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Free U.S. shipping on orders over $150Snapshot: PEG-MGF (PEGylated Mechano-Growth Factor) is a regulated IGF-1 Ec-derived peptide used in preclinical research to study IGF-1R, PI3K/Akt, and MAPK/ERK signaling in tissue-repair and regeneration models. Experimental studies have explored its roles in skeletal muscle recovery, periodontal ligament remodeling, bone and cartilage repair, and injury-response pathways.
PEG-MGF (Polyethylene Glycol–Modified Mechano-Growth Factor) is a chemically-modified peptide related to the IGF-1 Ec splice-variant sequence (also called MGF). In research settings, it is used as a pathway probe to study IGF-axis signaling, skeletal muscle regeneration programs, and injury-response biology in both in vitro and in vivo models [1, 2, 3]. Pegylation is applied to increase peptide persistence and stability, allowing for longer exposure windows compared with non-pegylated fragments in time-course and distribution studies [4].
Experimental studies most often evaluate PEG-MGF in contexts including skeletal muscle injury and repair, cardiac ischemia and hypoxia, bone healing and osteoblast activity, cartilage and chondrocyte migration, and periodontal ligament cell differentiation. Mechanistically, its actions are linked to IGF-1 receptor activation and downstream PI3K/Akt and MAPK/ERK signaling pathways, which are associated with cell growth, migration, and survival responses [3].
PEG-MGF has been investigated in preclinical and mechanistic research models, with findings suggesting potential roles in muscle repair and regeneration [5], modulation of inflammatory mediator expression and immune-cell clearance kinetics [6], osteoblast proliferation [7], chondrocyte migration and mechanotransduction pathways [2], and apoptosis and remodeling in cardiac injury models [8].
In experimental settings, key considerations include the fact that IGF-axis activation is linked to cell-proliferation signaling, which warrants caution in models involving abnormal or uncontrolled cell growth [2]. Effects may also vary depending on delivery method and PEGylation format, and current evidence remains largely limited to controlled preclinical studies. These findings are model-specific and should be interpreted within a lab-research context.
PEG-MGF and related MGF-derived peptides are frequently studied in models of muscle injury and repair. These experiments typically measure changes in inflammation, oxidative stress, and expression of genes involved in tissue recovery and remodelling [2]. Cell-based studies using myoblasts and muscle-cell cultures also study cell growth, migration, and IGF-1R-linked PI3K/Akt and MAPK/ERK signaling, which are pathways associated with hypertrophy and regeneration rather than performance enhancement [2].
Across multiple studies, MGF peptides support satellite-cell activation, proliferation, and fusion, which are key steps in muscle maintenance and repair [5, 3]. In primary human muscle cell cultures, the MGF-24aa-E peptide increased the proliferative lifespan of satellite cells and delayed cellular aging in younger tissue, while promoting hypertrophy across all age groups [5]. These effects are interpreted as enhanced regenerative capacity, particularly relevant to age-related muscle loss and sarcopenia [5]. Other experimental models show that early increases in MGF splice-variant expression tend to coincide with the initial, proliferation-focused phase of muscle repair, followed later by differentiation and myofiber maturation [3].
MGF-related peptides have also been studied in cardiac injury settings. In animal models of myocardial infarction, delivery of MGF E-domain peptides has been associated with better preservation of cardiac function, smaller regions of compromised tissue, reduced cell-death signaling, and slower progression of adverse remodeling [8, 9]. In some studies, localized delivery using peptide-eluting biomaterial structures further improved hemodynamic recovery following injury [9].
Overall findings suggest benefits for repair, survival, and regeneration-linked signaling programs both in skeletal and cardiac muscle, with applications focused on tissue-healing rather than performance outcomes.
MGF-related peptides have also been studied in periodontal ligament (PDL) regeneration models, particularly under mechanical loading conditions such as occlusal force.
In vitro and in vivo studies show that MGF produced in response to mechanical stimulation can enhance PDL remodelling and promote periodontal ligament stem-cell proliferation and fibrogenic differentiation [10, 11]. These effects are linked to Fyn-FAK-mediated mechanochemical signaling, activation of ERK1/2 and p38 pathways, and the Fyn-RhoA-YAP phosphorylation axis, which together support matrix remodeling and fibroblast-like differentiation [10].
