FGL
preclinicalAlso known as: FG Loop peptide, FGL(L)
**Mechanism of Action** FGL (FG Loop peptide) is a synthetic peptide derived from the neural cell adhesion molecule (NCAM) that mimics the FG loop region of NCAM’s fibronectin type III domain. It selectively binds to and activates fibroblast growth factor receptor 1 (FGFR1), initiating downstream signaling cascades such as MAPK/ERK and PI3K/Akt pathways. This activation promotes neurite outgrowth, synaptogenesis, and long-term potentiation (LTP), thereby enhancing synaptic plasticity and memory consolidation in preclinical models. **Key Research Findings** Preclinical studies demonstrate that FGL improves spatial learning and memory in rodent models of aging and neurodegeneration, including Alzheimer’s disease. It reduces amyloid-beta pathology and tau hyperphosphorylation while increasing hippocampal neurogenesis. FGL also shows neuroprotective effects against excitotoxicity and oxidative stress. However, its short half-life and limited blood-brain barrier penetration remain challenges for translational development. **Clinical Relevance** FGL is in preclinical development as a potential therapeutic for cognitive decline associated with neurodegenerative disorders. Its ability to enhance synaptic plasticity and neuroprotection positions it as a candidate for conditions like Alzheimer’s disease and age-related memory impairment. No human trials have been conducted to date. For research purposes only — not medical advice.
Key data
Research & studies
FGL-1 is a potent factor for interorgan communication between the liver and immune system in primary Sjögren disease.; Liver FGL-1 production is induced by interleukin-6 from CD4+ T cells.; Fgl1-deficient mice show earlier onset of autoimmune lesions compared to wild-type mice.; FGL-1 levels are significantly elevated in patients with primary Sjögren disease and correlate with serum IL-6 levels.
Comparable overall survival across chemotherapy, chemoimmunotherapy, and immunotherapy regimens without unexpected adverse events.; Genomic analysis reveals NSCLC-like (KEAP1, KRAS, STK11) and SCLC-like (RB1, TP53) LCNEC subtypes, with 80% aligning with SCLC transcriptional profiles.; Elevated FGL-1 and SPINK1 expression in NSCLC-like LCNECs, and higher DLL3 levels in SCLC-like LCNECs.; Fewer tumor-infiltrating lymphocytes in LCNECs compared to other lung cancers.
GL and FGL supplementation reduced fasting blood glucose levels and enhanced muscle strength and skeletal muscle cross-sectional area in T2DM mice.; Both GL and FGL ameliorated ubiquitin-proteasome system (UPS)-related pathways, while only FGL attenuated skeletal muscle inflammation and apoptosis.; FGL, administered at half the dose of GL, demonstrated greater efficacy in regulating molecular markers, including improved mTOR-autophagy pathway.; Bioconversion of guava leaf with L. plantarum produced unique metabolites (e.g., hydroxyl-isocaproic acid) and may offer additive or synergistic anti-diabetic and muscle-protective effects.
Major CAF types exhibit three activation states with distinct interactions and prognostic relevance for immunotherapy.; Minor CAF components can originate from other TME components such as endothelia and macrophages.; Endothelial-to-mesenchymal transition CAFs are ubiquitously present and may interact with SPP1+ tumor-associated macrophages, impacting survival.
The GGM assumption of independent pairwise interactions is often implausible in psychological research.; MNMs allow each pairwise interaction to be moderated by a subset of other variables in the model.; Simulations show MNMs outperform split-sample methods (NCT and FGL) for detecting moderation effects.; The R-package mgm provides a reproducible tutorial for estimating MNMs.
FGL-1 expression was significantly higher in placental trophoblasts of subjects with GDM compared to controls.; FGL-1 increased trophoblast proliferation via an extracellular signal-regulated kinase 1/2-dependent pathway.; Plasma FGL-1 concentrations were higher in GDM subjects and disrupted insulin action in HepG2 cells and L6 myotubes.; Placental FGL-1 may play a role in impairing insulin function and could be a novel biomarker for GDM.
NCAM mimetic peptides induce downstream signaling pathways and exhibit neuritogenic and neuroprotective effects.; These peptides modulate synaptic function in both in vitro and in vivo models.; Preclinical studies demonstrate therapeutic potential for stroke, traumatic brain injury, and Alzheimer's disease.; C3, plannexin, and FGL are specifically identified as promising therapeutic candidates.
FGL peptide improves cognition by activating PKC pathway, leading to AMPA receptor delivery to synapses.; PTD4-PI3KAc peptide enhances hippocampal memory by promoting synapse and spine formation via PI3K signaling.; PTEN-derived peptide prevents memory deterioration in Alzheimer's mouse model by blocking pathological PTEN-PDZ interactions.; Synaptic function is a valid target for cognitive enhancement through peptide treatment.
Frequently asked questions
What is FGL?
**Mechanism of Action** FGL (FG Loop peptide) is a synthetic peptide derived from the neural cell adhesion molecule (NCAM) that mimics the FG loop region of NCAM’s fibronectin type III domain. It selectively binds to and activates fibroblast growth factor receptor 1 (FGFR1), initiating downstream signaling cascades suc
How does FGL work?
NCAM-derived FG-loop peptide that activates FGFR1 to enhance synaptic plasticity and memory in animal models.
What is the research status of FGL?
FGL is currently classified as preclinical, with 262 research references on record. This is for research purposes only and is not medical advice.
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