Comparison
Follistatin (FST) vs. GHRP-6
Two peptides side-by-side — identity, evidence base, legal status and known adverse events.
Identity
Category
Growth
Growth
CAS no.
122956-17-2
87616-84-0
Molecular weight
35000 g/mol
873.02 g/mol
Half-life
no data
0.4 h
Sequence
Glykoprotein, ~315 Aminosäuren in der zirkulierenden Hauptform (Sequenz isoformabhängig, kein einheitliches kurzes Peptid)His-D-Trp-Ala-Trp-D-Phe-Lys-NH2Mechanism of action
Follistatin (FST)
Follistatin binds with high affinity to activin and to myostatin (GDF-8), as well as related TGF-β ligands such as GDF-11 and some BMPs, preventing their binding to the activin type-II receptors. Myostatin is a negative regulator of skeletal muscle mass; by sequestering myostatin, its growth-inhibiting signalling is removed (de-repression). Because follistatin additionally neutralises activin, it acts on several muscle-inhibiting pathways at once — in animal models this produced greater muscle gain than knocking out myostatin alone. Several isoforms exist (including FST-288 and FST-315) that differ in tissue binding via heparan sulfate. The FST344 variant used in gene therapy was chosen to reduce binding to off-target structures.
GHRP-6
GHRP-6 is a high-affinity agonist of the growth-hormone secretagogue receptor 1a (GHSR-1a) — the same receptor later shown to bind the endogenous hormone ghrelin. The identification of GHRP-6 as a pharmacological anchor led to cloning of GHSR in 1996 and the discovery of ghrelin itself in 1999. GHRP-6 stimulates pituitary GH secretion via a pathway independent of GHRH and can be combined synergistically with GHRH. Via GHSR in the hypothalamus it additionally activates NPY/AgRP neurons, producing an orexigenic (appetite-stimulating) effect in animal models.
Evidence base
Highest evidence
Human trial
Human trial
Studies
4
4
of which in humans
1
2
Effects recorded
4
4
Open conflicts
1
1
Documented adverse events
1
2
Legal status
Full entries
Frequently asked questions
- What is the difference between Follistatin (FST) and GHRP-6?
- Follistatin (FST) is classified as "Growth", while GHRP-6 is classified as "Growth". Follistatin (FST): Follistatin is an endogenous glycosylated binding protein (~35 kDa, considerably larger than typical peptides) that binds and neutralises members of the TGF-β superfamily, including activin and myostatin (GDF-8). In animal models, raising follistatin de-represses muscle growth. Clinically it has been studied mainly via AAV gene therapy (FS344) in muscular dystrophies. Follistatin is not an approved drug; human efficacy and safety data are limited and stem mostly from early gene-therapy trials and preclinical research. A 'follistatin-344' product is sold on the grey market, the identity and purity of which cannot be verified without analytics. GHRP-6: Synthetic hexapeptide that founded the class of growth-hormone-releasing peptides (GHRPs). Cyril Bowers identified GHRP-6 in the late 1970s as the first orally and parenterally active GH secretagogue with no structural similarity to GHRH. Never approved as a medicine; downstream analogs (GHRP-2, hexarelin, ipamorelin) were pursued clinically. This page contrasts both neutrally and source-based — with no usage or dosing recommendation.
- Which peptide is better supported by science, Follistatin (FST) or GHRP-6?
- The highest available evidence level is "Human trial" for Follistatin (FST) and "Human trial" for GHRP-6. A higher evidence level means more robust data, but says nothing about suitability for an individual. The full body of evidence is on each peptide's own page.
- What is the legal status of Follistatin (FST) and GHRP-6 in Germany and the United States?
- Germany: Follistatin (FST) — Unapproved, GHRP-6 — Unapproved. United States: Follistatin (FST) — Unapproved, GHRP-6 — Unapproved. These are factual summaries with source and review date on the individual pages.