El factor de crecimiento mecánico pegilado (PEG-MGF) es una forma truncada y ligeramente alterada del factor de crecimiento similar a la insulina 1 (IGF-1). Las investigaciones muestran que estimula la proliferación y diferenciación de mioblastos (células musculares). También se ha explorado en investigaciones centradas en aumentar la resistencia, estimular la función del sistema inmunológico, reducir el colesterol y reducir la grasa corporal total. También hay alguna evidencia que sugiere que PEG-MGF mejora la función inmune relacionada con la curación y, por lo tanto, podría reducir el tiempo que tardan las heridas en sanar.

La pegilación es un proceso de unión de polietilenglicol a otro compuesto químico. A menudo se hace para reducir la reacción inmune natural del cuerpo a un agente o, como en el caso de PEG-MGF, para aumentar la vida media del compuesto en la sangre al reducir la eliminación en los riñones. La pegilación es común, segura y tiene varias ventajas. PEG-MGF fue desarrollado porqueMGFtiene una vida media muy corta en sangre. Aunque persiste durante períodos más prolongados en el tejido muscular, el MGF administrado de forma exógena tiene una vida media corta porque pasa primero por el torrente sanguíneo a menos que se inyecte directamente en el tejido muscular. PEG-MGF ayuda a compensar esta desventaja particular.

PEG-MGF y músculo esquelético

Las lesiones musculares son comunes en los deportes e incluyen desde torceduras y esguinces hasta lesiones por avulsión. En muchos casos, este tipo de lesiones requieren reparación quirúrgica. Sin embargo, independientemente del tratamiento, la recuperación tiende a ser larga y los resultados no siempre son perfectos. Sin embargo, la investigación en un modelo de lesión muscular en ratones sugiere que el MGF inyectado directamente en el músculo protege las células al disminuir la expresión de ciertas hormonas inflamatorias y reducir el estrés oxidativo.^[1].

Similar research by Sun et. al. shows that MGF modulates muscle inflammation and improves the recruitment of macrophages and neutrophils to the site of injury^[2]. Both studies are based on the previous knowledge that exercise-induced muscle damage stimulates the release of IGF-1Ea and IGF-1Eb, both of which are closely related to MGF^[3].

Studies carried out by an international group of endocrinology researchers reveals that MGF stimulates the insulin-like growth factor 1 receptor just as much as IGF-1^[4]. Stimulation of this receptor has been linked to decreased aging, increased lean body mass, and improved energy homeostasis in humans. This function suggests that PEG-MGF can produce effects similar to IGF-1 leading to improved muscle repair, enhanced fat metabolism, and overall increases in lean body mass.

Research in mice also shows a 25% increase in mean muscle fiber size when MGF is administered to mice that are exercising^[5]. In this study, the MGF was injected directly into the muscle, something that authors Goldspink and Jakeman point out as a serious limitation as the protein would have to be injected into every muscle in which hypertrophy is to be optimized. PEG-MGF solves this particular problem by increasing the plasma half-life of MGF and allowing it to be administered via a single intravenous injection rather than multiple intramuscular injections.

PEG-MGF Research in Heart Muscle Repair

Research carried out in the department of bioengineering at the University of Illinois shows that MGF inhibits the programmed cell death that cardiac muscle cells undergo following hypoxia. Furthermore, the peptide appears to recruit cardiac stem cells to the site of injury and may therefore help in regeneration and healing following heart attack. Rats in the study were administered MGF within eight hours of hypoxia and showed less cell death and greater stem cell recruitment compared to controls that did not receive MGF^[6]. Dr. Doroudian, lead author of the research, believes that using nanorods to deliver MDF in the setting of heart damage may be an effective way to provide localized, long-term therapy of the bioactive peptide to areas of injury.

Similar research indicates that localized delivery of MGF shows that it can improve cardiac function following heart attack by reducing pathologic hypertrophy. Rats in the study that were treated with PEG-MGF showed better hemodynamics and less cardiac remodeling than untreated rats^[7]. Carpenter et. al. have similarly shown that MGF injected in the setting of acute myocardial infarction can reduce cardiomyocyte injury by as much as 35%.

Bone Repair and Growth

Research in rabbits indicates that PEG-MGF can increase the rate of bone repair by boosting the proliferation of osteoblasts, the cells that mineralize bone. Rabbits treated with high doses of MGF showed the same level of healing at four weeks that was seen in controls at six weeks^[8]. There is hope that this technique can help scientists learn how to promote bone healing and reduce time that people must spend immobilized to allow for healing.

Protecting Cartilage

Research indicates that MGF can improve the function of chondrocytes, the cells primarily responsible for cartilage health and deposition. Research in mice shows that MGF enhances the migration of chondrocytes from bone, where the cells develop, into cartilage where they have an effect^[9]. This is a perfect setting for PEG-MGF because it could be injected into compromised joint spaces and would remain for long periods of time. A single injection could, in theory, be useful for weeks or even months whereas standard MGF has an effect limited to minutes or perhaps hours.

Dental Applications

Research in cell cultures of human periodontal ligament cells indicates that PEG-MGF can improve osteogenic differentiation and boost expression of MMP-1 and MMP-2^[10]. These factors act to improve repair of the ligaments that attach the tooth to bone and may offer an alternative to too extractions and implants, allowing people to keep their natural teeth after injury. There is even speculation that PEG-MGF may make it possible to save damaged or avulsed teeth after they are surgically re-implanted.