Collectively, these findings suggest a potential role for MGF-centered signaling as an adjunct approach in periodontal regeneration research.
PEG-MGF peptides have been studied in multiple injury- and regeneration-focused models. In cardiac ischemia, MGF expression rises rapidly and peptide delivery has been associated with reduced apoptosis, preservation of myocardium, improved hemodynamics, and possible stimulation of precursor cell recruitment [4].
In neural and hypoxia-ischemia models, MGF shows neuroprotective activity independent of IGF-1R signaling, supporting cell survival pathways [4]. MGF has also been reported to influence chondrocyte and mesenchymal-cell differentiation, matrix remodelling, and cytoskeletal dynamics under stress or damage conditions [4].
References
1 Liu, X., Zeng, Z., Zhao, L., Chen, P. and Xiao, W. (2019) Impaired skeletal muscle regeneration induced by macrophage depletion could be partly ameliorated by MGF injection. Front. Physiol., Frontiers Media SA 10, 601
2 Liu, Y., Duan, M., Zhang, D. and Xie, J. (2023) The role of mechano growth factor in chondrocytes and cartilage defects: a concise review. Acta Biochim. Biophys. Sin. (Shanghai), China Science Publishing & Media Ltd. 55, 701–712
3 Matheny, R. W., Jr, Nindl, B. C. and Adamo, M. L. (2010) Minireview: Mechano-growth factor: a putative product of IGF-I gene expression involved in tissue repair and regeneration. Endocrinology, The Endocrine Society 151, 865–875
4 Zabłocka, B., Goldspink, P. H., Goldspink, G. and Górecki, D. C. (2012) Mechano-Growth Factor: an important cog or a loose screw in the repair machinery? Front. Endocrinol. (Lausanne), Frontiers Media SA 3, 131
5 Kandalla, P. K., Goldspink, G., Butler-Browne, G. and Mouly, V. (2011) 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. 132, 154–162
6 Lin, Y.-C., Chen, B.-M., Tran, T. T. M., Chang, T.-C., Al-Qaisi, T. S. and Roffler, S. R. (2023) Accelerated clearance by antibodies against methoxy PEG depends on pegylation architecture. J. Control. Release, Elsevier BV 354, 354–367
7 Deng, M., Zhang, B., Wang, K., Liu, F., Xiao, H., Zhao, J., et al. (2011) Mechano growth factor E peptide promotes osteoblasts proliferation and bone-defect healing in rabbits. Int. Orthop., Springer Science and Business Media LLC 35, 1099–1106
8 Carpenter, V., Matthews, K., Devlin, G., Stuart, S., Jensen, J., Conaglen, J., et al. (2008) Mechano-growth factor reduces loss of cardiac function in acute myocardial infarction. Heart Lung Circ., Elsevier BV 17, 33–39
9 Peña, J. R., Pinney, J. R., Ayala, P., Desai, T. A. and Goldspink, P. H. (2015) Localized delivery of mechano-growth factor E-domain peptide via polymeric microstructures improves cardiac function following myocardial infarction. Biomaterials, Elsevier BV 46, 26–34
10 Feng, F., Tu, T., Wang, H., Song, R., Li, J., Zhu, Y., et al. (2024) Mechano-growth factor regulates periodontal ligament stem cell proliferation and differentiation through Fyn-RhoA-YAP signaling. Biochem. Biophys. Res. Commun., Elsevier BV 733, 150450
11 Zhao, Y., Zhang, S., Cheng, B., Feng, F., Zhu, Y., Liu, Y., et al. (2024) Mechanochemical coupling of MGF mediates periodontal regeneration. Bioeng. Transl. Med., Wiley 9, e10603
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). PEG-MGF is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
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No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
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FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
What is Pinealon Peptide? Pinealon is a synthetic, bioactive, tripeptide (Glu-Asp-Arg) derived from the pineal gland [3]. It is classified as a peptide bioregulator due to its unique ability to bypass typical cell-surface or cytoplasmic receptors [3]. Instead, evidence suggests that it’s exceptionally small structure enables the molecule to cross both cellular and nuclear membranes [3]. Lab studies find that Pinealon can enter the cell nucleus, where it is thought to interact with DNA or DNA-associated proteins [3]. This ability to reach the genome provides a potential explanation for its wide-ranging effects, which align better with gene-expression changes rather than modulating traditional signalling pathways [3]. Inside the nucleus, Pinealon seems to modulate genes involved in antioxidant defenses, cell repair, and protection from cellular stress [1]. Animal model research reveals reductions in reactive oxygen species and apoptosis, and increased activity of endogenous antioxidant