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Peptide — NCAM-Derived FGF Receptor Agonist

FGL

Phase 1

FG loop peptide · fibroblast growth loop · FGL(L) / FGLL (two-chain form) · FGLs (shorter two-chain form) · NCAM mimetic peptide

A lab-made copy of 15 amino acids from NCAM, a protein on the surface of nerve cells, developed by a University of Copenhagen group to switch on the FGF receptor. Sold online as a memory peptide; the memory results come from rats.

Reconstituting this? Do the math.
Molecular Weight
1,649.8 (15-residue chain, supplier datasheet)
Sequence
EVYVVAENQQGKSKA (NCAM residues 681–695)
Half-life
Not in the human study’s abstract · ~45 min in rats (FGLs)
Route
Nasal (human study) · SubQ, nasal, into the brain (animals)
FDA Status
Not approved · on no FDA list
Published Studies
35 PubMed records (FGL with NCAM), 2004–2019
Human Studies
1 published (24 men, single nasal dose, 2007) · 1 unpublished
WADA Status
Not named · S0 covers unapproved drugs
Evidence Strength
Memory: rat studies only
Human: one safety study
Cost & Access
Research chemical (online sellers)

Research only · not on any FDA 503A list · Tell me if this changes →

The other four questions

What does it do? In rats it improved memory in learning tests. In rodent models of amyloid-beta damage, stroke and aging it protected brain cells or damped inflammation. In cells it switches on the FGF receptor and helps synapses form. No study has measured what it does to memory in a person.
Who uses it? Researchers, in animal and cell studies, most of them co-authored by the Copenhagen lab that developed it. Online, it is sold as a nootropic, labeled for research use, and forum users pair it with Dihexa.
Does the evidence hold up? Not for people. The one published human study (2007) gave 24 healthy men a single nasal dose to measure safety and blood levels, not memory. Most of the animal work lists the developers as authors, and two studies found fewer brain cells in healthy young rats given it.
Bottom line? A rat memory peptide that reached human safety testing; its planned proof-of-concept study was not completed, according to its EU project report. What a vial sold online contains, and whether it does anything for a person’s memory, no document shows.

Dosing from the Literature

Published for memory: rat doses only; the one published human study gave single nasal doses of 25–200 mg to test safety, not memory. Not published: any dose tested for memory in people.

No study has tested any dose of FGL for memory or focus in people. The table records doses exactly as published: the one human trial, a selection of animal studies (per kilogram of body weight in rats and mice) and one promoter’s stated regimen. They are not recommendations, and the animal doses are not human doses.

SourceAmountFrequency & DurationPopulationNotes
Trial doses — Anand et al., 200725, 100 or 200 mg FGL(L), into the noseOnce; 8-day open-label study24 healthy men, mean age 42 (range 24–55)Safety and blood levels only; no memory test. Plasma levels were undetectable after 25 mg.
Animal study — Knafo et al., 20126.6 mg/kg under the skin (two-chain form)Two injections, 5 and 2 days before trainingMale rats, 8–9 weeks oldWater-maze learning improved; “No side effects were observed following these treatments.”
Animal study — Popov et al., 20088 mg/kg under the skinEvery 2 days until day 19Aged rats (22 months)Changed synapse and dendritic spine structure; hippocampal volume unchanged.
Animal study — Corbett et al., 201310.8 mg/kg under the skin (FGLL)Every third day, day 7 to day 25Young adult male rats, 4 per groupPrevented amyloid-induced memory loss; healthy rats given it alone had 40% fewer CA1 pyramidal cells.
Animal study — Zellinger et al., 20142 or 10 mg/kg under the skin (four-chain dendrimer)60 minutes before each daily kindling stimulation, 16 stimulation daysMale mice, 8 per groupFewer stimulations were needed to reach a generalized seizure at both doses.
Stated regimen — Campbell, 20221–2 mg under the skin of the abdomen; 1 mg for people “in their 30s and under”Once a day, “5 day on, 2 day off”; 6 weeks for the younger groupNot statedAttributed to William Seeds’ book Peptide Protocols, Volume 1. No study has tested it.
Dosing Disclaimer

No dose of FGL has been tested for memory in a person. The one published human study measured safety and blood levels after a single nasal dose; the animal doses are per kilogram of a rat or mouse; the promoter’s regimen has not been tested in any study. These rows document what was published; they are not a dosing guide. Always work with a licensed healthcare provider.

