Human pathway context: MSTN genetics and sarcopenia
A child with an MSTN splice-site mutation showed marked muscle hypertrophy. In a separate 24-week sarcopenia trial, the activin-receptor antibody bimagrumab increased lean mass but did not significantly improve the primary physical-performance endpoint versus placebo.
Context: Single human genetic case and randomized trial in community-dwelling older adults with sarcopenia. Neither study administered FLGR-242.
Limitations: Human pathway evidence cannot establish FLGR-242 efficacy, safety or dosing. Lean mass and functional performance are separate outcomes.
Structural work shows direct binding of FST288 to myostatin. Hill et al. found binding and inhibitory activity for FLRG (FSTL3), a distinct protein. FST-344 refers to a precursor of mature FST315 in the primary sequence literature.
Context: Structural, serum binding, reporter assay and precursor sequence studies of named molecules.
Limitations: These findings establish pathway biology and nomenclature. They do not determine the sequence, composition or ligand selectivity of FLGR-242.
Transgenic skeletal-muscle expression of FS I-I increased muscle mass and strength in mice and improved selected outcomes in mdx mice. FS I-I bound myostatin at 46.8 nM and activin at 64.3 micromolar. In separate work, the synthetic DF-3 14-mer increased mouse muscle mass after intramuscular injection and inhibited myostatin without inhibiting activin A or TGF-beta1 in the reported reporter assay.
Context: FS I-I was expressed from a muscle-specific transgene. DF-3 was an injected peptide and a separate sequence.
Limitations: Neither study tested a vial identified as FLGR-242. Transgene expression and IM DF-3 cannot establish FLGR-242 administration, potency or PK.
FLGR242 / FLGR-242: proposed identity and human evidence gaps
FLGR242 is marketed as a modified follistatin construct designed to inhibit myostatin (GDF-8), with claimed albumin binding and prolonged exposure. Full product sequence, formulation, independent identity testing, ligand selectivity and human target engagement were not verified.
Context: Owner-supplied article and promotional interview description compared with the patent and primary literature. The Atlas registry snapshot returned no matching studies for FLGR-242. Direct registry retrieval was unavailable during this audit.
Limitations: No compound-specific human dose-response, dosing protocol, safety, hypertrophy, strength, functional benefit, sarcopenia outcome or post-discontinuation effect was established by sources reviewed.
Route: Not documented · Human SC, oral and IM pharmacokinetics and absolute bioavailability are not established. No verified human terminal half-life or duration of effect.
US12377158B1 discloses an SA21-based binder, describes a Klotho fusion and states a seven-day half-life for a canine follistatin construct. It also asserts approximately 19 days for human binder-linked proteins, a figure it gives for human albumin itself.
Context: Patent specification and Dennis et al. albumin-binding experiments. The Dennis study measured binding in vitro and extended exposure of a different fusion construct in animals.
Limitations: No primary human concentration-time data for FLGR-242 or demonstrated equivalence between the commercial vial and the patent example. The patent figures do not establish dosing frequency.