This is a working overview of melanocortin receptors, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-04-10. Anything still debated is marked as such rather than presented as settled.
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.
Published pharmacokinetic information is limited and comes mainly from small studies rather than registrational trials. Plasma half-life is usually described as short, on the order of tens of minutes, followed by rapid tissue distribution and clearance of the intact peptide. Metabolites and low concentrations of parent compound have been reported in urine, a detail relevant to anti-doping and forensic testing. Whether repeated exposure changes receptor sensitivity or clearance over time remains an open question. Values differ noticeably between analytical assays, so published numbers should be read as approximate rather than definitive.
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.
No regulatory authority has approved melanotan-2 for human use, and several countries classify it as a prescription-only or controlled substance, which restricts lawful supply. Material sold online is generally labelled as a research chemical and is not required to meet pharmaceutical standards of identity or purity. Published human data consist mainly of small uncontrolled studies, case reports and adverse-event notifications, so the evidence base is descriptive rather than confirmatory. Whether repeated melanocyte stimulation alters long-term naevus behaviour remains an open question that no completed trial has resolved.
Melanotan-2 is a synthetic cyclic heptapeptide designed as a structural analogue of alpha-melanocyte-stimulating hormone, the endogenous tridecapeptide that regulates pigment production. Two modifications distinguish it from the natural hormone: norleucine replaces methionine at the N-terminus, which limits oxidation, and a D-phenylalanine substitution raises receptor affinity. The ring is closed through an aspartate-lysine lactam bridge, giving the molecule a constrained conformation. The free base has a molecular mass near 1024 daltons, and commercial material is usually supplied as an acetate salt. It appears in the literature as a research peptide rather than an approved therapeutic agent.
Receptor studies place melanotan-2 among non-selective melanocortin agonists, binding MC1R, MC3R, MC4R and MC5R rather than a single subtype. Activation of MC1R on cutaneous melanocytes raises tyrosinase activity and shifts pigment synthesis toward eumelanin, which is darker and more photostable than pheomelanin. Central receptors, particularly MC4R, are associated with appetite suppression and with reported effects on sexual function. Because subtype selectivity is low, the same molecule engages pigment, metabolic and vascular pathways at once, and this breadth is a common explanation offered for the range of adverse events described in user reports.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C50H69N15O9 | Cyclic heptapeptide, C-terminally amidated |
| Approximate molecular mass | 1024 Da | Monoisotopic mass of the free peptide |
| Appearance | White to off-white powder | Typically supplied as a lyophilised solid |
| Solubility class | Soluble in water and polar solvents | Also dissolves in neutral aqueous buffer |
| Common synonyms | Melanotan II, MT-II, MT-2 | Described as a melanocortin agonist in early literature |
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.
Research interest has centred on photoprotection and pigmentation, with a smaller body of work on appetite and sexual function. Published human data remain limited to small, frequently uncontrolled studies, and the compound has never received marketing approval from a national medicines regulator. Most laboratory work treats it as a pharmacological tool for probing melanocortin signalling in cell culture or animal models. Whether pigmentation changes observed in people translate into measurable protection against ultraviolet-induced DNA damage remains an open question.
Melanotan-2 is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone, the naturally occurring peptide involved in pigmentation signalling. Its sequence is conventionally written as Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2, with a lactam bridge joining the aspartate side chain to the lysine side chain. The empirical formula is C50H69N15O9 and the monoisotopic mass lies near 1023.5 daltons. N-terminal acetylation and the D-configured phenylalanine both increase resistance to enzymatic breakdown compared with the parent hormone.
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 peptide analog modeled on alpha-melanocyte-stimulating hormone, a naturally occurring signaling peptide involved in pigmentation. Its structure is a cyclic heptapeptide containing two non-natural substitutions, norleucine at position four and D-phenylalanine at position seven. These modifications resist enzymatic breakdown and extend the molecule's activity relative to the native hormone. The compound binds melanocortin receptors and is studied mainly as a pharmacological tool rather than a therapeutic product. It has never received approval as a medicine in any major jurisdiction.