→ Peptide Calculator — vial-to-syringe math

What It Is

FGL is a synthetic pentadecapeptide, EVYVVAENQQGKSKA, corresponding to residues 681 to 695 of the second fibronectin domain of NCAM (Knafo et al., 2012). NCAM, the neural cell adhesion molecule, is a membrane glycoprotein on the surface of neuronal and glial cells (Aonurm-Helm et al., 2010). In 2003 the Copenhagen group showed that this part of NCAM binds the FGF receptor 1 directly (Kiselyov et al., 2003), and the FG loop of the module, the stretch FGL copies, was mapped by NMR as a binding site for the receptor (Li et al., 2010). The group published FGL as an FGF receptor agonist in 2004, from the Protein Laboratory at the University of Copenhagen (Neiiendam et al., 2004).

The name covers several molecules. The 15-residue chain is sold as a laboratory reagent: MedChemExpress lists it at a molecular weight of 1,649.80 (CAS 499993-62-3) “For research use only” (product data sheet). Studies often used linked copies; a dimer or tetramer promotes receptor dimerization and thereby activation, according to a review by the group (Li et al., 2010). FGLL, written FGL(L) in the human study’s abstract (Anand et al., 2007), is two FGL chains joined at their N-terminal ends (Knafo et al., 2012; Corbett et al., 2013); other studies used a dendrimer of four chains on a lysine backbone (Cambon et al., 2004; Zellinger et al., 2014). FGLs, or FGLS, is two shorter 11-residue chains (VAENQQGKSKA) joined the same way (NeuroFGL Final Report Summary; Turner et al., 2019). A version linked to hyaluronate, HA-FGL, was made for nose-to-brain delivery in a 2019 animal study (Kim et al., 2019). An online seller, Functional Peptides, lists “FGL” in 10 mg vials and describes “FGL(L) is a peptide with neurotrophic and memory enhancing properties”; its page does not say which form the vial holds.

ENKAM Pharmaceuticals A/S, a Danish company, “owns the FGL peptide” (Knafo et al., 2012, competing-interests statement). From January 2012 to December 2014 the EU funded NeuroFGL, a project coordinated by the University of Copenhagen with ENKAM as a participant, with an EU contribution of €5,978,735 toward “the clinical advancement” of FGLs for neurological disorders (CORDIS fact sheet). The project’s final report names Alzheimer’s disease and mild cognitive impairment as the target indications, says FGLs reached a single ascending dose study in people, and says the next clinical study “could therefore not be completed within the project period” (NeuroFGL Final Report Summary).

A PubMed search for FGL with NCAM in the title or abstract returns 35 records, published from 2004 to 2019 (September 29, 2026); one reports a human study. Online, it is marketed as a nootropic: a 2022 article by the peptide promoter Jay Campbell calls it “a recreational nootropic peptide” (Campbell, 2022).

Mechanism of Action

Everything below comes from cell and animal studies. None of it has been measured in people.

  • NCAM → FGFR1 (the contact FGL copies) — Surface plasmon resonance showed a direct interaction between NCAM’s fibronectin type III modules 1 and 2 and FGFR1’s Ig modules 2 and 3; NMR showed the second NCAM module interacting with FGFR1’s Ig module 3 and with ATP, which inhibited the binding. The NCAM module induced FGFR phosphorylation and neurite outgrowth (Kiselyov et al., 2003).
  • FGFR1 → MAPK and PI3K–Akt (growth and survival of neurons) — FGL binds to and induces phosphorylation of FGFR without prior NCAM–NCAM binding. In dopaminergic, hippocampal and cerebellar granule neurons it induced neurite outgrowth and promoted survival after induced cell death, and both effects depended on FGFR, MAPK and PI3K (Neiiendam et al., 2004).
  • FRS2α, ShcA, PLCγ (part of the FGF signal, not all of it) — FGL induced phosphorylation of FGFR1, FRS2α, ShcA and PLCγ, but its activation of FRS2α was significantly lower than FGF1’s (Chen et al., 2010). In transfected cells in a later study, FGL did not phosphorylate FRS2 at all, and in the rat hippocampus it did not phosphorylate TrkB, the BDNF receptor (Knafo et al., 2012).
  • PKC → CaMKII → AMPA receptors (the proposed memory mechanism) — FGL triggered a long-lasting increase in synaptic transmission in hippocampal CA1 neurons through facilitated synaptic delivery of AMPA receptors, with enhanced NMDA receptor-dependent LTP; both the LTP and the learning gain depended on an initial PKC activation followed by persistent CaMKII activation (Knafo et al., 2012). In the dentate gyrus of rats in vivo, FGL facilitated the induction and maintenance of LTP without altering basal synaptic transmission (Dallérac et al., 2011).
  • Transmitter release and synapse formation — In cultured hippocampal neurons, FGL enhanced presynaptic function through FGFR1 and raised the density of synaptophysin-positive spots to 122% and 128% of control after 2 and 4 days (Cambon et al., 2004).
  • GSK3β inhibition — FGL increased the fraction of GSK3β phosphorylated on Ser9, a modification that inhibits the kinase (Klementiev et al., 2007). After FGL, a larger proportion of CA1 pyramidal neurons contained inactive GSK3β (Corbett et al., 2013).
  • Glia: IL-4 → CD200, and IGF-1 — FGL enhanced IL-4 release from glial cells, and IL-4 raised neuronal CD200 through ERK signaling (Downer et al., 2010). FGL promoted IGF-1 release from neurons, and IGF-1 was needed for its effect on Akt and CD200 (Downer et al., 2009). Its damping of LPS-induced glial activation did not occur in cells from CD200-deficient mice (Cox et al., 2013).
  • Signaling in NCAM-deficient mice — Mice lacking NCAM had lower basal phosphorylation of FGFR1, CaMKII and CaMKIV in the hippocampus, and FGL restored it (Aonurm-Helm et al., 2010).

