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FGL Peptide

Also known as FGL, FGLL, FG loop peptide, NCAM mimetic peptide, EVYVVAENQQGKSKA

NCAM-derived FGFR1 agonist peptide with substantial rodent data and no demonstrated clinical benefit.

preclinical Neuro & cognition research chemical

At a glance

Category
Neuro & cognition
Status
research chemical
Route
intranasal in the human study; intracerebroventricular, subcutaneous and intraperitoneal in the animal work
Half-life
A phase 1 study in 24 healthy male volunteers measured pharmacokinetics after single intranasal doses of 25, 100 and 200 mg 3 - unusually for compounds in this reference, some human PK data exist. Plasma exposure is very low: undetectable at 25 mg, mean Cmax 0.52 ng/ml and AUC24 1.27 ng.h/ml at 100 mg, rising to 1.38 ng/ml and 4.05 ng.h/ml at 200 mg 3. The delivery rationale was direct nose-to-brain transport rather than systemic exposure, and these figures are why.
Onset
Not established in humans. Animal effects on synaptic plasticity are reported over hours to days; cognitive effects over days to weeks of dosing
Molecular weight
Approximately 1651 g/mol for the linear pentadecapeptide; the compound is also used as a dendrimeric (multimeric) construct in some studies, which has a very different mass.
Sequence
Glu-Val-Tyr-Val-Val-Ala-Glu-Asn-Gln-Gln-Gly-Lys-Ser-Lys-Ala (EVYVVAENQQGKSKA), corresponding to residues E681-A695 of the second fibronectin type III module of NCAM

Not approved anywhere. Developed as a drug candidate by ENKAM Pharmaceuticals (Denmark) with the University of Copenhagen; the programme reached early-phase clinical testing including a phase 1 intranasal study in 24 healthy male volunteers 3, and no positive controlled efficacy result has been published. Where it is sold today it is an unapproved research chemical.

Doping status: Not listed by name; as a non-approved substance it falls under the S0 residual category and is prohibited at all times

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

This is a short entry. There is little or no published research on this compound, so there is correspondingly little to report. Empty dosing or reconstitution sections mean no credible figures exist — not that they were left out.

Mechanism of action

FGL is a 15-residue fragment of the neural cell adhesion molecule (NCAM), taken from the FG loop of its second fibronectin type III module - the region through which NCAM binds fibroblast growth factor receptor 1. The peptide acts as an FGFR1 agonist, reproducing part of the receptor activation that NCAM-mediated cell contact normally provides. This is a well-defined and biologically sensible mechanism, and it distinguishes FGL from most compounds in this category: the target is named, the binding site is mapped, and the pharmacology follows from structure rather than from a doctrine.

Downstream, FGL has been reported to promote neurite outgrowth and neuronal survival in primary neurons, enhance presynaptic function and synaptogenesis, facilitate long-term potentiation in the dentate gyrus in vivo, alter synapse and dendritic spine ultrastructure in aged rats, mobilise neural stem cells, and exert anti-inflammatory effects on microglia partly through CD200 and IGF-1 and interferon-gamma modulation. Whether any of this occurs in a human brain at an achievable dose has not been shown.

What the research shows

FGL has a genuine, internationally published preclinical literature from independent academic groups in Denmark, Ireland and elsewhere - which is considerably more than most compounds in this category can claim. What it does not have is any published controlled trial showing clinical benefit. The compound was taken into early clinical development for Alzheimer's disease and did not emerge with a positive result; it should be read as a preclinical compound whose translation was attempted and has not been demonstrated.

Research in humans

The one clearly documented human study is a phase 1 tolerability, safety and pharmacokinetic study of intranasal FGLL in healthy male volunteers, published in Clinical Pharmacokinetics in 2007, in which a single dose was well tolerated 3. Further phase 1 studies, a phase 2a study in Alzheimer's disease and a pilot in stroke patients have been described in company and consortium communications, but no peer-reviewed publication reporting positive efficacy outcomes from those studies was found. Absence of a published positive result from a completed phase 2 is itself informative.