Like the Aztecs, the Pueblo, Navajo and Apache tribes cherished turquoise for its amuletic use; the latter tribe believe the stone to afford the archer dead aim. In Navajo culture it is used for "a spiritual protection and blessing." Among these peoples turquoise was used in mosaic inlay, in sculptural works, and was fashioned into toroidal beads and freeform pendants. The Ancestral Puebloans (Anasazi) of the Chaco Canyon and surrounding region are believed to have prospered greatly from their production and trading of turquoise objects. The distinctive silver jewellery produced by the Navajo and other Southwestern Native American tribes today is a rather modern development, thought to date from around 1880 as a result of European influences. In Persia, turquoise was the de facto national stone for millennia, extensively used to decorate objects (from turbans to bridles), mosques, and other important buildings both inside and out, such as the Medresseh-i Shah Husein Mosque of Isfahan. The Persian style and use of turquoise was later brought to India following the establishment of the Mughal Empire there, its influence seen in high purity gold jewellery (together with ruby and diamond) and in such buildings as the Taj Mahal. Persian turquoise was often engraved with devotional words in Arabic script which was then inlaid with gold. Cabochons of imported turquoise, along with coral, was (and still is) used extensively in the silver and gold jewellery of Tibet and Mongolia, where a greener hue is said to be preferred.
Medical societies issue guidelines for when physicians should use MRI on patients and recommend against overuse. MRI can detect health problems or confirm a diagnosis, but medical societies often recommend that MRI not be the first procedure for creating a plan to diagnose or manage a patient's complaint. A common case is to use MRI to seek a cause of low back pain; the American College of Physicians, for example, recommends against imaging (including MRI) as unlikely to result in a positive outcome for the patient.
The country was mostly savannah, although the moist and mountainous eastern highlands supported areas of tropical evergreen and hardwood forests. Trees found in these Eastern Highlands included teak, mahogany, enormous specimens of strangling fig, forest newtonia, big leaf, white stinkwood, chirinda stinkwood, knobthorn and many others. In the low-lying parts of the country, fever trees, mopane, combretum and baobabs abound. Much of the country was covered by miombo woodland, dominated by brachystegia species and others. Among the numerous flowers and shrubs were hibiscus, flame lily, snake lily, spider lily, leonotus, cassia, tree wisteria and dombeya. There were around 350 species of mammals that can be found in Rhodesia. There were also many snakes and lizards, over 500 bird species, and 131 fish species.
At high pressures, above approximately 10 GPa and temperatures of a few hundred kelvin or less, α-iron changes into another hexagonal close-packed (hcp) structure, which is also known as ε-iron. The higher-temperature γ-phase also changes into ε-iron, but does so at higher pressure. The physical properties of iron at very high pressures and temperatures have been studied extensively because of their relevance to theories about the cores of the Earth and other planets. The Earth's inner core is generally presumed to consist of an iron-nickel alloy with ε (or β) structure. Some controversial experimental evidence exists for a stable β phase at pressures above 50 GPa and temperatures of at least 1500 K. It is supposed to have an orthorhombic or a double hcp structure. (Confusingly, the term "β-iron" is sometimes also used to refer to α-iron above its Curie point, when it changes from being ferromagnetic to paramagnetic, even though its crystal structure has not changed.)
== Clinical significance == Toxic vacuolation is associated with sepsis, particularly when accompanied by toxic granulation. The finding is also associated with bacterial infection, alcohol toxicity, liver failure, and treatment with granulocyte colony-stimulating factor, a cytokine drug used to increase the absolute neutrophil count in patients with neutropenia. The formation of toxic vacuoles represents increased phagocytic activity, which is stimulated by the release of cytokines in response to inflammation or tissue injury. Toxic vacuolation frequently occurs in conjunction with toxic granulation and Döhle bodies in inflammatory states, and these findings are collectively referred to as toxic changes. Neutrophilia and left shift (the presence of immature neutrophil precursors such as band neutrophils and metamyelocytes in the peripheral blood) often accompany toxic changes, as these phenomena also occur in response to inflammation. It has been suggested that neutrophil vacuoles not be labelled "toxic vacuoles" unless they are accompanied by other toxic changes, as vacuolation can occur in other conditions.
Sources: en.wikipedia.org
=== Eating behaviors and energy conservation === An increased presence of MCH can cause increased eating levels and has been linked to an increase in body mass. Inversely, a decrease in the amount of MCH present can cause decreased levels in eating. Increased amounts of MCH in olfactory regions, among others, have also been linked to an increased intake of fatty foods with high caloric content. Food that is found to taste good also seems to promote MCH, which reinforces the eating of that food. Sugar, specifically glucose, seems to promote MCH's role in sleep and energy conservation. This promoting of energy conservation has also been linked to higher body mass even when diet is controlled.
=== European Union === Use of zinc pyrithione is prohibited within cosmetic products in the European Union since December 2021. The substance was considered safe for use in rinse-off and leave-in products of different tested concentrations, but due to potential environmental toxicity consideration of the use of zinc pyrithione was made against potential alternative substance ingredients. Due to no industry submission to the regulators supporting the continued use of zinc pyrithione and/or an absence of indications that there were no suitable alternatives to the substance: the use of zinc pyrithione became automatically prohibited within cosmetic products as an intended ingredient. This was as a consequence of zinc pyrithione addition to the Cosmetic Product Regulation (EC) No 1223/2009 Annex II list.