What the Research Shows

All of the results below are from rats, mice, gerbils or cultured cells.

  • Memory in healthy rats — Injected into the brain (5 µg) right after training, FGL strengthened fear-conditioning memory for at least a month, and treated rats found a water-maze platform twice as fast as controls at 24 hours, one week and two weeks (Cambon et al., 2004). Under the skin, it prolonged social memory in adult rats, and given into the nose of newborn rats it sped the development of coordination skills (Secher et al., 2006). Two injections of the two-chain form improved water-maze learning (Knafo et al., 2012). On a different schedule, healthy rats given FGL showed no memory improvement (Corbett et al., 2013).
  • Amyloid-beta damage (an Alzheimer’s-type model) — After amyloid-beta 25–35 was injected into rat brains, FGL given into the cisterna, the nose or under the skin prevented or strongly reduced all the signs of damage and short-term memory loss the authors measured (Klementiev et al., 2007; an erratum was published in 2014). In a second study, amyloid-beta caused a 40% loss of pyramidal cells in the dorsal CA1, which FGL partially alleviated, and FGL prevented the social memory impairment (Corbett et al., 2013).
  • Aging — In aged rats, FGL reduced markers of activated microglia and the rise in IL-1β and lessened the impairment in LTP (Downer et al., 2010), reversed the age-related fall in hippocampal IGF-1 (Downer et al., 2009), lowered the density of microglia carrying activation markers and reduced GFAP staining (Ojo et al., 2011), and limited the age-related loss of synaptophysin and of astrocyte–synapse contacts without changing synapse number (Ojo et al., 2012). At 8 mg/kg every two days in 22-month-old rats, it changed the fine structure of spines and synapses without changing hippocampal volume or synapse density (Popov et al., 2008). Given during four weeks of chronic stress at midlife, it prevented the stress-related decline in spatial memory at 18 months (Borcel et al., 2008).
  • Stroke and ischemia — A single injection 24 hours before a transient global ischemia protected hippocampal CA1 neurons from death in gerbils (Skibo et al., 2005). In rats, FGL under the skin increased neural stem cell proliferation (Klein et al., 2014) and, after stroke, increased stem cell mobilization and remyelination and affected neuroinflammation (Klein et al., 2016). The EU project report says the effects of FGLs were “much attenuated” in the chronic phase after stroke (NeuroFGL Final Report Summary).
  • Brain injury — After a cold-induced brain injury in adolescent rats, FGL changed the activity of genes that regulate apoptosis, signal transduction and metabolism. The study measured gene expression, not recovery (Pedersen et al., 2008).
  • Mood — FGL reduced depression-like behavior in NCAM-deficient mice and had no effect on their normal littermates (Aonurm-Helm et al., 2008). In rats, a single dose of FGLL increased anxiety-like behavior, while 16 days of daily doses had antidepressant-like effects (Turner et al., 2019).
  • A schizophrenia model — In rats given phencyclidine as newborns, long-term FGL treatment brought working memory almost back to control levels but did not change the reversal-learning deficit (Secher et al., 2009).
  • An epilepsy model — In mice being kindled toward seizures, FGL at 2 and 10 mg/kg reduced the number of stimulations needed to reach a generalized seizure (Zellinger et al., 2014). See Side Effects & Risks.
Research Limitations — Rodents, One Circle of Authors, Several Molecules

Every result above is from animals or cells. Of the 27 animal and cell studies of FGL and its linked forms cited on this page, 18 list Elisabeth Bock or Vladimir Berezin of the Copenhagen group as authors, and in 2012 both held shares in ENKAM Pharmaceuticals, which owns the peptide (less than 0.01% each; Knafo et al., 2012). The studies used different molecules under one name, from different makers, and some groups were small: 4 rats per group in Corbett et al. (2013). Results also conflict: social memory improved in one study of healthy rats and not in another (Secher et al., 2006; Corbett et al., 2013), and dorsal hippocampal volume fell in young healthy rats, while hippocampal volume did not change in aged ones (Ojo et al., 2013; Popov et al., 2008). No result has been tested in people.

