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Free U.S. shipping on orders over $150Melanotan II is a synthetic α-MSH analogue with the ability to bind MC1R, MC3R, MC4R, and MC5R receptors [R]. Compared to Melanotin I, it shows an ability to cross the blood-brain barrier, resulting in central nervous system effects including sexual behavior, appetite, and mood regulation. It has a shorter duration of action,
Melanotan II has documented effects on sexual arousal and erectile dysfunction because of its affinity for specific receptors in the brain [1]. By activating MC4R and MC3R, researchers found that it stimulated neural pathways involved in sexual motivation and performance, independent of direct sexual stimulation [1]. In animal studies, Melanotan II induced spontaneous erections and increased libido in both males and females [2, 3].
In a small study of men with psychological (not physical) erectile dysfunction, Melanotan-II triggered erections in most participants and kept them firm for much longer than a placebo [4]. Some men experienced mild side effects like nausea or yawning, but these were temporary and didn’t need treatment [4].
Melanotan analogs stimulate melanocytes to increase eumelanin production, leading to darker skin pigmentation [5]. While Melanotan I is highly selective for the MC1R receptor (which leads to more predictable tanning effects), Melanotan II activates multiple other receptors, which can cause broader systemic effects [6].
Melanotan II is thought to influence energy balance and appetite regulation via MC3R and MC4R activation in key regions of the brain that control hunger and satiety, the hypothalamus and nucleus accumbens [7].
In an animal study, researchers gave Melanotan II to rats and found that it caused a sharp drop in food intake over two days and significantly reduced body fat and insulin levels [8]. Even when combined with another brain chemical, neuropeptide Y, which normally increases hunger and fat storage, Melanotan II blocked most of these effects [8].
By acting on specific brain regions, melanotan II seems to reduce food intake, suppress appetite, and increase thermogenesis by activating brown adipose tissue [9].
Emerging research has suggested that melanotan II may modulate dopamine and oxytocin pathways, potentially influencing reward processing, mood, and addiction-related behaviors [10].
One study in rats found that injecting melanotan II into the bloodstream was able to activate oxytocin-producing brain cells, a hormone linked to bonding and social behavior. While it did not directly cause oxytocin release inside the brain, it increased the activity of neurons and was able to increase blood levels, suggesting it may indirectly boost levels through brainstem pathways [11].
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Melanotan II 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.
Orders are processed within 1–3 business days after payment confirmation. Orders placed after 3:00 PM Pacific time or on weekends and holidays will begin processing the next business day. We offer free standard shipping on orders over $150. All orders are shipped in insulated packaging with ice packs when necessary. Standard delivery typically takes 2–4 business days within the continental US.
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.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
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.
Snapshot MGF (IGF-1 Ec) is a specialized form of IGF-1 released after exercise or muscle strain to jump-start the body’s repair process. It helps activate muscle stem cells, supports recovery, and promotes healthy tissue rebuilding. Research also shows MGF may aid nerve protection and balanced immune responses, making it a key peptide for repair and resilience. What Is MGF (IGF-1) Ec? Mechano-growth factor (MGF), also known as IGF-1 Ec, MGF-E, and MGF Ec, is a 24-amino acid splice variant of the insulin-like growth factor-1 (IGF-1) gene that is uniquely expressed in response to mechanical loading, tissue strain, and muscular microdamage [1]. While classical IGF-1 isoforms (such as IGF-1 Ea, the most ubiquitous form) participate in endocrine and paracrine signaling related to growth, metabolism, and recovery, MGF represents a specialized version with distinct biological roles. The key difference lies in its E-domain sequence, which alters receptor binding dynamics and shifts its function toward local tissue repair rather than systemic growth signaling. Native IGF-1 promotes pathways like PI3K/Akt and mTOR, while MGF is believed to stimulate satellite cell activation, promoting local cellular proliferation and preparing damaged fibers for subsequent IGF-1–mediated differentiation [2]. Because of its rapid, short-lived expression following mechanical stress, endogenous MGF acts as the body’s