hint that the mixed dimer is not simply a blend of the two 1
- A minor species in people: a specific assay found it in bulk in cow, sheep and pig follicular fluid and at about a two-hundredth of that in human follicular fluid 2
In medicine
- Nothing is measured or treated: no assay used in care separates it from activin A and activin B
- The approved activin traps catch it as they catch the other two, so it is covered by treatment without ever being named
Beyond the body’s own use
- It can be told apart in the laboratory. A two-site assay cross-reacts less than 0.2 per cent with the other activins, the inhibins and follistatin, so the limit is clinical interest, not chemistry 2
- Followed through six whole pregnancies it was undetectable at every visit while activin A rose 22-fold, which is the clearest evidence that the heterodimer is not a circulating hormone in people 3
Sources
- Olsen et al., Activins as dual specificity TGF-beta family molecules, SMAD activation via activin- and BMP-type 1 receptors, Biomolecules 2020
- Evans et al., Development, validation and application of a two-site ELISA for activin-AB, Journal of Endocrinology 1997
- Fowler et al., A longitudinal study of maternal serum inhibins, activins and follistatin during pregnancy, Human Reproduction 1998
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.