Human Data

No study has measured memory, focus or any other benefit of FGL in people, and none has tested repeated doses. One human study has been published:

  • Single nasal doses in 24 healthy men (Anand et al., 2007) — An 8-day, open-label, phase I study with an ascending-dose, sequential-cohort design: single intranasal doses of FGL(L) at 25, 100 and 200 mg, in men with a mean age of 42 (range 24–55). All three doses were “well tolerated,” with no clinically notable abnormalities in ECG recordings, vital signs or laboratory tests. Plasma levels were undetectable at every time point after 25 mg and measurable up to 1 hour after 100 mg and up to 4 hours after 200 mg; mean Cmax was 0.52 and 1.38 ng/mL and mean AUC(24) 1.27 and 4.05 ng·h/mL for 100 and 200 mg. The adverse events are under Side Effects & Risks. The authors wrote that studies in patients with Alzheimer’s disease were being planned.

One more human study is reported but not published:

  • Single intravenous doses of FGLs (EU project report) — The NeuroFGL final report says its single ascending dose study “demonstrated that FGLs was safe and well tolerated administered in single intravenous doses up to very high doses,” with a pharmacokinetic profile “very similar to animals.” It gives no doses, participant numbers or data, and no paper or registry record of it was found. The multiple-dose proof-of-concept study that was to follow “could therefore not be completed within the project period” (NeuroFGL Final Report Summary).
  • Forum posts — A 2020 LongeCity thread has posts from people who say they use FGL, and from a seller of a hyaluronate-linked version, HA-FGL, who described early user reports as “very mixed, at best” (LongeCity, 2020). These are posts, not data.

ClinicalTrials.gov lists no trial of FGL, FGLL or FGLs, and the EU Clinical Trials Register showed none (both searched September 29, 2026). The evidence meter on the FGL card reads “Animal only” because it counts published human data for the use on its tag, memory, and the one published human study measured safety and blood levels.

Reconstitution & Storage

The seller’s page lists “FGL” at 10 mg per vial and does not say whether the vial holds powder or liquid. MedChemExpress sells the 15-residue peptide as a powder and gives its solubility in water as at least 100 mg/mL (product data sheet). None of the documents read for this page gives a mixing volume for injection. The table is arithmetic only: how volume maps to milligrams for the 1 mg and 2 mg amounts in the stated regimen above (U-100 insulin syringe: 100 units = 1 mL). It is not a recommendation.

Vial SizeWater AddedConcentration1 mg2 mg
10 mg1 mL10 mg/mL10 units (0.10 mL)20 units (0.20 mL)
10 mg2 mL5 mg/mL20 units (0.20 mL)40 units (0.40 mL)
  • Doses larger than a vial — The human study’s nasal doses, 25 to 200 mg (Anand et al., 2007), are each more than a whole 10 mg vial.
  • Storage of the laboratory reagent — MedChemExpress lists the 15-residue powder at −80 °C for 2 years or −20 °C for 1 year, and in solution at −80 °C for 6 months or −20 °C for 1 month, sealed and away from moisture (product data sheet).
  • Storage of FGLs, the project’s drug substance — The EU report found no degradation by HPLC after 24 months at −20 °C, 98% of the starting value after 6 months at 25 °C, and stability in its dosing solution through three freeze–thaw cycles, 26 hours at room temperature and 18 days at 4 °C and at −20 °C (NeuroFGL Final Report Summary). FGLs is a different molecule from the 15-residue chain.
  • Storage of vials sold as “FGL” — The seller’s page gives none. Campbell (2022): “I also don’t know what the optimal storage conditions are.”

→ Peptide Calculator — vial-to-syringe math

Side Effects & Risks

What Happened in Healthy Animals

Two studies from The Open University in the UK gave FGL to healthy young adult rats. In one, rats given FGL alone had 40% fewer CA1 pyramidal cells, and the authors wrote that “FGL administered to healthy animals can be detrimental to the hippocampus” (Corbett et al., 2013). In the other, FGL reduced the volume of the dorsal hippocampus, with fewer pyramidal neurons in CA1 and CA3 (Ojo et al., 2013). In mice being kindled toward seizures, FGL reduced the number of stimulations needed to reach a generalized seizure, and the authors wrote that the results “raise some concern regarding a putative effect, which might promote the formation of a hyperexcitable network” (Zellinger et al., 2014). No human study has looked for either effect.