immediate “alert” peptide for muscle and connective-tissue adaptation. MGF (IGF-1) Ec Mechanism of Action and Benefits Muscle Growth and Repair MGF (IGF-1 Ec) is most recognized for its involvement in the early stages of muscle repair, where it acts as a rapid-response signal following mechanical strain or localized microdamage. Unlike systemic IGF-1 isoforms that are involved in sustained anabolic activity, MGF initiates the activation and proliferation of satellite cells, the stem-like cells responsible for muscle regeneration. An in vitro study used primary human muscle cell cultures from donors of different ages (neonatal, young adult, old adult) to investigate the effects of MGF (IGF-1 Ec) on muscle regeneration pathways [3]. MGF (IGF-1 Ec) administration resulted in: Increased proliferative lifespan of satellite cells in neonatal and young adult cultures. Strong satellite cell activation and myogenic fusion, supporting enhanced muscle repair potential. Hypertrophy-like changes across all age groups, and a significant reduction in reserve satellite cells, indicating increased recruitment. The peptide substantially enhanced satellite cell activation, proliferation, and fusion, supporting improved muscle repair and maintenance. Because its effects are strongest in neonatal and young adult muscle, MGF (IGF-1 Ec) may represent a promising therapeutic strategy for preventing age-related sarcopenia. Neuroprotection and Neurogenesis Beyond its well-established role in muscular adaptation, MGF (IGF-1 Ec) has been investigated for its influence on neural resilience and regenerative signaling within the central and peripheral nervous systems. A preclinical in vivo/in vitro model of neuronal ischemia evaluated neuroprotective mechanisms of MGF (IGF-1 Ec) [4]. Results showed: Substantial protection to neurons typically highly vulnerable to ischemic injury, in the gerbil in vivo model. After ischemia, endogenous MGF expression increased in resistant hippocampal neurons, suggesting a natural protective role. MGF (IGF-1 Ec) peptide was as potent and longer lasting than full-length IGF-1 in preventing neurodegeneration. Neuroprotective effects of MGF (IGF-1 Ec) occurred independently of the IGF-1 receptor, indicating a novel mode of action. The MGF (IGF-1 Ec) peptide demonstrates potent, sustained neuroprotective effects in both in vivo and in vitro ischemia models. Its ability to act independently of the IGF-1 receptor makes this peptide a promising therapeutic candidate for stroke recovery. Immune Modulation and Tissue Repair MGF (IGF-1 Ec) also plays a meaningful role in coordinating immune activity, especially in environments where mechanical stress or localized injury triggers an inflammatory response. Because MGF is rapidly upregulated in damaged tissue, it acts as an early signaling cue that helps transition the microenvironment from acute inflammation toward controlled regeneration. An animal study investigated whether exogenous MGF can rescue impaired muscle regeneration in a mouse model of skeletal muscle contusion combined with macrophage depletion [5]. Mice underwent muscle contusion injury followed by macrophage depletion to model impaired regenerative conditions. After the injection of injured muscles with synthetic MGF (IGF-1 Ec), results showed: Substantially reduced fibrosis markers Reduced pro-inflammatory mediators (TNF-α, IFN-γ, IL-1β, and TGF-β) Reduced chemokine receptor expression, indicating suppression of inflammatory cell recruitment Reduced gp91phox, an oxidative stress marker Although MGF did not directly enhance muscle fiber regeneration lost due to macrophage depletion, it improved the detrimental effects of macrophage loss by modulating inflammation. 1 Schlegel, W., Raimann, A., Halbauer, D., Scharmer, D., Sagmeister, S., Wessner, B., et al. (2013) Insulin-like growth factor I (IGF-1) Ec/Mechano Growth factor--a splice variant of IGF-1 within the growth plate. PLoS One, Public Library of Science (PLoS) 8, e76133 2 Dai, Z., Wu, F., Yeung, E. W. and Li, Y. (2010) IGF-IEc expression, regulation and biological function in different tissues. Growth Horm. IGF Res., Elsevier BV 20, 275–281 3 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 4 Dluzniewska, J., Sarnowska, A., Beresewicz, M., Johnson, I., Srai, S. K. S., Ramesh, B., et al. (2005) A strong neuroprotective effect of the autonomous C-terminal peptide of IGF-1 Ec (MGF) in brain ischemia. FASEB J., Wiley 19, 1896–1898 5 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