enzymes [4]. It appears to reduce the activity of caspase-3, an enzyme involved in programmed cell death, across several tissue types, suggesting a potential role in supporting cell survival under stressful conditions [4]. Pinelon may impact pathways related to healthy cell cycling and interact with the pineal gland to influence its function and regulate circadian rhythm [5]. Pinealon peptide benefits Its unique mechanism, which bypasses conventional cell-surface receptors, has led to growing interest in its potential roles in neuroprotection, metabolism, stress resilience, and cognitive support. Learning and Memory Through directly interacting with DNA to influence gene expression involved in neural function, Pinealon may support learning and memory. Studies suggest it can reduce oxidative stress in brain tissue, preserve neuronal viability, and modulate pathways related to information retention. In a study of prenatal rats exposed to high levels of homocysteine, maternal administration of Pinealon improved offspring cognitive function, enhancing performance in spatial orientation and navigation tasks while reducing reactive oxygen species and neuronal necrosis in the cerebellum [6]. Another found Pinealon was able to produce improvements in the Morris labyrinth task, showing faster acquisition of navigation tasks compared to untreated controls and those treated with a comparator peptide [7]. Improvements were also accompanied by reductions in caspase-3 activity in brain regions, suggesting that this peptide supports neuronal survival and resilience under hypoxic stress [4]. In a review, authors highlight findings to suggest that Pinealon enhances learning indices, decreases age- and stress-related neuronal apoptosis, and improves overall memory performance in animal models. It is thought these benefits are related to Pinealon’s ability to penetrate the nucleus and modulate gene expression, upregulating protective pathways and antioxidant systems while stabilizing cell-cycle and cell-death processes [8]. Neuroprotection Studies have found that Pinealon may help protect neurons through multiple and complementary mechanisms, primarily demonstrated in preclinical models. One major pathway involves reducing oxidative stress, a key contributor to neuronal injury and neurodegeneration. In cell studies, Pinealon was found to decrease ROS accumulation, reduce necrotic cell death, and modulate ERK1/2 activation, a signalling pathway involved in cell survival and stress response [1]. These findings suggest Pinealon may help maintain neuronal integrity under conditions of metabolic or oxidative stress, through direct genomic interactions that influence cell-cycle regulation [1]. Experimental hypoxia models further demonstrate neuroprotective effects. In hypobaric hypoxia and aged rat studies, Pinealon was able to increase neuronal resistance to oxygen deprivation, potentially by stimulating superoxide dismutase and glutathione peroxidase, and by limiting NMDA receptor-mediated excitotoxicity [7]. Pinealon was also found to normalize pro-inflammatory cytokines such as IL-6 and TNF‑α, indicating a dual role reducing programmed cell death and neuroinflammation [4]. At a molecular level, Pinealon is thought to modulate gene expression pathways associated with neurodegeneration [8]. Evidence suggests it can interact with histones and RNA, influencing pathways such as MAPK/ERK, as well as pro-apoptotic proteins and antioxidant genes [8]. This makes it a candidate for further study in neurodegenerative conditions. Antioxidant and Anti-aging Pinealon shows promise as an antioxidant and cellular longevity support. It supports brain cell viability by reducing reactive oxygen species (ROS) and limiting cell death, while also influencing cell survival pathways like ERK1/2 [1]. It also shows benefits for strengthening cell membranes and preventing lipid peroxidation, helping support the brain’s resistance to oxidative stress [8]. Pinealon has been shown to modulate the activity of antioxidant enzymes, including SOD and GPx, and support antioxidant genes like SOD2 and GPX1 [8]. In aging and low-oxygen models, it protects neurons by reducing excitotoxicity, lowering caspase‑3 activity, and normalizing inflammatory signals, which supports cell survival and new neuron growth [4]. In human neurons from older donors, it also reduces DNA damage and helps maintain dendritic structures [9]. Overall, Pinealon combines antioxidant, anti-aging, and anti-inflammatory effects, though human studies are still limited.
