FGL

What it is

A synthetic pentadecapeptide (sequence: EVYVVAENQQGKSKA) derived from the FG loop of the second fibronectin type III module of Neural Cell Adhesion Molecule (NCAM). The N-terminal glutamate is modified to pyroglutamic acid in the functional form. Critically, FGL is biologically active only as a tetrameric dendrimer — four peptide copies coupled to a lysine backbone — because FGFR1 activation requires receptor dimerization. Developed by Elisabeth Bock and Vladimir Berezin at the University of Copenhagen, and commercialized by Enkam Pharmaceuticals A/S. A Phase I intranasal safety trial in 24 healthy volunteers was completed (Anand et al., 2007), but no efficacy trials have been conducted and clinical development appears to have stalled after an EU-funded grant period (~2012).

Community-reported ranges

Dose values in mcg (1000 mcg = 1 mg). Community-reported SC ranges extrapolated from preclinical literature (2-10 mg/kg SC in rodents) and sparse community discussion. Phase I trial used 25-200 mg intranasal in humans (safety only, not efficacy). Not dosing guidance.

Frequently discussed alongside

Based on community forum discussions. Not a recommendation to combine compounds.

Published research

FGL has an extensive preclinical record across multiple species (rats, mice, gerbils, dogs, primates). Cambon et al. (2004) showed a single ICV injection enhanced memory consolidation for over one month. Knafo et al. (2012) demonstrated FGL facilitated AMPA receptor synaptic delivery via PKC-CaMKII signaling, nearly doubling LTP in hippocampal CA1 neurons. Anti-inflammatory effects are mediated through neuronal CD200 upregulation and IGF-1 release. Klein et al. (2016) showed endogenous neural stem cell mobilization after stroke. A Phase I trial (Anand et al., 2007, n=24 healthy males) confirmed intranasal safety and tolerability at 25-200 mg. The 6 million Euro EU-funded NeuroFGL project (~2012) supported further development, but no Phase II or efficacy trials have been reported. Clinical development appears stalled.

Reported side effects

From community self-reports. Not from controlled studies.

The Phase I human trial (n=24) reported mild nasal burning in 2 of 24 subjects at the 200 mg intranasal dose, with no systemic adverse effects. However, preclinical studies raise significant safety concerns: high-dose treatment in young rats produced widespread hippocampal apoptosis despite improved memory performance (attributed to GSK-3β inhibition sensitizing extrinsic apoptosis pathways). In a mouse kindling model, FGL reduced the number of stimulations needed to induce generalized seizure, suggesting potential pro-convulsant risk at certain doses. Community-reported side effects are sparse due to limited adoption.

Regulatory status