What is MOTS-c peptide? MOTS-c is a mitochondrial-derived and exercise-induced peptide whose levels decrease with age [1]. It improves insulin sensitivity, glucose metabolism, and metabolic homeostasis [2]. Animal studies suggest that, by activating AMPK, it can mitigate obesity resulting from high-fat diets, aging, and menopause [3, 2]. It also regulates age-related inflammation and various aspects of age-related physical decline, such as bone and muscle losses [1]. MOTS-c peptide benefits and side effects Metabolic and cardiovascular health In pancreatic cells, MOTS-c lowers insulin secretion and increases glucagon production [4]. In mice with aberrant lipid metabolism, MOTS-c treatment significantly reduced lipid buildup in liver cells [5]. In rodents, high-fat diet-induced obesity can promote insulin resistance and fat accumulation that triggers chronic inflammation. In mice, MOTS-c administration protects against both age-related and high-fat diet-induced insulin resistance, and diet-induced obesity [6]. Hormonal changes during pregnancy can affect insulin sensitivity and cause high blood sugar, leading to gestational diabetes. In pregnant women and mouse models of gestational diabetes, MOTS-c normalized blood sugar, and enhanced insulin sensitivity and glucose tolerance. The MOTS-c treatment lowered both the birth weight-associated complications and mortality of offspring caused by gestational diabetes [7]. Low estrogen during menopause can cause weight gain and fat redistribution in favor of white fats, which increases insulin resistance and the risk of metabolic disorders. In contrast, the more mitochondria-dense brown fats burn more calories, and improve glucose and lipid metabolisms. In ovarectomized mice, MOTS-c increases brown fat activation, and reduces fat accumulation and inflammation in white adipose tissue, which contributes to the lower level of fats in serum and liver [3]. In heart failure, fluid buildup and increased pressure in the lungs can cause lung injury. MOTS-c reduced heart dysfunction and remodeling caused by heart failure and lowered inflammation while boosting antioxidant activity in the hearts of sick mice [8]. It can also prolong injured heart and lung cells’ life cycle [9, 10]. Muscle building and bone health Age-related sarcopenia can reduce overall healthspan and independence, while increasing various metabolic health risks. MOTS-c suppresses myostatin and lipid infiltration that contributes to muscle atrophy, even in immobilized animals [11, 12]. Older adults with higher circulating MOTS-c have better muscle performance and lean mass, while those with lower levels experienced more sarcopenia [13]. In a mouse model of aging, MOTS-c can significantly increase physical performance by activating genes related to skeletal muscle metabolism and myoblast adaptation to metabolic stress [1]. In an in vitro model of muscle development, MOTS-c peptide helps muscle cells to form properly, affecting their integral parts such as myotubes. It supports muscle cell formation at the expense of lipid accumulation while protecting muscle cells from the breakdown effects of inflammatory cytokine IL-6 [14]. Age-related bone loss often parallels muscle loss, and various anti-sacropenic stimuli also protect bone health. Importantly, metabolic dysfunction and inflammation tend to accelerate bone loss. MOTS-c mitigates age-related bone loss by stimulating osteoblasts and suppressing osteoclasts by modulating AMPK and inflammatory responses [15]. In a mouse bone damage model, MOTS-c treatment reduced bone loss and inflammation and prevented the formation of osteoclasts [16]. Anti-inflammatory and antioxidant benefits Sepsis is a potentially lethal condition characterized by systemic overactive immune reactions towards an infection or noninfectious agents. MOTS-c greatly improves survival and lowers bacterial counts in MRSA-infected experimental mice. It also reduces levels of pro-inflammatory cytokines like TNF-α, IL-6, and IL-1β, while increasing the anti-inflammatory cytokine IL-10 [17]. Type 1 diabetes patients have lower endogenous MOTS-c levels than healthy controls. In a mouse model of type 1 diabetes, exogenous MOTS-c prevents pancreatic β cell destruction by shifting CD4+ T cells towards a less self-destructive phenotype, suggesting that MOTS-c may be beneficial as an autoimmune treatment [18]. Age-related inflammation and declining antioxidant capacity are key drivers of aging and related diseases. Older adults aged 70–81 years have 20% less MOTS-c than younger adults 18–30 years old [19]. In a mouse model of type 2 diabetes, MOTS-c administration increased antioxidant enzymes like SOD and CAT, protecting myocardial cells from oxidative stress [20]. Neuropathic pain Unlike acute pain, neuropathic pain is pain caused by nervous system dysfunction related to nerve damages, rather than by injury or inflammation. MOTS-c’s antinociceptive effects pertain to its ability to restore mitochondrial health, and inhibit microglial and pain signals in the spinal cord [21]. Furthermore, compared to morphine, MOTS-c has far fewer side effects such as gastrointestinal transit inhibition and motor incoordination [22].