In people, the only published safety data are from single nasal doses. The rest is from animals:

  • In the human study — Three of 24 men (13%) reported five adverse events. Two had a burning sensation in the nose lasting under 3 minutes at 200 mg, and one had runny eyes lasting under 2 minutes at 25 mg; these began right after dosing, and a relationship to FGL(L) was suspected. One of the men with nasal burning had dizziness, vomiting and headache starting more than 2 days later, not considered related (Anand et al., 2007).
  • Anxiety and fear — In rats, a single dose of FGLL increased anxiety-like behavior (Turner et al., 2019). After fear conditioning, rats given FGL froze more to the conditioning cues a month later, which the authors read as a stronger, more persistent fear memory (Cambon et al., 2004).
  • Toxicology of FGLs — In the EU project’s animal program, the no-observed-adverse-effect levels were 1,000 mg/kg a day intravenously, the highest dose tested, in a two-week non-rodent study and 750 mg/kg a day in a 14-day rat study; possible FGLs-related changes at the injection site after subcutaneous doses were swelling from 250 mg/kg and hematoma and hemorrhage at 750 mg/kg, a 2,000 mg/kg intravenous group in the 14-day rat study was stopped early for local intolerance at the injection site, and the genetic toxicology tests were negative (NeuroFGL Final Report Summary). These are data on FGLs, the shorter two-chain molecule.
  • Cancer questions — No cancer data on FGL exist. In ovarian cancer, NCAM’s interaction with the FGF receptor drove cancer cell migration and invasion in culture and spread in mice, and a different NCAM-derived peptide that activates the receptor, Encamin-C, increased cancer cell migration and invasion in culture (Zecchini et al., 2011). FGL itself was not tested.
  • What is in a vial — The published studies used the two-chain FGLL, a four-chain dendrimer and the shorter FGLs, at purities reported as “at least 85%” (Knafo et al., 2012), “more than 99%” (Zellinger et al., 2014) and “higher than 80%” for FGLs (NeuroFGL Final Report Summary). The seller’s page read for this page names both “FGL” and “FGL(L)” and states no form, purity or test result; the HA-FGL seller on LongeCity posted in October 2020 that there was “No COA currently.” No independent analysis of FGL sold online has been published.
  • WADA — The 2026 Prohibited List does not name FGL. Its S0 section prohibits at all times unapproved substances that no other section addresses, and S2.3 prohibits growth factors, fibroblast growth factors among them, and “growth factor modulators.”
  • Pregnancy and drug interactions — Unstudied.

Bloodwork & Monitoring

No monitoring guidance for FGL has been published. What the studies measured:

  • In the human study — ECG recordings, vital signs and laboratory tests, with no clinically notable abnormalities after single nasal doses (Anand et al., 2007).
  • In the animal safety program — For FGLs, ECG, blood pressure, hematology and clinical pathology; the 15-day non-rodent study found no electrocardiographic evidence of cardiotoxicity (NeuroFGL Final Report Summary).
  • The brain — The neuron losses in healthy rats were found by counting cells in brain tissue after death (Corbett et al., 2013; Ojo et al., 2013). No human study has looked for them.
  • Which tests fit a given person — A question for a licensed healthcare provider. This page can’t answer it.

Commonly Stacked With

The only combination the documents show is with Dihexa, recorded as published. No study has tested FGL with anything.

Dihexa

Campbell’s 2022 article quotes an unnamed peptide physician: “I have personally used it paired with DIHEXA and found it very useful for memory.” In a 2020 LongeCity thread, users describe pairing the two; the thread’s first post was later edited to warn that it “might not be safe to take dihexa & FGL at the same time.” No study has tested the pair.

→ Peptide Calculator — vial-to-syringe math

Legal Status

Current Status — September 2026

Not on any FDA list. FGL is not FDA-approved: openFDA’s Drugs@FDA data return no product for it (searched September 29, 2026). It does not appear on FDA’s 503A bulk drug substances categories list (updated May 14, 2026) or on the 503A bulks list in 21 CFR 216.23. Sellers label it for research: “Only legal application for peptides is for research purposes” (Functional Peptides); “For research use only” (MedChemExpress).

WADA’s 2026 Prohibited List does not name FGL. Its S0 section prohibits at all times “Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use,” and S2.3 prohibits growth factors, fibroblast growth factors (FGFs) among them, and “other growth factors or growth factor modulators affecting muscle, tendon or ligament protein synthesis/degradation, vascularisation, energy utilization, regenerative capacity or fibre type switching” (Prohibited List 2026).

