Shaanxi BLOOM Tech Co., Ltd. is one of the most experienced manufacturers and suppliers of mt2 injection in China. Welcome to wholesale bulk high quality mt2 injection for sale here from our factory. Good service and reasonable price are available.
MT2 injection, namely Melanotan II injection, features Melanotan II (MT2) as its core active ingredient. It is a synthetic cyclic heptapeptide and a structural analog of human endogenous α-melanocyte-stimulating hormone (α-MSH). Compared with endogenous hormones, MT2 undergoes structural optimization, conferring stronger receptor-binding capacity, superior biological stability and enhanced resistance to enzymatic degradation. Its biological activity is nearly one thousand times that of native α-MSH, making it the predominant non-selective melanocortin receptor agonist for research and application at present.
The formulation was initially developed at the University of Arizona, USA, in the 1980s. The original research objective was to explore UV-free skin tanning technology for protection against ultraviolet-induced cutaneous damage. With advancing research, scientists discovered that it can target and activate multiple human melanocortin receptors, exerting multifaceted effects including modulation of pigment synthesis, energy metabolism, appetite and physiological functions.
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Melanotan II COA
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| Certificate of Analysis | ||
| Compound name | Melanotan II | |
| Grade | Pharmaceutical grade | |
| CAS No. | 121062-08-6 | |
| Quantity | 30g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202601090056 | |
| MFG | Jan 9th 2026 | |
| EXP | Jan 8th 2029 | |
| Structure |
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| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.54% |
| Loss on drying | ≤1.0% | 0.42% |
| Heavy Metals | Pb≤0.5ppm | N.D. |
| As≤0.5ppm | N.D. | |
| Hg≤0.5ppm | N.D. | |
| Cd≤0.5ppm | N.D. | |
| Purity (HPLC) | ≥99.0% | 99.90% |
| Single impurity | <0.8% | 0.52% |
| Total microbial count | ≤750cfu/g | 95 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 500ppm |
| Storage | Store in a sealed, dark, and dry place below -20°C | |
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| Chemical Formula | C50H69N15O9 |
| Exact Mass | 1023.54 |
| Molecular Weight | 1024.2 |
| m/z | 1023.54 (100.0%), 1024.54 (54.1%), 1025.55 (14.3%), 1024.54 (5.5%), 1025.54 (3.0%), 1025.54 (1.8%), 1026.55 (1.7%), 1026.55 (1.0%) |
| Elemental Analysis | C, 58.64; H, 6.79; N, 20.51; O, 14.06 |
Mechanism of Action
Currently, MT2 injection is primarily employed as a research reagent in biomedicine and endocrine metabolism studies. Owing to its unique melanogenic property, it is widely adopted in research on skin photoprotection and skin tone homogenization. Nevertheless, its non-targeted receptor activation leads to certain side effects; it has not been approved for routine clinical administration and is restricted exclusively to research use.
Core Target: Activation Mechanism of Melanocortin Receptor Family
The core mechanism underlying the physiological activity of the product lies in the non-selective activation of human melanocortin receptors (MCRs). Belonging to the superfamily of G protein-coupled receptors, MCRs are widely distributed in human skin, central nervous system, endocrine glands and visceral tissues. Four key subtypes have been identified: MC1R, MC3R, MC4R and MC5R. Each subtype exhibits highly specific tissue distribution and physiological functions, which constitute the fundamental basis for the multiple pharmacological effects of MT2.
Native α-MSH presents relatively high binding selectivity yet weak affinity toward individual receptor subtypes. By virtue of cyclic lactam structural modification, MT2 constrains its molecular spatial conformation, enabling stable binding to various melanocortin receptors with markedly improved binding efficiency. It can durably activate downstream receptor signaling cascades and continuously regulate physiological and metabolic processes in the body.
After administration into the organism, MT2 diffuses rapidly to all target tissues via body fluid circulation, and can bind to and activate melanocortin receptors spontaneously without external stimuli such as ultraviolet radiation.