What is NAD+? Nicotinamide adenine dinucleotide (oxidized form), commonly abbreviated as NAD⁺, is a naturally occurring coenzyme found in all living cells. It has gained interest in research due to its roles in mediating various cellular anti-aging processes. It plays a central role in redox reactions, acting as an electron carrier in metabolic processes such as glycolysis, the Krebs cycle, and oxidative phosphorylation [1, 2, 3]. Structurally, NAD⁺ consists of two nucleotides joined through their phosphate groups: one nucleotide contains an adenine base, and the other contains nicotinamide [4]. Image source [4] NAD+ functions In cellular systems, NAD⁺ functions as a substrate for a range of enzymes, including: Sirtuins: deacetylases and ADP-ribosyltransferases responsible for the regulation of metabolism, cellular stress response, and aging [5] Poly(ADP-ribose) polymerases (PARPs): enzymes responsible for DNA repair, genomic stability, and programmed cell death [6] CD38/CD157: cell surface proteins found in immune cells [7] In its oxidized form (NAD⁺), the molecule accepts electrons and is converted into its reduced counterpart, NADH, which subsequently donates those electrons to the mitochondrial electron transport chain for ATP production [8]. However, NAD⁺ itself remains a molecule of focus for research exploring its direct biochemical interactions within various intracellular compartments, including the cytoplasm, nucleus, and mitochondria. NAD+ and anti-aging Intracellular NAD⁺ levels decline with cellular aging, demonstrated in several mammalian tissues [9]. Various anti-aging hormeses, such as caloric restriction and cold exposure, work partly by increasing cellular NAD+. This observation has created interest in longevity research and has launched multiple investigations into NAD⁺ precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) in both animals and humans [10], [11]. Age-associated declines in NAD⁺ levels have been linked to impaired mitochondrial function, increased oxidative stress, and reduced sirtuin activity [9]. Lower NAD⁺ concentrations correlate with diminished autophagy, shortened telomeres, and lowered PARP DNA repair activity [12, 13]. Age-related NAD⁺ depletion also impairs endothelial function and contribute to chronic low-grade inflammation [14]. NAD+ and DNA repair Although NAD+ is a PARP substrate, it’s unclear whether increasing physiologic NAD+ concentration can meaningfully improve DNA repair. A clinical trial with 21 healthy smokers orally supplemented nicotinic acid (0, 50, or 100 mg/day) over 14 weeks to track various biological and DNA associated parameters. After 14 weeks, results found [15]: Supplementation with 50 and 100 mg/day of nicotinic acid elevated blood nicotinamide and lymphocyte NAD⁺ concentrations. The rise in NAD⁺ was most pronounced in individuals with initially low NAD⁺ levels. There was no significant reduction in HPRT variant frequencies or micronuclei induction, common measures of DNA damage. Although nicotinamide supplementation did not activate markers of DNA repair, larger sample size studies and comparison to healthy individuals are needed. NAD+ and metabolic health NAD+ supplementation can tangibly improve whole-body metabolic health. An RCT of 30 overweight or obese adults over 45 received 1,000 mg/day of β-nicotinamide mononucleotide (MIB-626) (2 x 500 mg tablets twice daily) vs. placebo for 28 days to see whether NAD⁺ levels could be safely boosted and improve markers of cardiometabolic health [16]. Results showed that MIB-626 supplementation: Significantly increased circulating levels of NAD⁺ and related metabolites significantly increased (p < 0.05). Increased body weight by ~1.9 kg (p = .008). Reduced diastolic blood pressure by ~7 mmHg (p = .034). Significantly reduced total cholesterol by ~27 mg/dL (p = .004) and LDL by ~19 mg/dL (p = .007). NAD+ and addiction NAD+ supplementation is a powerful way to curb addictive behaviors. A pilot study investigated the effects of intravenous NAD+ and enkephalinase combination infusions on cravings and psychological outcomes in 50 individuals with Substance Use Disorder (SUD) [17]. The cohort included a diverse group of poly-drug-dependent individuals. Behavioral changes were evaluated using Likert scales, measuring craving, anxiety, and depression levels before and after infusion therapy. IV NAD+ infusions resulted in: A significant reduction in withdrawal symptoms such as craving, anxiety, and depression (p < 0.0005) Reduced relapse risks as participants had no detectable illicit substances based on the urine tests All reductions followed a dose-dependent linear trend, with greater improvements observed over time. The study shows the potential application of NAD/NADH as a stand-alone treatment in attenuating symptoms of addiction.