No trial of FGL is registered on ClinicalTrials.gov, and the EU Clinical Trials Register showed none (searched September 29, 2026). The NeuroFGL report says its clinical trial application for FGLs “was assembled and approved by regulatory authorities (DMA)”; the project ended on December 31, 2014 without completing its proof-of-concept study.

Cost & Access

FGL is sold online as a research chemical. Functional Peptides, an online seller, lists “FGL” in 10 mg vials; MedChemExpress sells the 15-residue peptide as a laboratory reagent. In 2022 Jay Campbell wrote that there was “no place I feel comfortable recommending for people who want to buy the FGL peptide online.”

Pricing and availability vary and are set by the seller. Kalios does not sell compounds.

References

  1. Kiselyov VV, Skladchikova G, Hinsby AM, Jensen PH, Kulahin N, Soroka V, Pedersen N, Tsetlin V, Poulsen FM, Berezin V, Bock E. Structural basis for a direct interaction between FGFR1 and NCAM and evidence for a regulatory role of ATP. Structure. 2003;11(6):691-701. PMID: 12791257.
  2. Neiiendam JL, Køhler LB, Christensen C, Li S, Pedersen MV, Ditlevsen DK, Kornum MK, Kiselyov VV, Berezin V, Bock E. An NCAM-derived FGF-receptor agonist, the FGL-peptide, induces neurite outgrowth and neuronal survival in primary rat neurons. J Neurochem. 2004;91(4):920-935. PMID: 15525346.
  3. Cambon K, Hansen SM, Venero C, Herrero AI, Skibo G, Berezin V, Bock E, Sandi C. A synthetic neural cell adhesion molecule mimetic peptide promotes synaptogenesis, enhances presynaptic function, and facilitates memory consolidation. J Neurosci. 2004;24(17):4197-4204. PMID: 15115815.
  4. Skibo GG, Lushnikova IV, Voronin KY, Dmitrieva O, Novikova T, Klementiev B, Vaudano E, Berezin VA, Bock E. A synthetic NCAM-derived peptide, FGL, protects hippocampal neurons from ischemic insult both in vitro and in vivo. Eur J Neurosci. 2005;22(7):1589-1596. PMID: 16197499.
  5. Secher T, Novitskaia V, Berezin V, Bock E, Glenthøj B, Klementiev B. A neural cell adhesion molecule-derived fibroblast growth factor receptor agonist, the FGL-peptide, promotes early postnatal sensorimotor development and enhances social memory retention. Neuroscience. 2006;141(3):1289-1299. PMID: 16784819.
  6. Anand R, Seiberling M, Kamtchoua T, Pokorny R. Tolerability, safety and pharmacokinetics of the FGLL peptide, a novel mimetic of neural cell adhesion molecule, following intranasal administration in healthy volunteers. Clin Pharmacokinet. 2007;46(4):351-358. PMID: 17375985.
  7. Klementiev B, Novikova T, Novitskaya V, Walmod PS, Dmytriyeva O, Pakkenberg B, Berezin V, Bock E. A neural cell adhesion molecule-derived peptide reduces neuropathological signs and cognitive impairment induced by Abeta25-35. Neuroscience. 2007;145(1):209-224. PMID: 17223274. Erratum: Neuroscience. 2014;266:136-137.
  8. Popov VI, Medvedev NI, Kraev IV, Gabbott PL, Davies HA, Lynch M, Cowley TR, Berezin V, Bock E, Stewart MG. A cell adhesion molecule mimetic, FGL peptide, induces alterations in synapse and dendritic spine structure in the dentate gyrus of aged rats: a three-dimensional ultrastructural study. Eur J Neurosci. 2008;27(2):301-314. PMID: 18215229.
  9. Borcel E, Pérez-Alvarez L, Herrero AI, Brionne T, Varea E, Berezin V, Bock E, Sandi C, Venero C. Chronic stress in adulthood followed by intermittent stress impairs spatial memory and the survival of newborn hippocampal cells in aging animals: prevention by FGL, a peptide mimetic of neural cell adhesion molecule. Behav Pharmacol. 2008;19(1):41-49. PMID: 18195593.
  10. Aonurm-Helm A, Jurgenson M, Zharkovsky T, Sonn K, Berezin V, Bock E, Zharkovsky A. Depression-like behaviour in neural cell adhesion molecule (NCAM)-deficient mice and its reversal by an NCAM-derived peptide, FGL. Eur J Neurosci. 2008;28(8):1618-1628. PMID: 18973581.