Potential Neuroprotective Effects

Alexander Walker, Editorial Assistant at BioMed Central, has recently reviewed a study exploring the long-term effects of increased levels of MGF in the brain and central nervous system. The study reveals that higher levels of MGF help to reduce the effects of age-related neuron degeneration, resulting in mice that retain their cognitive functions and operate a peak cognitive performance longer into old age. According to Walker, “the efficacy of MGF in the brain is age-dependent” as mice in the study had improved results both initially and over the long-term if MGF overexpression occurred earlier in life^[11].

Treatment with MGF has also been shown to improve muscle weakness and reduce the loss of motor-neurons in mouse models of ALS^[12]. According to Dluzniewska et al., MGF is naturally expressed in the brain following hypoxic injury and is over-expressed in regions of the brain where neuron regeneration is greatest. By administering exogenous MGF, it may be possible to reduce the impact of a number of neurological diseases, no

PEG-MGF exhibits minimal side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. PEG-MGF for sale at

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Paul Goldspink, PhD is the Principal Investigator and Associate Professor at the Department of Physiology within the Medical College of Wisconsin. The research in Dr. Goldspink’s laboratory is focused on understanding the actions of IGF-1 isoforms in the heart and other tissues. We are investigating the role of IGF-1 isoforms in response to stresses such a mechanical overload, hypoxia, oxidative stress and age in the heart. We have focused on a particular isoform called Mechano-Growth Factor (MGF), which plays a protective role in preventing cell death, preserving contractility and preventing pathologic hypertrophy of the heart following myocardial infarction. We are currently investigating the underlying mechanisms utilizing peptide analogs derived from the E-domain region of MGF which serve as allosteric modulators of excitation-transcription pathways in muscle. Through collaborations we have been able to exploit our findings by developing a technology that combines a microscopic physical scaffold to deliver peptide therapeutics, with the goal of improving cardiac function during the progression of heart failure by using implantable cell-sized “biomimetic devices”. The development of these intelligent drug delivery platforms which we have recently employed in the heart, also have applicability of other tissues and disease states.

Paul Goldspink, PhD is being referenced as one of the leading scientists involved in the research and development of PEG-MGF. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between

1. [1] X. Liu, Z. Zeng, L. Zhao, P. Chen, and W. Xiao, “Impaired Skeletal Muscle Regeneration Induced by Macrophage Depletion Could Be Partly Ameliorated by MGF Injection,” Front. Physiol., vol. 10, p. 601, 2019.
2. [2] K.-T. Sun, K.-K. Cheung, S. W. N. Au, S. S. Yeung, and E. W. Yeung, “Overexpression of Mechano-Growth Factor Modulates Inflammatory Cytokine Expression and Macrophage Resolution in Skeletal Muscle Injury,” Front. Physiol., vol. 9, 2018.
3. [3] A. Philippou et al., “Expression of IGF-1 isoforms after exercise-induced muscle damage in humans: characterization of the MGF E peptide actions in vitro,” Vivo Athens Greece, vol. 23, no. 4, pp. 567–575, Aug. 2009.
4. [4] J. A. M. J. L. Janssen, L. J. Hofland, C. J. Strasburger, E. S. R. van den Dungen, and M. Thevis, “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, vol. 11, no. 3, Mar. 2016./a>
5. [5] G. Goldspink, “Research on mechano growth factor: its potential for optimising physical training as well as misuse in doping,” Br. J. Sports Med., vol. 39, no. 11, pp. 787–788, Nov. 2005.
6. [6] G. Doroudian, J. Pinney, P. Ayala, T. Los, T. A. Desai, and B. Russell, “Sustained delivery of MGF peptide from microrods attracts stem cells and reduces apoptosis of myocytes,” Biomed. Microdevices, vol. 16, no. 5, pp. 705–715, Oct. 2014.
7. 7] J. R. Peña, J. R. Pinney, P. Ayala, T. A. Desai, and P. H. Goldspink, “Localized delivery of mechano-growth factor E-domain peptide via polymeric microstructures improves cardiac function following myocardial infarction,” Biomaterials, vol. 46, pp. 26–34, Apr. 2015.
8. [8] M. Deng et al., “Mechano growth factor E peptide promotes osteoblasts proliferation and bone-defect healing in rabbits,” Int. Orthop., vol. 35, no. 7, pp. 1099–1106, Jul. 2011.
9. [9] X. Jing et al., “Mechano-growth factor protects against mechanical overload induced damage and promotes migration of growth plate chondrocytes through RhoA/YAP pathway,” Exp. Cell Res., vol. 366, no. 2, pp. 81–91, May 2018.
10. [10] J.-T. Chen, Y. Wang, Z.-F. Zhou, and K.-W. Wei, “[Mechano-growth factor regulated cyclic stretch-induced osteogenic differentiation and MMP-1, MMP-2 expression in human periodontal ligament cells by activating the MEK/ERK1/2 pathway],” Shanghai Kou Qiang Yi Xue Shanghai J. Stomatol., vol. 28, no. 1, pp. 6–12, Feb. 2019.
11. [11] A. W. graduated from the U. of L. with a Bs. in Z. in 2015 H. joined B. C. as E. A. for the L. S. department in May 2017, I. P. I. in Parasitology, entomology, and E. Biology, “Hearts and Minds of Mice and Men: Mechano Growth Factor a new tool in the battle against age-related neuron loss?,” On Biology, 20-Jul-2017. [BMC]
12. [12] J. Dluzniewska et al., “A strong neuroprotective effect of the autonomous C-terminal peptide of IGF-1 Ec (MGF) in brain ischemia,” FASEB J. Off. Publ. Fed. Am. Soc. Exp. Biol., vol. 19, no. 13, pp. 1896–1898, Nov. 2005.

ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATONAL AND EDUCATIONAL PURPOSES ONLY.

The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body.  These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease.  Bodily introduction of any kind into humans or animals is strictly forbidden by law.