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Peptide Evidence Registry

Growth hormone axis · Metabolic & endocrine

FLGR-242

A branded follistatin-derived protein construct marketed with muscle-growth claims. No FLGR-242-specific animal outcome study, human study or registered human trial has been identified; related evidence is not compound-specific evidence.

L1Theory onlyNot approved for this useUnclearBiologic / other
How settled this rating is:
very-low confidence in the current evidence rating
Routes studied:
Not established
Also known as:
FLGR242, follistatin-derived albumin-binding construct
Last reviewed:
2026-10-11
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Evidence passport

FLGR-242

A one-screen evidence identity for this compound. These fields describe research maturity, confidence and legal status. They are not a safety guarantee, efficacy percentage or recommendation.

Reviewed 2026-10-11
Evidence level
L1Theory only
Confidence
Very low confidence in rating
Regulatory status
Not approved for this use
Development status
Unclear

Evidence strength

Human efficacy evidence0 of 100 evidence strength

Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.

Human safety evidence1 of 100 evidence strength

Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number.

The 0-100 values rate the strength and maturity of evidence, not how effective or safe the compound is.

Evidence base
Mostly animal and laboratory research
Furthest established stage
Not established
Human research maturity
Preclinical concept / no compound-specific outcome study identified
Source curation
Sources fully curated

Routes recorded

Most of this evidence comes from animals and cells

The supporting research for FLGR-242 is predominantly preclinical (Level 1–2). That is a legitimate starting point for science and a poor basis for personal decisions. Human results are not simply a scaled-up version of mouse results.

Overview

Human efficacy evidence strength0 of 100 evidence strength

Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.

Preclinical (animal / lab) evidence strength8 of 100 evidence strength

Higher = more animal, tissue or cell research. Preclinical results are a starting point, not proof of a human benefit.

Human safety evidence strength1 of 100 evidence strength

Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number.

Evidence for the assessed benefit

L1Theory onlyVery low confidence in rating

Level 1 (theory only). The rationale rests on related constructs (FS I-I, native follistatin and other myostatin inhibitors) and on a patented albumin-binding technology. None of that is FLGR-242-specific outcome evidence and it is not transferred to this profile.

Human research context: None identified.

Research maturity, benefit evidence, safety and approval are different questions.

How to read these scores

Every number here rates the evidence, not the compound. They are editorial 0-100 strength ratings, not percentages, and not a rating out of five stars.

  • Human efficacy evidence strength — Higher = more and better-quality human evidence. It does not mean the effect is bigger or that the compound works for you.
  • Preclinical evidence strength — Higher = more animal, tissue or cell research. Preclinical results are a starting point, not proof of a human benefit.
  • Human safety evidence strength — Higher = more mature, better-documented human safety data. It does not mean the compound is safer than one with a lower number. A score of 80 does not mean “80% safe”.
  • Evidence level (L0-L5) — the strongest type of study behind the compound, from anecdote (L0) to large replicated human trials (L5). It is a description of the study evidence, not a quality, safety or recommendation rating.
  • Confidence — how likely we think it is that this rating changes as new research lands. Low confidence means the picture is unsettled, not that the compound is bad.

None of these ratings is medical advice, a safety guarantee, or a recommendation to use anything. How we grade evidence.

How far human research has progressed: Preclinical concept / no compound-specific outcome study identified

Routes & formulations

No studied or approved route is established for FLGR-242. Nothing here describes how it is or should be used.

Route availability is not evidence of efficacy, and evidence from one route does not transfer to another. The Registry never provides dosing or sourcing information.

Peptide lifecycle

  1. Discovery

  2. Preclinical

  3. Phase I

  4. Phase II

  5. Phase III

  6. Approved

UnclearFurthest stage not established in our curated record

Associated with Epiq Bio Consulting LLC. No registered trial, regulatory filing or peer-reviewed compound-specific study was identified. The FLGR242 word mark was filed on 20 January 2026 and registered in the US on 6 October 2026 (Reg. 8482755); a trademark establishes a brand, not efficacy or safety.

Last documented development: 6 October 2026 — US trademark registration (brand only)

What it is

A branded recombinant construct described commercially as a fragmented or modified follistatin fused to an albumin-binding peptide. The exact full construct identity is not established in peer-reviewed literature, and those descriptions are commercial claims, not independently validated science. It is better understood as a protein/biologic construct than a conventional short peptide.