Animal and lab research

The rodent literature is broad and reasonably consistent: protection of hippocampal neurons from ischaemic insult in vitro and in vivo 2; neurite outgrowth and survival in primary rat neurons 1; facilitation of long-term plasticity in the dentate gyrus 7; changes in synapse and spine structure in aged rats 4; rescue of spatial learning deficits after neonatal phencyclidine treatment 5; mobilisation of neural stem cells 9; and attenuation of LPS-induced glial activation 8. Several of these come from groups independent of the originators, which is unusual and counts in the compound's favour. The limitation is the familiar one: rodent neuroprotection and plasticity findings have an extremely poor record of predicting clinical benefit, as davunetide demonstrated.

Caveats. No published controlled efficacy trial in any human condition. No established human dose. Studies differ in whether they use the linear peptide or a dendrimeric construct, and the two are not interchangeable - a point routinely ignored when preclinical results are cited for material sold as 'FGL'. The peptide is unmodified and protease-labile, so systemic delivery is a real problem that the intranasal route was chosen to circumvent, with unproven success. No long-term safety data exist.

What it is used for

  • Investigated preclinically for cognitive impairment, Alzheimer's disease, stroke and neuroinflammation 128
  • Taken into early clinical development for Alzheimer's disease; the only published human study is a single-dose phase 1 3, and no positive efficacy result has been published
  • Self-administered as a research chemical for claimed cognitive and neuroprotective effects, which no clinical evidence supports

Dosing

Route
intranasal in the human phase 1 study; subcutaneous in vendor protocols, a route with no human data
  • No efficacious dose has been established in humans for any indication, because no trial has demonstrated efficacy. The only doses ever given to a human in a published study are the single intranasal 25, 100 and 200 mg of the phase 1 3, and those were tolerability and pharmacokinetic doses, not therapeutic ones.
  • Animal studies use microgram-to-milligram per kilogram doses by routes including direct intracerebroventricular injection; these do not translate into a human subcutaneous dose.
  • Vendor protocols circulating for subcutaneous use are not derived from any published study. Left null rather than manufacturing a protocol.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Reconstitution

Vial sizes
10 mg, 30 mg (lyophilised powder, research chemical)
Solvent
bacteriostatic water (0.9% benzyl alcohol); sterile water only if used within the same session
Storage
Supplier guidance: lyophilised powder at -20 °C protected from light; reconstituted at 2-8 °C for roughly 2-4 weeks. No stability study for this peptide has been published; these are handling conventions, not pharmacopoeia specifications.

Let the diluent run down the vial wall, swirl and do not shake; discard if cloudy. Note that some of the preclinical literature uses a dendrimeric multimer rather than the linear 15-mer; material sold as FGL is generally the linear peptide, so results obtained with the dendrimer do not necessarily apply to it.

Work it out for FGL Peptide

Safety

Side effects

  • In the phase 1 study all three single intranasal doses were well tolerated, with no clinically notable abnormalities in ECG, vital signs or laboratory tests; the adverse events reported were minor and local - transient nasal burning and watering eyes 3
  • Beyond that single-dose study of 24 men, there is no repeat-dose or long-term human safety data 3
  • Mechanistic consideration rather than an observed effect: FGFR1 agonism is a growth-factor pathway, and chronic systemic activation of a growth factor receptor has not been characterised for safety in humans

Do not use if

  • Pregnancy and breastfeeding - no data
  • Children and adolescents - no data
  • Hypersensitivity to the peptide or to benzyl alcohol in the diluent
  • Active, past or suspected malignancy - FGFR1 signalling drives proliferation and is an established oncogenic pathway in several tumour types; deliberate agonism of it has no safety characterisation and is a reasoned concern rather than a documented harm
  • No toxicology programme adequate to support chronic use has been published

Interactions

Not studied. No interaction data exist. Any interplay with FGFR inhibitors used in oncology would be pharmacologically direct and opposing, but this is reasoning from mechanism, not an observed interaction.

Sources