Its receptor activation pattern is saturable and long-acting; single administration sustains biological activity for several days, far exceeding the short-lived effects of native hormones. Meanwhile, the cyclic structure of the molecule effectively resists hydrolytic degradation by endogenous peptidases to avoid rapid metabolic inactivation, ensuring persistent signal activation. Differential activation of distinct receptor subtypes mediates a series of biological responses including pigment synthesis, energy homeostasis, appetite regulation, glandular secretion and physiological function modulation. These signaling pathways operate independently while exerting synergistic regulation, collectively forming the complete functional network of MT2.
Targeting MC1R: Mechanism Mediating Melanogenesis and Skin Pigmentation
MC1R is the most critical and thoroughly investigated target of MT2. It is specifically expressed on the cell membrane of epidermal melanocytes and hair follicle melanocytes, serving as a vital receptor governing human melanin generation, skin tone formation and cutaneous photoprotection. Upon specific binding between MT2 and MC1R, the canonical Gs protein-coupled signaling pathway is initiated. Adenylyl cyclase (AC) on the cell membrane is rapidly activated, inducing a sharp elevation of intracellular second messenger cyclic adenosine monophosphate (cAMP) and disrupting basal metabolic homeostasis within melanocytes.
Sustained high levels of cAMP further activate downstream protein kinase A (PKA). Activated PKA undergoes nuclear translocation and catalyzes phosphorylation of cyclic adenosine monophosphate response element-binding protein (CREB) in the cell nucleus, triggering the transcriptional activity of CREB.
Activated CREB specifically binds to the promoter region of the tyrosinase gene, significantly upregulating gene expression and protein synthesis of tyrosinase, and boosting the biological activity of key melanogenic enzymes including tyrosinase, dopachrome tautomerase and isomerase.
As the rate-limiting enzyme for melanin synthesis, elevated tyrosinase activity accelerates the oxidation of tyrosine into DOPA and dopaquinone, followed by a sequence of oxidation and polymerization reactions that ultimately produce eumelanin.
Unlike UV-induced melanogenesis, pigment production mediated by MT2 injection predominantly generates eumelanin, which possesses stronger antioxidant and anti-ultraviolet properties. It achieves homogeneous skin pigmentation without photodamage and effectively improves cutaneous sun resistance.
Furthermore, MT2 suppresses melanocyte apoptosis via the MC1R pathway to prolong melanocyte survival. It also facilitates the transportation and distribution of melanosomes to keratinocytes, yielding more uniform and long-lasting skin pigmentation. Long-term administration stably elevates basal cutaneous pigment content and lowers risks of UV sunburn, uneven pigmentation and photoaging. This signaling pathway represents MT2's primary functional mechanism. Distinct from physical and chemical shielding in conventional sunscreen products, it achieves endogenous hormonal regulation to realize active cutaneous anti-photodamage, granting unique physiological advantages.
Meanwhile, excessive activation of this pathway constitutes the main cause of excessive skin darkening and pigment deposition in some users, reflecting dose-dependent pharmacological characteristics.
Targeting MC3R/MC4R: Mechanism Regulating Energy Metabolism and Appetite Balance
MC3R and MC4R are predominantly expressed in the hypothalamic central nervous system, acting as core receptor subtypes modulating appetite, energy homeostasis and lipid metabolism.
Activation of these two receptors underpins MT2's metabolic regulatory effects. MC4R plays a dominant role in appetite suppression and energy expenditure control, whereas MC3R mainly assists in maintaining systemic energy balance and regulating fat storage efficiency. The two subtypes synergistically participate in the modulation of feeding behavior and metabolic rhythms.
After crossing the blood-brain barrier into the central nervous system, MT2 specifically binds to MC3R and MC4R on hypothalamic neurons and initiates downstream regulatory responses through the identical cAMP-PKA signaling pathway.
In terms of appetite modulation, receptor activation inhibits synthesis and release of orexigenic neuropeptide Y and agouti-related protein in the hypothalamus, while promoting secretion of anorexigenic neuropeptides. It bidirectionally modulates central feeding signals, markedly alleviating hunger and reducing voluntary food intake, especially suppressing cravings for high-calorie and high-fat food. With regard to energy metabolism, MT2 enhances basal metabolic rate by activating the two receptors, accelerates catabolism of white adipose tissue to reduce lipid accumulation in adipocytes, moderately improves thermogenesis efficiency, and speeds up excess energy consumption to sustain body fat homeostasis.
