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Context, anatomy, and key evidence

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activin antagonist

Follistatin 315

Published evidence · coverage incomplete

Anatomy in the research

Anatomy evidence is still being assembled.

These are anatomical mentions in cited research—not established treatment targets or proof of benefit in people.

This publication has no anatomy passages that meet our source-linking checks yet. Read the available findings ↓

General anatomy view only. No peptide-specific structures are highlighted.

At a glance

What is it—and why does it matter?

An introduction is not yet available. The findings below address specific research questions, not a complete account of this peptide.

This published profile is a reference in progress. Findings retain their source context; missing topics are marked below.

What is it?

A molecule, not a product name.

Identity

Follistatin (human) is described as a regulatory glycoprotein, indicating a protein with regulatory biological roles.

Human research · design must be checked

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Human follistatin is a regulatory glycoprotein

    An engineered human follistatin variant: insights into the pharmacokinetic and pharmocodynamic relationships of a novel molecule with broad therapeutic potential. · Abstract

    pubmed:23249626:bdc9f4ba1d68:bdc9f4ba1d68

How does it work?

Target, response, and disposition.

Mechanism

Follistatin is described as a myostatin-inhibiting protein (i.e., it inhibits myostatin activity).

Animal / laboratory evidence

2 cited sources · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

5 cited passages across 2 source records. 2 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Follistatin, a myostatin-inhibiting protein,

    Detection of black market follistatin 344. · Abstract

    pubmed:31758732:f5e4ca131d7e:f5e4ca131d7e
  2. supports · Source-backed record
    Activin A is an autocrine inhibitor of cell growth in the liver.

    Possible endocrine control by follistatin 315 during liver regeneration based on changes in the activin receptor after a partial hepatectomy in rats. · BACKGROUND/AIMS

    pubmed:15782995:ca9c7c75937e:ca9c7c75937e
  3. supports · Source-backed record
    The biological activity of activin A is mediated by a heteromeric receptor complex.

    Possible endocrine control by follistatin 315 during liver regeneration based on changes in the activin receptor after a partial hepatectomy in rats. · BACKGROUND/AIMS

    pubmed:15782995:ca9c7c75937e:ca9c7c75937e
  4. supports · Source-backed record
    Follistatin (FS) binds to activin and inhibits its biological effects

    Possible endocrine control by follistatin 315 during liver regeneration based on changes in the activin receptor after a partial hepatectomy in rats. · BACKGROUND/AIMS

    pubmed:15782995:ca9c7c75937e:ca9c7c75937e
  5. supports · Source-backed record
    and acts as a negative regulator of muscle cells.

    Possible endocrine control by follistatin 315 during liver regeneration based on changes in the activin receptor after a partial hepatectomy in rats. · BACKGROUND/AIMS

    pubmed:15782995:ca9c7c75937e:ca9c7c75937e

Mechanism

Protein engineering changes described include Fc fusion (murine IgG(1) Fc) and elimination of heparan sulfate-binding activity to alter PK characteristics.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    we leveraged protein engineering to modify the PK characteristics of the native molecule by fusing FST315 to a murine IgG(1) Fc and removing the intrinsic heparan sulfate-binding activity of follistatin.

    An engineered human follistatin variant: insights into the pharmacokinetic and pharmocodynamic relationships of a novel molecule with broad therapeutic potential. · Abstract

    pubmed:23249626:bdc9f4ba1d68:bdc9f4ba1d68

Mechanism

The work includes in-depth characterization of pharmacokinetic/pharmacodynamic relationships for native FST315.

Human research · design must be checked

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    we performed in-depth analyses of the PK/PD relationships of native follistatin-315 (FST315).

    An engineered human follistatin variant: insights into the pharmacokinetic and pharmocodynamic relationships of a novel molecule with broad therapeutic potential. · Abstract

    pubmed:23249626:bdc9f4ba1d68:bdc9f4ba1d68

Mechanism

The described analytical workflow uses immunomagnetic purification and then protein separation/detection by SDS-PAGE and Western blotting using a monoclonal anti-His antibody.

Molecular / pharmacology evidence

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    The detection method is based on immunomagnetic purification followed by SDS-PAGE and Western blotting with a monoclonal anti-His antibody.

    Detection of black market follistatin 344. · Abstract

    pubmed:31758732:f5e4ca131d7e:f5e4ca131d7e

What has been studied?

What the evidence says.

Study findings

The source attributes multiple functional effects to human follistatin, including antiinflammatory activity, wound healing, and muscle stimulation.

Human research · design must be checked

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Human follistatin is a regulatory glycoprotein with widespread biologic functions, including antiinflammatory activities, wound-healing properties, and muscle-stimulating effects.

    An engineered human follistatin variant: insights into the pharmacokinetic and pharmocodynamic relationships of a novel molecule with broad therapeutic potential. · Abstract

    pubmed:23249626:bdc9f4ba1d68:bdc9f4ba1d68

Risks and interactions

Risks, organized for scanning.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Products and regulatory status

Same ingredient. Different records.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Administration context

The practical clinical context.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Additional research & classification gaps

2 archived statements are kept separate from drug-effect findings. Media studies, economic models, methods, and records with unresolved scope are not used as medical-effect evidence.

Inspect contextual research (2)
Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The presence of a His-tag enables clear discrimination of the detected protein from endogenous (naturally occurring) follistatin.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The immunoprecipitation step uses a polyclonal anti-follistatin antibody.

Research context only—not evidence of a treatment effect.

Research status + gaps

What still needs better answers?

  • No publishable claim yet for: administration, contraindication, interaction, regulatory, safety
  • 27 compiled claim(s) withheld by automated assurance: assurance_score_below_0.58 (17), assurance_score_below_0.72 (8), current_regulatory_source_required (10), extraction_ambiguity (19), high_risk_requires_regulatory_or_two_independent_sources (10), no_direct_support (18)
  • A source-backed introductory overview is not yet available.

These are the limits of this profile, not an exhaustive list of scientific uncertainties.

References + discovery

Open the records yourself.

  1. Possible endocrine control by follistatin 315 during liver regeneration based on changes in the activin receptor after a partial hepatectomy in rats.

    pubmed · published 2005-01-01 · retrieved 2026-09-09T18:02:18Z

  2. An engineered human follistatin variant: insights into the pharmacokinetic and pharmocodynamic relationships of a novel molecule with broad therapeutic potential.

    pubmed · published 2013-03-01 · retrieved 2026-09-04T19:33:24Z

  3. Detection of black market follistatin 344.

    pubmed · published 2019-11-01 · retrieved 2026-09-09T21:48:18Z

Publication history and provenance

Version 1 · Automated assessment · 2026-09-09T21:48:18Z

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