What is Myostatin (GDF-8)?

The TGF-β-family brake that limits skeletal muscle mass. Structurally it is TGF-β superfamily growth/differentiation factor (secreted dimer).

How strong is the evidence for GDF-8?

PeptideHormone grades GDF-8 at the "Established" evidence tier — its mechanism and core effects are settled across the peer-reviewed literature. It is catalogued as an endogenous signal the body produces itself, and the tier is an editorial judgment about the public literature that can change as the science does.

What is the half-life of GDF-8?

The reported circulating half-life of GDF-8 is Long (circulates as a latent complex).

MyostatinGDF-8

The TGF-β-family brake that limits skeletal muscle mass.

EndogenousEstablished

The body writes brakes as carefully as accelerators. Muscle has a ceiling because something is actively holding it there.

Identity

Class: TGF-β superfamily growth/differentiation factor (secreted dimer)
Source: Skeletal muscle
Receptor: Activin type II receptors (ActRIIB) → Smad2/3

Key properties

Evidence floorPreclinicalREF1PRE1

Molecular weight

≈ 25,000 Da

REF

Half-life (native)

Long (circulates as a latent complex)

PRE

Approximate values for the native hormone; engineered analogs are often deliberately larger and far longer-acting. Each figure carries its own provenance tier, and the floor is the weakest of them - the Standard.

Mechanism

Myostatin signals through activin type II receptors and the Smad2/3 pathway to restrain muscle growth — a negative regulator. Animals and rare humans lacking functional myostatin develop pronounced muscle hypertrophy, which is why blocking it is pursued therapeutically.

Reference notes

Loss of myostatin causes dramatic muscle overgrowth across species — the clearest evidence of its braking role.
It signals through activin type II receptors and Smad2/3, not a GPCR.
Blocking myostatin is a leading strategy for muscle preservation, including during incretin-driven weight loss.

Common questions

What is Myostatin (GDF-8)?: The TGF-β-family brake that limits skeletal muscle mass. Structurally it is TGF-β superfamily growth/differentiation factor (secreted dimer).
How does GDF-8 work?: Myostatin signals through activin type II receptors and the Smad2/3 pathway to restrain muscle growth — a negative regulator. Animals and rare humans lacking functional myostatin develop pronounced muscle hypertrophy, which is why blocking it is pursued therapeutically.
How strong is the evidence for GDF-8?: PeptideHormone grades GDF-8 at the "Established" evidence tier — its mechanism and core effects are settled across the peer-reviewed literature. It is catalogued as an endogenous signal the body produces itself, and the tier is an editorial judgment about the public literature that can change as the science does.
What is the half-life of GDF-8?: The reported circulating half-life of GDF-8 is Long (circulates as a latent complex).

Selected literature

Curated peer-reviewed reviews, sourced from PubMed. Selected for relevance, not exhaustive — open any entry on PubMed for the full record and its primary citations.

1.Mechanisms regulating skeletal muscle growth and atrophy · The FEBS journal, 2013 · PMID 23517348
2.Myostatin/Activin Receptor Ligands in Muscle and the Development Status of Attenuating Drugs · Endocrine reviews, 2022 · PMID 34520530

External references

GDF-8 in the public knowledge graph — the same entity resolved across the authoritative chemistry and protein databases.