  11. Pedersen MV, Helweg-Larsen RB, Nielsen FC, Berezin V, Bock E, Penkowa M. The synthetic NCAM-derived peptide, FGL, modulates the transcriptional response to traumatic brain injury. Neurosci Lett. 2008;437(2):148-153. PMID: 18436381.
  12. Downer EJ, Cowley TR, Cox F, Maher FO, Berezin V, Bock E, Lynch MA. A synthetic NCAM-derived mimetic peptide, FGL, exerts anti-inflammatory properties via IGF-1 and interferon-gamma modulation. J Neurochem. 2009;109(5):1516-1525. PMID: 19457161.
  13. Secher T, Berezin V, Bock E, Glenthøj B. Effect of an NCAM mimetic peptide FGL on impairment in spatial learning and memory after neonatal phencyclidine treatment in rats. Behav Brain Res. 2009;199(2):288-297. PMID: 19133297.
  14. Downer EJ, Cowley TR, Lyons A, Mills KH, Berezin V, Bock E, Lynch MA. A novel anti-inflammatory role of NCAM-derived mimetic peptide, FGL. Neurobiol Aging. 2010;31(1):118-128. PMID: 18468731.
  15. Aonurm-Helm A, Berezin V, Bock E, Zharkovsky A. NCAM-mimetic, FGL peptide, restores disrupted fibroblast growth factor receptor (FGFR) phosphorylation and FGFR mediated signaling in neural cell adhesion molecule (NCAM)-deficient mice. Brain Res. 2010;1309:1-8. PMID: 19909731.
  16. Chen Y, Li S, Berezin V, Bock E. The fibroblast growth factor receptor (FGFR) agonist FGF1 and the neural cell adhesion molecule-derived peptide FGL activate FGFR substrate 2alpha differently. J Neurosci Res. 2010;88(9):1882-1889. PMID: 20175207.
  17. Li S, Bock E, Berezin V. Neuritogenic and neuroprotective properties of peptide agonists of the fibroblast growth factor receptor. Int J Mol Sci. 2010;11(6):2291-2305. PMID: 20640153. (Review.)
  18. Dallérac G, Zerwas M, Novikova T, Callu D, Leblanc-Veyrac P, Bock E, Berezin V, Rampon C, Doyère V. The neural cell adhesion molecule-derived peptide FGL facilitates long-term plasticity in the dentate gyrus in vivo. Learn Mem. 2011;18(5):306-313. PMID: 21508096.
  19. Ojo B, Rezaie P, Gabbott PL, Cowely TR, Medvedev NI, Lynch MA, Stewart MG. A neural cell adhesion molecule-derived peptide, FGL, attenuates glial cell activation in the aged hippocampus. Exp Neurol. 2011;232(2):318-328. PMID: 21978973.
  20. Zecchini S, Bombardelli L, Decio A, Bianchi M, Mazzarol G, Sanguineti F, Aletti G, Maddaluno L, Berezin V, Bock E, Casadio C, Viale G, Colombo N, Giavazzi R, Cavallaro U. The adhesion molecule NCAM promotes ovarian cancer progression via FGFR signalling. EMBO Mol Med. 2011;3(8):480-494. PMID: 21739604. (Encamin-C, not FGL.)
  21. Ojo B, Rezaie P, Gabbott PL, Davies H, Colyer F, Cowley TR, Lynch M, Stewart MG. Age-related changes in the hippocampus (loss of synaptophysin and glial-synaptic interaction) are modified by systemic treatment with an NCAM-derived peptide, FGL. Brain Behav Immun. 2012;26(5):778-788. PMID: 21986303.
  22. Knafo S, Venero C, Sánchez-Puelles C, Pereda-Peréz I, Franco A, Sandi C, Suárez LM, Solís JM, Alonso-Nanclares L, Martín ED, Merino-Serrais P, Borcel E, Li S, Chen Y, Gonzalez-Soriano J, Berezin V, Bock E, Defelipe J, Esteban JA. Facilitation of AMPA receptor synaptic delivery as a molecular mechanism for cognitive enhancement. PLoS Biol. 2012;10(2):e1001262. PMID: 22363206. (Sequence, dimeric form, doses and competing-interests statement from the full text.)
  23. Ojo B, Gabbott PL, Rezaie P, Corbett N, Medvedev NI, Cowley TR, Lynch MA, Stewart MG. An NCAM mimetic, FGL, alters hippocampal cellular morphometry in young adult (4 month-old) rats. Neurochem Res. 2013;38(6):1208-1218. PMID: 23076631.
  24. Corbett NJ, Gabbott PL, Klementiev B, Davies HA, Colyer FM, Novikova T, Stewart MG. Amyloid-beta induced CA1 pyramidal cell loss in young adult rats is alleviated by systemic treatment with FGL, a neural cell adhesion molecule-derived mimetic peptide. PLoS One. 2013;8(8):e71479. PMID: 23951173.
