MC1R is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Updated 2026-06-08. Numbers and descriptions here follow the published literature rather than marketing material.
The compound was developed in the late 1980s and 1990s by academic researchers investigating photoprotection. The rationale held that stimulating melanin production might reduce ultraviolet damage to skin and lower skin cancer risk. Early work examined receptor binding, pigment response, and short-term tolerability in small studies. That program did not produce an approved drug, and formal development stalled after early-phase trials. Whether induced pigmentation confers meaningful photoprotection remains an open question.
Outside regulated medicine, melanotan II circulates through online vendors as a research chemical, often marketed for tanning. Products sold this way vary widely in purity, concentration, and labeling accuracy, and independent testing has documented discrepancies. Published reports describe both pigment effects and adverse reactions, including nausea, flushing, and darkening of existing moles. Long-term safety data are sparse, and no large controlled trial has established a risk profile. Questions about cumulative effects on melanocytes remain unresolved in the literature.
Melanotan II is a synthetic cyclic heptapeptide with the sequence Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2, corresponding to a molecular formula of C50H69N15O9 and a monoisotopic mass near 1024 daltons. It was designed as a structural analogue of alpha-melanocyte-stimulating hormone, a peptide hormone produced by cleavage of proopiomelanocortin. A lactam bridge between the aspartate and lysine side chains closes the ring, and the C-terminal amide removes a free carboxyl group. Both modifications increase resistance to enzymatic degradation compared with the linear parent hormone. Four substitutions distinguish it from afamelanotide, the linear analogue studied under the name melanotan I.
Receptor-binding studies classify melanotan II as a non-selective melanocortin agonist. It interacts with MC1R, MC3R, MC4R and MC5R, with reported affinities in the low nanomolar range and no strong subtype preference. Activation of MC1R on dermal melanocytes shifts pigment synthesis toward eumelanin, the dark polymer deposited in melanosomes and transferred to keratinocytes. Because the same peptide engages MC4R in the hypothalamus, it also appears in animal work on food intake and erectile response, which is why it is discussed in both pigment and metabolic research. Which receptor populations dominate after systemic exposure in humans is not fully established.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic cyclic heptapeptide | Belongs to the melanocortin agonist family |
| Key substitutions | Nle4 and D-Phe7 | Improve resistance to enzymatic degradation |
| Molecular formula | C50H69N15O9 | Approximately 1024 g/mol |
| Regulatory status | Not approved as a medicine | Distributed as a research chemical |
| Common synonyms | Melanotan II, MT-II, MT-2 | Spelling varies across sources |
Melanotan-2, also written Melanotan II, is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone. Its sequence is Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2, and the lactam bridge between the aspartate and lysine side chains constrains the peptide into a ring. This structural change increases receptor affinity and metabolic stability relative to the native hormone. The compound was created in the 1980s as a research tool for studying pigmentation biology.
Melanocytes are the pigment-producing cells of the skin, and they carry melanocortin-1 receptors on their surface. When the receptor is activated, cyclic adenosine monophosphate rises inside the cell and raises the activity of enzymes such as tyrosinase, which increases melanin output. Melanotan-2 binds melanocortin-1 receptors in vitro and in animal models, and this binding is generally described as the basis for the tanning effect. Other receptors account for different effects: melanocortin-4 receptors contribute to appetite and erectile signalling, while melanocortin-3 and melanocortin-5 receptors contribute to energy balance and exocrine function.
Early published reports described melanotan-2 as a tanning agent without sun protection, which means darkening is not the same as protection against ultraviolet radiation. Later studies explored the peptide in erectile dysfunction, hemorrhagic shock, and some skin conditions. No regulator in the United States or Europe has approved it for clinical use. Many products labelled melanotan-2 are sold without approval and their identity and purity are unverified. Its long-term safety in humans remains an open question.
β-catenin recruits other transcriptional coactivators, such as BCL9, Pygopus and Parafibromin/Hyrax. The complexity of the transcriptional complex assembled by β-catenin is beginning to emerge thanks to new high-throughput proteomics studies. However, a unified theory of how β‐catenin drives target gene expression is still missing, and tissue-specific players might assist β‐catenin to define its target genes. The extensivity of the β-catenin interacting proteins complicates our understanding: β-catenin may be directly phosphorylated at Ser552 by Akt, which causes its disassociation from cell-cell contacts and accumulation in cytosol, thereafter 14-3-3ζ interacts with β-catenin (pSer552) and enhances its nuclear translocation. BCL9 and Pygopus have been reported, in fact, to possess several β-catenin-independent functions (therefore, likely, Wnt signaling-independent).
On 17 September, the "All American" Division conducted its fourth and final combat jump of World War II. Fighting off German counterattacks, the division captured its objectives between Grave, and Nijmegen. The division failed to initially capture Nijmegen Bridge when the opportunity presented itself early in the battle. When the British XXX Corps arrived in Nijmegen, six hours ahead of schedule, they found themselves having to fight to take a bridge that should have already been in Allied hands. In the afternoon of Wednesday 20 September 1944, the 82nd Airborne Division successfully conducted an opposed assault crossing of the Waal river. War correspondent Bill Downs, who witnessed the assault, described it as "a single, isolated battle that ranks in magnificence and courage with Guam, Tarawa, Omaha Beach. A story that should be told to the blowing of bugles and the beating of drums for the men whose bravery made the capture of this crossing over the Waal possible." The Market Garden salient was held in a defensive operation for several weeks until the 82nd was relieved by Canadian troops, and sent into reserve in France. During the operation, 19-year-old Private John R. Towle of the 504th PIR was posthumously awarded the 82nd Airborne Division's second Medal of Honor of World War II.
