Protein / target

Growth/differentiation factor 8

Encoded byMSTNO14793Homo sapiensSwiss-Prot

UniProt: O14793 Ensembl: ENSG00000138379 HGNC: HGNC:4223 NCBI Gene: 2660

Clinical-stage

Therapeutic maturity

Clinical candidates

Antibody-tractable

Druggability

Advanced Clinical

Research papers

Protein at a glance

Biological role

Protein homodimerization

Strongest disease association

Proximal spinal muscular atrophy

Via encoding gene MSTN · Literature evidence · score 0.36

Therapeutic position

Clinically advancing target

Antibodies

Research activity

Emerging research

2 papers · latest 2025

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Acts specifically as a negative regulator of skeletal muscle growth

Subcellular location

Secreted

Domains and Gene Ontology detail (35)

Gene Ontology

Cextracellular space
Fcytokine activity
Fgrowth factor activity
Fheparin binding
Fidentical protein binding
Fprotein homodimerization activity
Fsignaling receptor binding
Pcellular response to hypoxia
Pmuscle cell cellular homeostasis
Pmuscle organ development
Pmyoblast migration involved in skeletal muscle regeneration
Pnegative regulation of insulin receptor signaling pathway

375 aa · 43 kDa

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Cell migrationGOImmune signallingGO

View supporting evidence

Cell migration

·positive regulation of macrophage chemotaxis
·trophoblast cell migration

Immune signalling

·cytokine activity
·trophoblast cell migration

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene MSTN

Gene-level evidence surfaced through the gene MSTNthat encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Proximal spinal muscular atrophy

0.48Limited support

Clinical evidence dominant · Open Targets 0.36

Muscular Atrophy, Spinal

0.44Limited support

Clinical evidence dominant · Open Targets 0.35

Obesity disorder

0.36Limited support

Animal model evidence dominant · Open Targets 0.12

Muscular Dystrophy, Duchenne

0.26Limited support

Literature evidence dominant · Open Targets 0.11

Sarcopenia

0.22Preliminary

Literature evidence dominant · Open Targets 0.13

View evidence synthesis (5)

Proximal spinal muscular atrophyLimited support

0.48

agreement 0.33–0.64

Clinical77%Literature23%

Open Targets aggregate 0.36 · 2 independent evidence families

Muscular Atrophy, SpinalLimited support

0.44

agreement 0.29–0.60

Clinical91%Literature9%

Open Targets aggregate 0.35 · 2 independent evidence families

Obesity disorderLimited support

0.36

agreement 0.23–0.49

Animal model50%Literature28%Clinical22%

Open Targets aggregate 0.12 · 3 independent evidence families

Muscular Dystrophy, DuchenneLimited support

0.26

agreement 0.14–0.39

Literature42%Animal model36%Clinical22%

Open Targets aggregate 0.11 · 3 independent evidence families

SarcopeniaPreliminary

0.22

agreement 0.06–0.37

Literature60%Clinical40%

Open Targets aggregate 0.13 · 2 independent evidence families

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations

Proximal spinal muscular atrophy0.36

Muscular Atrophy, Spinal0.35

Sarcopenia0.13

Obesity disorder0.12

Muscular Dystrophy, Duchenne0.11

Drug development

6 compounds recorded · 6 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (6)

DOMAGROZUMABPhase 2

RAMATERCEPTPhase 2

LANDOGROZUMABPhase 2

STAMULUMABPhase 1 2

TREVOGRUMABPhase 2

APITEGROMABPhase 3

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Antibodies — Strong

Advanced Clinical and UniProt loc med conf support this modality.

Protein degraders — Emerging

Feasibility evidence (small molecule binder) — no clinical-stage drug of this modality recorded.

Other modalities — Strong

Advanced Clinical support this modality.

View underlying tractability evidence (6)

AB · Advanced ClinicalAB · UniProt loc med confAB · UniProt SigP or TMHMMAB · GO CC med confPR · Small Molecule BinderOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.