  25. Cox FF, Berezin V, Bock E, Lynch MA. The neural cell adhesion molecule-derived peptide, FGL, attenuates lipopolysaccharide-induced changes in glia in a CD200-dependent manner. Neuroscience. 2013;235:141-148. PMID: 23337536.
  26. Zellinger C, Salvamoser JD, Seeger N, Russmann V, Potschka H. Impact of the neural cell adhesion molecule-derived peptide FGL on seizure progression and cellular alterations in the mouse kindling model. ACS Chem Neurosci. 2014;5(3):185-193. PMID: 24456603.
  27. Klein R, Blaschke S, Neumaier B, Endepols H, Graf R, Keuters M, Hucklenbroich J, Albrechtsen M, Rees S, Fink GR, Schroeter M, Rueger MA. The synthetic NCAM mimetic peptide FGL mobilizes neural stem cells in vitro and in vivo. Stem Cell Rev Rep. 2014;10(4):539-547. PMID: 24817672.
  28. Klein R, Mahlberg N, Ohren M, Ladwig A, Neumaier B, Graf R, Hoehn M, Albrechtsen M, Rees S, Fink GR, Rueger MA, Schroeter M. The Neural Cell Adhesion Molecule-Derived (NCAM)-Peptide FG Loop (FGL) Mobilizes Endogenous Neural Stem Cells and Promotes Endogenous Regenerative Capacity after Stroke. J Neuroimmune Pharmacol. 2016;11(4):708-720. PMID: 27352075.
  29. Turner CA, Lyons DM, Buckmaster CL, Aurbach EL, Watson SJ, Schatzberg AF, Akil H. Neural cell adhesion molecule peptide mimetics modulate emotionality: pharmacokinetic and behavioral studies in rats and non-human primates. Neuropsychopharmacology. 2019;44(2):356-363. PMID: 29703997.
  30. Kim YS, Sung DK, Kim H, Kong WH, Kim YE, Hahn SK. Nose-to-brain delivery of hyaluronate - FG loop peptide conjugate for non-invasive hypoxic-ischemic encephalopathy therapy. J Control Release. 2019;307:76-89. PMID: 31229472.
  31. European Commission, CORDIS. Development of a novel FGL therapy and translational tests for regenerative treatment of neurological disorders (NEUROFGL), FP7 grant agreement 278006: fact sheet. cordis.europa.eu/project/id/278006. Read September 29, 2026.
  32. European Commission, CORDIS. NEUROFGL Final Report Summary. cordis.europa.eu/project/id/278006/reporting. Read September 29, 2026. (Unpublished single-dose human study, toxicology, stability, structure of FGLs.)
  33. MedChemExpress. FGL peptide (Cat. No. HY-P3281) product data sheet. file.medchemexpress.com/batch_PDF/HY-P3281/FGL-peptide-DataSheet-MedChemExpress.pdf. Read September 29, 2026.
  34. Functional Peptides. FGL product page. functionalpeptides.com/shop/p/fgl. Read September 29, 2026.
  35. Campbell J. FGL Peptide: Benefits, Dosage & Side Effects. jaycampbell.com/blog/fgl-the-brain-power-peptide/. Last updated February 4, 2022. Read September 29, 2026.
  36. LongeCity. FGL peptide experiences/info (Nootropic Stacks forum), posts from April 2020 to December 2024. longecity.org/forum/topic/109111-fgl-peptide-experiencesinfo/. Read September 29, 2026.
  37. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances; S2.3, Growth factors and growth factor modulators. wada-ama.org.
  38. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act (categories 1–3). Updated May 14, 2026. fda.gov/media/94155/download. And 21 CFR 216.23, ecfr.gov, read September 29, 2026.
  39. openFDA Drugs@FDA API (api.fda.gov/drug/drugsfda.json), searches for “FGL” as generic name, brand name and active ingredient: no matches. September 29, 2026.
  40. ClinicalTrials.gov (searches for “FGL peptide,” “FGLL,” “FGL(L),” “FG loop peptide,” “NCAM mimetic” and “Enkam”) and the EU Clinical Trials Register (“FGL,” “FGLs,” “Enkam”): no record of a trial of FGL. PubMed: FGL[tiab] AND (NCAM[tiab] OR “neural cell adhesion molecule”[tiab]), 35 records. All searched September 29, 2026.

Last updated: September 29, 2026  |  Profile authored by Kalios Peptides research team

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