PT-141 peptide benefits PT‑141, also known as bremelanotide, is a synthetic cyclic heptapeptide structurally derived from α‑melanocyte‑stimulating hormone (α‑MSH). It acts primarily as an agonist at melanocortin receptors MC3R and MC4R, in the central nervous system [1]. By doing so, it activates hypothalamic pathways, resulting in downstream signals that influence sexual arousal and associated neurobiologic responses. Mechanistic target of PT-141 PT‑141 exerts its effect through binding and activation of melanocortin receptors, especially within the hypothalamus. Evidence from animal studies indicates that systemic administration of PT‑141 induces penile erection and activates hypothalamic neurons, as shown by increased c‑Fos immunoreactivity [1]. By working on sexual arousal and desires in the brain, PT-141’s mechanism of action differs from phosphodiesterase‑5 (PDE-5) inhibitors, which cause peripheral vasodilation. Instead, PT‑141 stimulates arousal via central neurochemical cascades, including increased dopamine release in key brain regions governing sexual function. This also means combining PT-141 with PDE5 inhibitors can have additive effects. Also, PT-141 is more effective in females than PDE5. PT-141 and erectile dysfunction Male erectile function Across preclinical and clinical studies, PT-141 demonstrated the ability to increase sexual arousal in both men and women, with dose-dependent efficacy and an acceptable safety profile in the controlled research setting. A randomized, double-blind, placebo-controlled clinical trial was combined with preclinical animal studies to investigate the effects of PT-141 on sexual dysfunction [1]. Preclinical results suggests that PT-141: Activated MC3 and MC4 melanocortin receptors in the central nervous system. Produced sexual arousal behaviors in rodents without directly affecting the vascular system. The parallel clinical trial found that intranasal PT-141 up to 20 mg, produced significant improvements in erectile function compared to placebo. The erectile response rates were dose-dependent, with higher doses achieving a significant increase in rigidity and duration of erection (p < 0.05). Adverse events were generally mild to moderate, with the most common being dose-dependent, transient nausea and flushing. Phase I data shows that subcutaneous doses of PT‑141 (10 mg, 20 mg) increased duration of base rigidity ≥ 80% in healthy males. Phase 2A results indicated significantly longer durations at the 20 mg dose, with common adverse events including flushing and nausea. PT-141 and female libido Two identical Phase 3 RCTs enrolled a total of 2,449 premenopausal women with hypoactive sexual desire disorder (HSDD). 1,247 participants were included in the safety population, and 1,202 in the modified intent-to-treat efficacy analysis [3]. Participants were randomized 1:1 to receive either bremelanotide 1.75 mg or placebo administered subcutaneously on an as-needed basis over 24 weeks. Bremelanotide administration resulted in: Increases in Female Sexual Function Index (FSFI) desire domain scores versus placebo (p < 0.01) Reductions in Female Sexual Distress (FSDS-DAO) scores (p < 0.01) The most common adverse events (≥10% in both studies) were nausea, flushing, and headache. Most events were mild to moderate in severity. These findings support the potential of bremelanotide in modulating sexual desire in female populations. PT-141 safety and side effect profile Preclinical and clinical evidence indicate that PT‑141 (bremelanotide) is generally safe in research settings, with most adverse events being mild to moderate and transient. Adverse events The most frequently reported side effects include nausea, flushing, and headaches [4]. Cardiovascular effects PT-141 is associated with transient and mild cardiovascular effects, including: Blood pressure elevation ( ~3 mm Hg systolic and 2 mm Hg diastolic) Heart rate reduction These effects peaked within a few hours and returned to baseline within approximately 8–10 hours. Importantly, there was no net increase in overall myocardial workload [5]. Pigmentation Activation of melanocortin receptors can contribute to hyperpigmentation on the face, gums, and breasts. This was rare with dosing protocols in research settings (fewer than eight doses per month). However, this became more common with daily consecutive dosing [6]. Rare events A single case of acute hepatitis was reported in a participant after approximately 20 subcutaneous doses over one year. Significant elevations in aminotransferases and mild hyperbilirubinemia, resolved after discontinuation of PT‑141 [6].