What people claim

  • Has a 19-day half-life in humans
  • Selectively blocks myostatin without activin effects
  • Builds large amounts of muscle in humans
  • Burns fat or improves metabolic health

What the evidence actually says

There is no FLGR-242-specific published animal outcome study, human efficacy study, human safety study or registered human trial in our record. Related research exists: FS I-I, a follistatin-derived myostatin inhibitor with much weaker activin binding than native follistatin, increased muscle mass and strength in transgenic mice, and FS I-I expression reduced fat mass and liver fat in mice. A US patent describes an albumin-binding linker construct. Related evidence is not compound-specific evidence: none of these findings show what FLGR-242 itself does in animals or people.

Related evidence

Useful next reads based on this compound — not recommendations.

Human evidence

  • None identified for FLGR-242.

Preclinical evidence

  • Related mechanism, not FLGR-242: Nakatani et al. (FASEB J 2008) reported that FS I-I, a follistatin-derived myostatin inhibitor with much weaker activin binding than native follistatin, increased muscle mass and strength in transgenic mice.
  • Related mechanism, not FLGR-242: FS I-I expression decreased adipose mass and hepatic steatosis in mice (PMID 21205933). Mouse findings for a different construct do not transfer to FLGR-242.
  • Related component, not FLGR-242: the original SA21 albumin-binding peptide bound human albumin with a Kd of about 467 nM (Dennis et al., J Biol Chem 2002). The <20 nM figure belongs to a later patented linker construct, not SA21.
  • Patent claims, not peer-reviewed evidence: US 12,377,158 B1 reports <20 nM human-albumin binding for its binder construct, says the technology may be used with follistatin, and mentions an approximately 7-day half-life for a follistatin construct in canine. This is not FLGR-242-specific peer-reviewed pharmacokinetic data.

Animal and cell findings are Level 1–2 evidence.

Mechanism and pathways

  • Claimed: a follistatin-derived domain binds myostatin, reducing activin receptor IIB signalling that limits muscle growth.
  • Claimed: an albumin-binding peptide extends circulation time. Neither claim has been independently verified for FLGR-242.

Safety and unknowns

  • No FLGR-242-specific human or animal safety data were identified. Safety is unknown.
  • Identity, purity and consistency of material sold under this name are unverified.
  • Native follistatin also binds activin and related signalling proteins; whether FLGR-242 avoids those effects is unverified.

Cancer relevance

This section covers questions raised by how the compound works in the body, plus anything regulators and trial teams keep an eye on. It is not a statement that this compound causes cancer — for most compounds here, no human data exist in either direction.

No established human signal

Unknown. No FLGR-242-specific data exist; growth-pathway interventions warrant study rather than assumption of risk or safety.

Regulatory status

Regulatory decisions apply to specific jurisdictions, products, formulations and indications. An approval elsewhere is not automatically an approval in your country.

Check the regulatory note and linked primary sources for jurisdiction-specific details.

Not an approved medicine anywhere in our record. No FLGR242 or FLGR-242 human trial was found in ClinicalTrials.gov or PubMed searches as of 11 October 2026. Listed under growth-hormone for discoverability only: the claimed mechanism is myostatin/activin-pathway ligand binding, not growth-hormone signalling. Anti-doping context: the WADA 2026 Prohibited List (S4.3) prohibits agents preventing activin receptor IIB activation, explicitly including myostatin-binding proteins such as follistatin; if FLGR-242 functions as claimed it would likely fall in that class. This is a classification note, not evidence that it is clinically active.

Evidence grade

L1Theory onlyVery low confidence in rating

Mechanistic rationale or early development without qualifying compound-specific outcome evidence. A registered trial is not a result.

What would change our rating?

  • Peer-reviewed disclosure of the full construct identity.
  • FLGR-242-specific animal outcome and pharmacokinetic studies.
  • A registered, controlled human trial with published safety and outcome data.

References and sources

Source transparency

A provenance snapshot of this profile. Counts show what kinds of sources are cited, not how much scientific weight each source deserves.

Sources fully curated
Last editorial review
2026-10-11
Recently reviewed · 5 days ago
Linked curated sources
6
Sources still pending
0
External specialist reviews
0
None recorded for this profile
Peer-reviewed: 3Patent / legal / policy record: 3

Review provenance

Registry editorial review: Colin Jackson-White, creator and editor, who is not a doctor or clinician. External specialist review is credited only when a named reviewer has completed a review of this exact profile.

Literature-discovery and AI tools may help locate or challenge candidate evidence, but they are not counted as evidence sources here. Registry judgements are tied to the underlying papers, trial records, regulator documents and official study records.

Source hierarchy: regulatory documents and trial registries first, peer-reviewed work next, sponsor material flagged as non-independent. We never use supplier or clinic marketing as evidence, and where a verified source has not yet been curated we say so rather than inventing one.

Evidence change history

These entries record changes to our assessment of the published evidence — not changes to the compound itself.

No recorded changes yet. Baseline position set on 2026-10-11.