In addition, activation of MC3R and MC4R modulates insulin sensitivity, enhances glucose uptake and utilization in peripheral tissues, mitigates blood glucose fluctuations, and assists in balancing glucose and lipid metabolism. Multiple research experiments have verified that continuous low-dose MT2 injection intervention effectively reduces body weight and body fat percentage and alleviates metabolic disorders.
Nevertheless, activation of this pathway carries side effects. Overdosing triggers excessive activation of central metabolic signals, resulting in symptoms such as anorexia, rapid weight loss and fatigue; metabolic rhythm disturbance may occur in certain individuals, demonstrating the bidirectional and dose-dependent nature of MT2 pharmacology. Moreover, MC4R also participates in human cardiovascular regulation, and its overactivation may slightly affect heart rate and vascular tone, contributing to mild cardiovascular adverse reactions.
The mainstream industrial and laboratory synthetic route for MT2 is solid-phase peptide synthesis (SPPS). The Fmoc protecting group strategy is adopted to assemble linear peptide chains, followed by intramolecular cyclization, purification and refinement to obtain high-purity cyclic heptapeptide products. The overall synthetic process is mature and yields high-purity products, complying with preparation requirements for research-grade formulations.
Synthesis commences with solid-phase resin as the carrier. Fmoc-protected amino acids are selected as raw materials. Following the specific amino acid sequence of MT2, repeated cycles of deprotection, coupling and washing reactions are carried out to sequentially assemble the linear heptapeptide chain.
Reaction temperature, duration and reagent ratio are strictly controlled throughout the process to suppress side reactions such as amino acid racemization and peptide chain cleavage. Special residues including D-phenylalanine require close process monitoring to guarantee precise stereoconfiguration.
Upon completion of linear peptide assembly, selective deprotection technology is implemented to specifically expose active side-chain groups of aspartic acid and lysine. Intramolecular amidation cyclization proceeds under mild liquid-phase conditions to construct MT2's signature cyclic lactam structure and lock the bioactive molecular conformation.
After cyclization, a trifluoroacetic acid system is used to cleave the peptide from the resin carrier and simultaneously remove all side-chain protecting groups to afford crude peptide products. Gradient purification is then performed via high-performance liquid chromatography (HPLC) to eliminate unreacted raw materials, short peptide impurities, isomers and other byproducts. Vacuum freeze-drying yields purified white powder.
This synthetic process achieves product purity exceeding 98% with robust structural stability. The purified material can be directly formulated into the product, representing the standardized synthetic protocol commonly adopted in research laboratories worldwide.
FAQ
Compared to oral and transdermal administration, what are the unique theoretical advantages of injectable formulations in regulating "peripheral" circadian rhythms (such as the heart and pancreas)?
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Injection can achieve a more rapid and reliable increase in systemic blood drug concentration, ensuring that the drug can act simultaneously and efficiently on the central nervous system (suprachiasmatic nucleus) and all peripheral organs expressing MT2 receptors (such as the heart, pancreas, and adipocytes), achieving synchronization of systemic rhythm.
Why may the "time window" for injection administration be more stringent than that for oral administration?
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Because injection administration avoids delayed intestinal absorption, the drug enters the systemic circulation almost instantly. If the injection time point (such as in the evening) does not match the "phase" of the individual's internal biological clock (such as night owls), it may exacerbate rhythm disorders. Therefore, more accurate medication timing prescriptions need to be based on individualized "time patterns".
In addition to sleep, what is the potential role of its injection type in controlling blood sugar in "type 2 diabetes" based on the rhythmic mechanism?
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MT2 receptors are expressed in pancreatic beta cells and participate in the diurnal regulation of insulin secretion. Directly and effectively activating peripheral MT2 receptors through injection may optimize the timing of insulin secretion and improve abnormal blood glucose rhythms such as the "dawn phenomenon", but this is a highly exploratory direction.
As an injection, what uncommon stability challenges may its drug formulation (such as solvents, pH values) face?
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MT2 receptor agonists are mostly hydrophobic molecules that may require the use of cyclodextrin, special surfactants, or co solvents (such as PEG) for solubilization. These excipients may affect the chemical stability of the drug, compatibility with packaging materials (such as adsorption), and even pose a risk of injection site reactions.
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