Description
MGF IGF-1 Ec Peptide: Muscle, Bone, and Cartilage Support
MGF IGF-1 Ec, or Mechano-Growth Factor C-terminal 24 (MGF-Ct24E), is a 24-amino-acid fragment cleaved from IGF-1 Ec. Unlike full-length IGF-1, MGF IGF-1 Ec bypasses classical IGF-1 receptor activation, signaling primarily through ERK pathways. It has been extensively studied for muscle hypertrophy, tissue repair, anti-apoptotic activity, and bone regeneration.
This peptide is a research tool for understanding noncanonical IGF-1 signaling, particularly in muscle, cartilage, bone, and neural-like cells, and offers potential for investigating cell survival, regeneration, and stress response mechanisms.
Chemical Makeup
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Molecular Formula: C124H204N42O41S1
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Molecular Weight: 2971.99 g/mol
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Other Names: Mechano-Growth Factor, MGF-Ct24E
Research and Clinical Insights
Muscle Cell Hypertrophy & Growth
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Activates Erk1/2 and Erk5, promoting muscle cell hypertrophy without IGF-1 receptor tyrosine phosphorylation.
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Increases cell volume and protein content in smooth muscle and myoblast cultures.
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Supports Erk5–MEF2C–dependent gene expression, enhancing α-smooth muscle actin, γ-actin, smoothelin, and desmin.
Muscle Cell Aging & Regeneration
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May mitigate aging in young satellite cells, prolonging division cycles in vitro.
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Effects are age-dependent, with limited benefit in older cells.
Anti-Fibrotic & Anti-Inflammatory Action
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Reduces muscle fibrosis, early collagen I/III expression, and pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1β, TGF-β).
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Modulates oxidative stress (gp91phox) and matrix metalloproteinases (MMP-1, 2, 9, 10, 14).
Anti-Apoptotic & Cell Survival
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Enhances Bcl-2 expression and reduces DNA fragmentation in hypoxic muscle cells.
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Preserves mitochondrial integrity, supporting intrinsic survival pathways.
Cartilage & Chondrocyte Support
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Potentiates TGF-β3-induced chondrogenesis, favoring Col2 and aggrecan expression.
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Reduces Col1 and pro-fibrotic markers in damaged cartilage.
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Supports cell migration and cytoskeletal organization via RhoA–YAP pathways.
Bone Cell & Osteoanabolic Activity
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Stimulates osteoblast proliferation, increasing S and G2/M phase cell populations.
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Acts through ERK1/2 signaling, independent of IGF-1 receptor.
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Promotes callus formation, cortical bridging, lamellar bone formation, and early fracture healing.
Neural-Like Cell Protection
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Enhances survival in SH-SY5Y neuroblastoma cells under mitochondrial stress.
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Reduces apoptosis and preserves mitochondrial function.
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Mechanism linked to HO-1 upregulation and ERK pathway activation.
Key Benefits of MGF IGF-1 Ec
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Supports muscle hypertrophy and regeneration
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Promotes bone formation and osteoblast proliferation
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Enhances cartilage repair and chondrocyte function
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Reduces fibrosis, oxidative stress, and inflammation
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Protects neural-like cells and supports cell survival under stress
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References:
- Janssen JA, Hofland LJ, Strasburger CJ, van den Dungen ES, Thevis M. Potency of Full-Length MGF to Induce Maximal Activation of the IGF-I R Is Similar to Recombinant Human IGF-I at High Equimolar Concentrations. PLoS One. 2016 Mar 18;11(3):e0150453. doi: 10.1371/journal.pone.0150453. PMID: 26991004; PMCID: PMC4798685.
- Li C, Vu K, Hazelgrove K, Kuemmerle JF. Increased IGF-IEc expression and mechano-growth factor production in the intestinal muscle of fibrostenotic Crohn’s disease and smooth muscle hypertrophy. Am J Physiol Gastrointest Liver Physiol. 2015 Dec 1;309(11):G888-99. doi: 10.1152/ajpgi.00414.2014. Epub 2015 Oct 1. PMID: 26428636; PMCID: PMC4669353.
- Kandalla PK, Goldspink G, Butler-Browne G, Mouly V. Mechano Growth Factor E peptide (MGF-E), derived from an isoform of IGF-1, activates human muscle progenitor cells and induces an increase in their fusion potential at different ages. Mech Ageing Dev. 2011 Apr;132(4):154-62. doi: 10.1016/j.mad.2011.02.007. Epub 2011 Feb 25. PMID: 21354439.
- Liu X, Zeng Z, Zhao L, Chen P, Xiao W. Impaired Skeletal Muscle Regeneration Induced by Macrophage Depletion Could Be Partly Ameliorated by MGF Injection. Front Physiol. 2019 May 17;10:601. PMID: 31164836; PMCID: PMC6534059.doi:10.3389/fphys.2019.00601





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