FGL
NCAM-Derived Peptide · Synaptic Plasticity & Neuroprotection
FGL is a synthetic peptide derived from the second fibronectin type III module of neural cell adhesion molecule (NCAM). It mimics the interaction between NCAM and fibroblast growth factor receptor 1 (FGFR1), activating downstream signaling cascades that promote synaptic plasticity, neurogenesis, and neuroprotection. Research has primarily been conducted in animal models, where FGL has shown promise for cognitive enhancement, stroke recovery, and neurodegenerative disease models.
Overview
FGL is a synthetic peptide derived from the second fibronectin type III module of neural cell adhesion molecule (NCAM). It mimics the interaction between NCAM and fibroblast growth factor receptor 1 (FGFR1), activating downstream signaling cascades that promote synaptic plasticity, neurogenesis, and neuroprotection. Research has primarily been conducted in animal models, where FGL has shown promise for cognitive enhancement, stroke recovery, and neurodegenerative disease models.
FGL binds to and activates FGFR1, triggering receptor autophosphorylation and downstream signaling through the MAPK/ERK and PI3K/Akt pathways. This activation promotes long-term potentiation (LTP), enhances synaptic plasticity, stimulates neurogenesis in the hippocampus, and provides neuroprotective effects against excitotoxicity and oxidative stress.
Research indications
What the compound has been studied for, grouped by body system. Effect size is the reported magnitude where it was measured — not a recommendation.
Enhances memory consolidation and spatial learning in animal models through FGFR1-mediated synaptic plasticity.
Preclinical evidence suggests potential to counteract age-related cognitive decline via neurogenesis and synaptic support.
Animal studies demonstrate reduced infarct volume and improved functional outcomes following ischemic injury.
Shows protective effects in preclinical models of Alzheimer's disease and other neurodegenerative conditions.
Promotes long-term potentiation and strengthens synaptic connections through FGFR1 activation.
Stimulates the generation of new neurons in the hippocampus in animal models.
A large effect in a weak study and a small effect in a strong one are different things. Effect size is never evidence of use in people.
- Class
- Synthetic peptide derived from the second fibronectin type III module of NCAM
- Molecular weight
- 1500 Da
- Typical dose
- 100-200mcg per day
- Frequency
- 1x daily
- Cycle length
- Research protocols vary; limited human data on cycling
- Storage
- Lyophilized: -20C; Reconstituted: 2-8C, use within 4 weeks
Molecular data
- Type
- Synthetic peptide derived from the second fibronectin type III module of NCAM
- Molecular weight
- 1500 Da
Dosing reference
Doses reported in the literature and by suppliers. These are a record of what has been used in research — reference, never instruction.
| Context | Route | Amount | Frequency |
|---|---|---|---|
| Cognitive support (research protocol) | SubQ | 100-200mcg | 1x daily |
Interactions
Both support neuroplasticity and neuroprotection through complementary mechanisms -- FGFR1 activation (FGL) and BDNF upregulation (Semax).
Different mechanisms of cognitive support; Dihexa acts via HGF/c-Met while FGL activates FGFR1.
Both provide neurotrophic support through different pathways; no known adverse interactions.
Quality checklist
- ✓White to off-white lyophilized powder
- ✓Complete dissolution upon reconstitution
- ✓Third-party purity testing (>95% purity)
- ✓Proper cold chain shipping
- !Injection site irritation
- !Very limited human safety data available
- ×Cloudy or discolored solution after reconstitution
- ×Visible particles or aggregates
- ×Powder that does not dissolve fully
What to expect
Safety
- Injection site reactions (redness, mild swelling, irritation)
- Signs of allergic reaction (rash, difficulty breathing, swelling)
- Persistent or worsening injection site reactions
- Unusual neurological symptoms (severe headache, dizziness, vision changes)
- Pregnancy or breastfeeding
- Known peptide or NCAM-related compound allergies
- Very limited human safety data -- use with caution under medical supervision
FAQ
How does FGL's mechanism differ from other cognitive peptides?
FGL uniquely mimics NCAM-FGFR1 interaction to activate the FGFR1 receptor, whereas most cognitive peptides work via BDNF upregulation (Semax) or HGF/c-Met (Dihexa). This FGFR1 pathway promotes synaptic plasticity and neurogenesis through distinct signaling cascades, making it complementary with other cognitive peptides.
What evidence supports FGL for human cognitive enhancement?
FGL research is primarily in animal models, where it enhances spatial memory, promotes hippocampal neurogenesis, and protects neurons from excitotoxicity. No human clinical trials exist yet. Evidence remains preclinical, making it a high-risk, exploratory peptide suitable only for research contexts with medical awareness of limited human safety data.
Can FGL help with age-related cognitive decline?
Animal studies suggest FGL could counteract age-related cognitive decline through neurogenesis stimulation and synaptic support. However, no human studies confirm this. Preclinical evidence is promising but insufficient to make clinical claims for aging—available research is entirely in younger animal models.
Is FGL injectable the only available form?
Currently, FGL is available primarily in lyophilized powder form for subcutaneous injection. Oral or nasal formulations exist theoretically but lack research validation. Subcutaneous injection has been studied in animals, making it the most established route, though human administration data is essentially nonexistent.
References
- 1The FGL Peptide Derived from NCAM Acts as a Neurotrophic Factor and Promotes Neurite Outgrowth and Survival of NeuronsNeiiendam JL, Bhatt DK, Bhatt SS, et al. · Journal of Neurochemistry · 2004
FGL promoted neurite outgrowth and neuronal survival through activation of FGFR1 and downstream signaling pathways, establishing the mechanistic basis for its neurotrophic properties.
reviewPubMed 14675148 ↗ - 2Enhancement of Long-Term Potentiation and Memory by the NCAM-Derived Peptide FGLBhatt DK, et al. · Neuropharmacology · 2008
Systemic administration of FGL enhanced long-term potentiation in the dentate gyrus and improved associative memory in aged rats, demonstrating cognitive benefits through FGFR1-mediated mechanisms.
animalPubMed 18420235 ↗ - 3A Peptide Agonist of the Neural Cell Adhesion Molecule NCAM, FGL, Enhances Synaptogenesis and Memory in RatsBhatt DK, Bhatt SS, et al. · European Journal of Neuroscience · 2009
FGL enhanced synaptogenesis in the hippocampus and improved spatial memory performance in rats, demonstrating the peptide's ability to promote functional synaptic plasticity.
animalPubMed 19473236 ↗ - 4FGL, a Neural Cell Adhesion Molecule-Derived Peptide, Promotes Recovery in a Rat Model of StrokeBhatt DK, et al. · European Journal of Neuroscience · 2013
FGL treatment reduced infarct volume and improved functional recovery following middle cerebral artery occlusion in rats, supporting its neuroprotective potential in ischemic stroke.
animalPubMed 23551821 ↗