=== Respiration === Cephalopods exchange gases with the seawater by forcing water through their gills, which are attached to the roof of the organism. Water enters the mantle cavity on the outside of the gills, and the entrance of the mantle cavity closes. When the mantle contracts, water is forced through the gills, which lie between the mantle cavity and the funnel. The water's expulsion through the funnel is used to power jet propulsion. If respiration is used concurrently with jet propulsion, large losses in speed or oxygen generation can be expected. The gills, which are much more efficient than those of other mollusks, are attached to the ventral surface of the mantle cavity. There is a trade-off with gill size regarding lifestyle. To achieve fast speeds, gills need to be small – water will be passed through them quickly when energy is needed, compensating for their small size. However, organisms which spend most of their time moving slowly along the bottom do not naturally pass much water through their cavity for locomotion; thus they have larger gills, along with complex systems to ensure that water is constantly washing through their gills, even when the organism is stationary. The water flow is controlled by contractions of the radial and circular mantle cavity muscles. The gills of cephalopods are supported by a skeleton of robust fibrous proteins; the lack of mucopolysaccharides distinguishes this matrix from cartilage. The gills are also thought to be involved in excretion, with NH4+ being swapped with K+ from the seawater.
Sources: en.wikipedia.org
A crystal structure of the serotonin 5-HT2B receptor bound to LSD reveals an extracellular loop that forms a "lid" over the diethylamide end of the binding cavity and "traps" LSD in the binding pocket, which explains the slow rate of LSD unbinding from serotonin receptors. The related lysergamide lysergic acid amide (LSA) that lacks the diethylamide moiety is far less potent in comparison. Moreover, a specific residue in the binding pocket is partially responsible for the prolonged action of LSD, and this residue is found in the human protein but not in the receptors of rodents. LSD is an extraordinarily potent psychoactive drug and is among the most potent psychedelics known in humans. The very high potency of LSD in producing psychedelic-like effects is also the case in animals, including rodents and monkeys. It is unclear why LSD is so potent. The affinity and activational potency of LSD at the human serotonin 5-HT2A receptor in vitro is unremarkable compared to other psychedelics such as DOI and DOB. There is no evidence for its greater potency being related to pharmacokinetics or metabolism. It appears that the N,N-diethylamide moiety of LSD fits into a sterically constrained region of the serotonin 5-HT2A receptor that specifically accommodates this moiety. LSD, like other psychedelics, has been found to increase the expression of genes related to synaptic plasticity and hence to have psychoplastogenic effects. This appears to be mediated by serotonin 5-HT2A receptor agonism.
=== Synthetic Biology === CRISPR – faster and more efficient gene editing technique Gene delivery/gene therapy – designing molecules to deliver modified or new genes into cells of live organisms to cure genetic disorders Metabolic engineering – modifying metabolism of organisms to optimize production of chemicals (e.g. synthetic genomics) Protein engineering – altering structure of existing proteins to enable specific new functions, or the creation of fully artificial proteins DNA-functionalized materials – 3D assemblies of DNA-conjugated nanoparticle lattices
It is marketed as a combination drug with mecobalamin under the brand names Agemax-P, Alphamix-PG, Freenerve-P, Gaben, Macraberin-P, Mecoblend-P, Mecozen-PG, Meex-PG, Methylnuron-P, Nervolin, Nervopreg, Neurica-M, Neuroprime-PG, Neutron-OD, Nuroday-P, Nurodon-PG, Nuwin-P, Pecomin-PG, Prebel-M, Predic-GM, Pregacent-M, Pregamet, Preganerv-M, Pregeb-M OD, Pregmic, Prejunate Plus, Preneurolin Plus, Pretek-GM, Rejusite, Renerve-P, Safyvit-PR, Vitcobin-P, and Voltanerv with Methylcobalamin and ALA by Cogentrix Pharma. In the US, Lyrica is marketed by Viatris after Upjohn was spun off from Pfizer.
Sources: en.wikipedia.org
It is a synthetic cyclic peptide designed as an analog of alpha-melanocyte-stimulating hormone. It acts on melanocortin receptors and is best known from research into pigmentation. It is not an approved pharmaceutical product.
No regulatory agency has approved it for any indication. It is encountered as a research chemical sold outside pharmaceutical supply chains. Products marketed this way are not subject to the manufacturing and labeling requirements that apply to approved drugs.
Reports describe increased skin pigmentation as well as side effects such as nausea, flushing, and changes to existing moles. Much of the evidence comes from small studies and case reports rather than large trials. The long-term safety profile is therefore uncertain.
No. It is a synthetic analogue carrying four amino acid changes, a lactam ring and an amidated C-terminus. The natural hormone is a linear thirteen-amino-acid peptide processed from proopiomelanocortin.