Cureus | Peptide Therapy

Peptide Therapy

Apr 22, 2024 | NEWS

There are many potential benefits of peptide therapy in different medical fields. This Cureus article explores the expression of antimicrobial peptides and cytokines in the human omentum following abdominal surgery, with the aim of understanding how these peptides can aid in the prevention of postoperative infections. The article below focuses on the effects of Mechano-Growth Factor (MGF) peptide, which has been shown to have favorable impacts on muscle growth, wound healing, cartilage repair, and brain development in animal studies. MGF peptide has also been shown to activate muscle stem cells and enhance heart health, among other benefits. 

There is a growing interest in peptide therapy as a potential solution to various medical problems, from muscle loss to postoperative infections.

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Peptide Research: an Overview

Mechano-Growth Factor (MGF) peptide is a splice variant of insulin-like growth factor [i] that has been suggested to have cardiological effects, favorably influencing muscle growth, wound healing, cartilage repair, and brain development in animal studies. MGF C-terminal has been speculated to enhance muscle healing after damage and hasten recovery. Moreover, data is suggesting it may help shield tissues from the mechanical stressors incurred during training and physical activity.

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What is the Mechano Growth Factor?

In contrast to IGF1, the peptide known as Mechano growth factor (MGF) [ii] has a slightly modified sequence. Research suggests it may significantly impact growth and development.

Animal studies purport that MGF peptide may promote tissue repair and development by activating muscle stem cells and increasing protein synthesis for tissue growth. Researchers are now exploring this peptide as a potential adjuvant for disorders that cause muscle loss and wasting in animals.

Animal studies support that MGF peptide may promote tissue repair and development by activating muscle stem cells and increasing protein synthesis for tissue growth. Researchers are now exploring this peptide as a potential therapy for disorders that cause muscle loss and wasting in animals.

MGF Peptide: Mechanism of Action

According to research, IGF and muscle growth factor (MGF) seem to work together to cause hypertrophy and speed up the healing process after muscle injury. Muscle satellite cells, also known as stem cells, are activated with their help, per experimental study results. [v]

Investigations purport the IGF-1Eb isoform, as it's more often known, may protect neurons, mitigate the atrophying effects of insulin, and speed up the healing of damaged muscle tissue in animals.

Studies in rats have asserted the efficacy of this peptide. After muscular damage, high levels of MGF were found in the rats' muscles, which have been hypothesized to have promoted skeletal muscle cell development. Research on MGF for disorders that cause muscle wasting or tissue damage is limited, but early results are encouraging.

MGF Peptide Properties

According to the scientific community's findings, MGF peptides have a wide range of applications. In a nutshell, here's what it can do, according to animal studies:

  • Encourage the growth of new muscle by stimulating stem cells

  • Facilitate healing, repair, and cell division

  • Facilitate the reduction of inflammation

  • Maximize workouts

  • Improve mental well-being and growth

  • Enhance heart health

Muscle Growth Factor's Effects

Recent studies have shown that MGF (Mechanical growth factor) may stimulate satellite cells in the body, leading to increased hypertrophy, larger muscles, and even muscle regeneration. According to animal studies, MGF administered to mice for three weeks resulted in a 25% increase in muscle growth. Researchers think this peptide has the potential to double the health benefits of exercise and cure muscle-wasting disorders.

An animal's basal metabolic rate and the pace at which it burns calories at rest benefit from muscle gain. Thus the animal may see more than simply an aesthetic advantage from exercising. Animal studies have demonstrated that increased lean body mass helps alleviate various diseases and health problems linked to obesity.

Transplantation of myogenic precursor cells enhances dystrophin expression, which may explain why MGF therapy is effective in the context of some muscle-wasting illnesses like Duchenne muscular dystrophy (DMD). As a result, the negative consequences of these states are mitigated.

Despite the treatment's encouraging name, post-transplant survival statistics are dismal. Animal studies suggest that C-terminal peptide may improve transplant outcomes by increasing the number of myogenic precursor cells that survive the procedure.

MGF Peptide and Injuries

Injuries, inflammatory diseases like arthritis, and overuse of joints may all lead to cartilage breakdown. Experts agree that poor blood flow and a lack of stem cells prevent cartilage from regenerating properly. Yet, research on MGF peptides in animals suggested that they might assist in overcoming many of the obstacles to cartilage regeneration.

Research indicates that C-terminal [iii] MGF might help chondrocytes (cells that promote cartilage health and repair) endure exposure to noxious stimuli, including damage and physical stress. By increasing cell survival, MGF supplementation has been theorized to aid in protecting and repairing cartilage when mechanical stress is applied, as per studies.

Rodent studies indicated that MGF peptide might stop disc degeneration by stopping cell apoptosis. [iv] 

Cardiological Consequences

Data from animal trials of acute myocardial infarction in sheep suggests that MGF peptide may prevent heart muscle damage caused by ischemia. Researchers also speculated that cardiomyocyte damage seemed reduced by 35% when MGF peptide was presented.

MGF Peptide and the Brain

In 2010, scientists asserted that MGF peptide was present in the brains of rats, suggesting the peptide's possible neuroprotective properties. Research in mice further indicates that MGF protein is expressed in the context of brain hypoxia and that it may protect neurons.

Studies purport that MGF peptide may relieve the increasing muscular weakness seen in Lou Gehrig's disease (ALS) and slow down the underlying cause of the illness, the degeneration of motor neurons.

Researchers have ascertained that mechano-growth factor peptides may protect neurons from disease progression more effectively than any other isoform. It has also been hypothesized to aid in recovering brain tissue damaged by ischemia. Scientists have high hopes that MGF peptide, with further study, may prove to be adjuvant and may save motor neurons from dying.


[i] Philippou A, Papageorgiou E, Bogdanis G, Halapas A, Sourla A, Maridaki M, Pissimissis N, Koutsilieris M. Expression of IGF-1 isoforms after exercise-induced muscle damage in humans: characterization of the MGF E peptide actions in vitro. In Vivo. 2009 Jul-Aug;23(4):567-75.

[ii] Moriggl, R, V Gouilleux-Gruart, R Jähne, S Berchtold, C Gartmicen, X Liu, L Hennighausen, A Sotiropoulos, B Groner, and F Gouilleux. “Deletion of the Carboxyl-Terminal Transactivation Domain of MGF-Stat5 Results in Sustained DNA Binding and a Dominant Negative Phenotype.” Molecular and Cellular Biology 16, no. 10 (October 1996): 5691–5700. doi:10.1128/mcb.16.10.5691.

[iii] Esposito, Simone, Koen Deventer, and Peter Van Eenoo. “Characterization and Identification of a C-Terminal Amidated Mechano Growth Factor (MGF) Analogue in Black Market Products.” Rapid Communications in Mass Spectrometry 26, no. 6 (February 10, 2012): 686–692. doi:10.1002/rcm.6144.

[iv] 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.

[v] Mills P, Dominique JC, Lafrenière JF, Bouchentouf M, Tremblay JP. A synthetic mechano growth factor E Peptide enhances myogenic precursor cell transplantation success. Am J Transplant. 2007 Oct;7(10):2247-59.

Editor's Note: This blog post was sponsored by Core Peptides LLC.