What is Selank? Selank is a 7-amino acid peptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP). It was developed at the Russian Institute of Molecular Genetics in the 1990s for its potential anxiolytic, neuroprotective, and nootropic properties. The peptide is an analog of the tuftsin molecule, which is naturally produced in the human body. It works primarily by allosterically modulating GABA receptors, similarly to benzodiazepines but without the same impairing side effects. Selank can function as a neuropsychotropic, antidepressant, and antistress, nootropic and immunomodulatory drug due to its anxiolytic activity [1]. Selank peptide benefits Selank has similar effects to tranquilizers like benzodiazepines at low doses without the unwanted side effects such as dependence, withdrawal, and amnesia. Moreover, animal studies suggest that Selank relieves aggression and fear reaction [1]. In addition, Selank modulates the expression of genes that influence different types of immune responses, suggesting that it may also work through immunomodulation [2]. A rat study suggests that Selank may help maintain immune homeostasis during stress [3]. Anxiolytic and antidepressant properties The pharmacological investigation of Selank has primarily focused on its anxiolytic and antidepressant properties. In patients with anxiety and depressive disorders, Selank effectively reduced anxiety, mood swings, and somatic symptoms [4]. In the experimental model of chronic mild stress, the combination of Selank with benzodiazepines was the most effective in reducing anxiety levels, and Selank independently was the most efficient in reducing anxiety levels after individual stressful events [5]. Adults living in Ukraine with adjustment disorder who were admitted to hospital for routine check ups were either given Selank or placebo. Selank reduced complaints in patients with adjustment disorders. Even two weeks after treatment, patients receiving Selank reported reduced somatic symptoms, nutritional problems, and alcohol misuse [6]. A 2016 rat study [1] examined the effect of intranasal Selank and GABA on the expression of genes related to neurotransmission in the frontal cortex. The study concluded that Selank exerts a significant and time-dependent effect on the expression of genes related to neurotransmission, supporting its pivotal role in modulating anxiolytic and antidepressant pathways. Moreover, Selank works as a GABA receptor modulator. If administered together, Selank and benzodiazepines can regulate the activity of GABA receptors in a peculiar manner, which is not cumulative and is different from either substance individually. Thus, Selank's anti-anxiety mechanism of action is also concentration-dependent allosteric modulation of GABA receptors [7]. Cognitive enhancement and neuroprotection A rat study suggests that intranasal selank may improve memory and learning by increasing BDNF in the hippocampus [1, 8]. Another study examined rats with strong alcohol preference fed with 10% ethanol as the only fluid source for 30 weeks to induce attention and memory disturbances mimicking chronic alcohol intoxication. Subsequently, both alcohol-fed and age-matched control rats received Selank intraperitoneally at 0.3 mg/kg. Both alcohol-fed and control rats experienced a cognitive stimulating effect with increased exploration time and reduced discrimination index in novel object recognition tests. In control animals, BDNF was unchanged. However, in alcohol-fed animals, alcohol cessation after 30 weeks elevated BDNF in the hippocampus and cortex, while administration of selank restored BDNF levels to values comparable to those of the control group. In conclusion, Selank helps modulate BDNF and other reparative processes in rats cognitively impaired from chronic alcohol [9]. Stress resilience and recovery A Russian article investigated the effects of Selank on behavior and serotonin/noradrenalin concentrations in the brains of adult rats exposed to hypoxia during 14-16 days of gestation. Intraperitoneal Selank resulted in [10]: 2–3-fold increase in sensory attention 1.5-fold changes in learning capacity Normalized exploratory activity in the open field and hole board Recovered balance of serotonergic and noradrenergic brain system activity These results suggest that Selank has a normalizing impact on neurobehavioral functions impaired by prenatal hypoxia, indicating its potential role in enhancing stress resilience and supporting recovery of serotonergic and noradrenergic system activity. Moreover, Selank was shown to have positive emotional effects and antistress actions [11]. Immune and inflammation modulation Inflammation is a complex process mediated by the interaction of various immune cells and cytokines including IL-1β, IL-6, and TGF-β1. A recent study [12] has evaluated the effect of Selank on the level of the cytokines in rats that have been exposed to inflammatory stress. There was a significant decrease in the concentration of IL-1β and IL-6 and restoration of the level of IL-4, as well as suppression of the production of TGF-β1 and TNF-α in the serum of rats treated with Selank.