The two substrates of this enzyme are (2S,3S)-2,3-dihydroxy-2,3-dihydrobenzoic acid and oxidised nicotinamide adenine dinucleotide (NAD+). Its products are 2,3-dihydroxybenzoic acid, reduced NADH, and a proton. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-CH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is 2,3-dihydro-2,3-dihydroxybenzoate:NAD+ oxidoreductase. This enzyme is also called 2,3-diDHB dehydrogenase. This enzyme participates in biosynthesis of siderophore group nonribosomal.
== Further reading == Gogarten, J Peter; Elena Hilario (2006). "Inteins, introns, and homing endonucleases: recent revelations about the life cycle of parasitic genetic elements". BMC Evol Biol. 6 (1): 94. doi:10.1186/1471-2148-6-94. ISSN 1471-2148. PMC 1654191. PMID 17101053.
Sources: en.wikipedia.org
Lynch, Britt-Gibson, and Black all initially auditioned for the role of Alamo before being assigned their parts. Rosalía's song "Malamente" had appeared in season 1 episode five "'03 Bonnie and Clyde, and she co-wrote "Lo Vas a Olvidar" with Billie Eilish for the 2021 special episode "Fuck Anyone Who's Not a Sea Blob". Hardison previously worked with Zendaya on her Disney Channel series K.C. Undercover, playing her character's father, Craig Cooper. In October, Colleen Camp, Gideon Adlon, Hemky Madera, Homer Gere, Jack Topalian, Jessica Blair Herman, Madison Thompson, Matthew Willig, Rebecca Pidgeon, and Sam Trammell joined the cast in more recurring roles.
{\displaystyle \Delta _{^{12}CH_{2}D_{2}}={\left({\frac {0.183798}{T}}\right)}-{\left({\frac {785.483}{T^{2}}}\right)}+\left({\frac {1056280.0}{T^{3}}}\right)+\left({\frac {9.37307\times 10^{7}}{T^{4}}}\right)-\left({\frac {8.919480\times 10^{10}}{T^{5}}}\right)+\left({\frac {9.901730\times 10^{12}}{T^{6}}}\right)}
== Bibliography == Oberg, Erik; Jones, Franklin D.; Horton, Holbrook L.; Ryffel, Henry H. (1996), Green, Robert E.; McCauley, Christopher J. (eds.), Machinery's Handbook (25th ed.), New York: Industrial Press, ISBN 978-0-8311-2575-2, OCLC 473691581.
a human embryo into which a nonhuman cell or cells (or the component parts thereof) had been introduced to render the embryo's membership in the species Homo sapiens uncertain; a chimera human/animal embryo produced by fertilizing a human egg with nonhuman sperm; a chimera human/animal embryo produced by fertilizing a nonhuman egg with human sperm; an embryo produced by introducing a nonhuman nucleus into a human egg; an embryo produced by introducing a human nucleus into a nonhuman egg; an embryo containing at least haploid sets of chromosomes from both a human and a nonhuman life form; a nonhuman life form engineered such that human gametes developed within the body of a nonhuman life form; or a nonhuman life form engineered such that it contained a human brain or a brain derived wholly or predominantly from human neural tissues. The bill would have prohibited the attempts to create a human-animal chimera, the transfer or attempt to transfer a human embryo into a nonhuman womb, the transfer or attempt to transfer a nonhuman embryo into a human womb, and the transport or receipt of an animal chimera for any purpose. Proposed penalties for violations of this bill included fines and/or imprisonment of up to 10 years. The bill was referred to the Subcommittee on Crime, Terrorism, Homeland Security, and Investigations on October 11, 2016, but died there.
== ECU Health-owned hospitals == ECU Health Medical Center, Greenville - Flagship Hospital ECU Health Beaufort Hospital, Washington ECU Health North Hospital, Roanoke Rapids ECU Health Bertie Hospital, Windsor ECU Health Chowan Hospital, Edenton ECU Health Duplin Hospital, Kenansville ECU Health Edgecombe Hospital, Tarboro ECU Health Roanoke-Chowan Hospital, Ahoskie The Outer Banks Hospital, Nags Head (jointly owned with Chesapeake Regional Healthcare) Former facilities:
Sources: en.wikipedia.org
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.
Afamelanotide is the linear analogue [Nle4-D-Phe7]-alpha-MSH, sometimes called melanotan I, while melanotan II is cyclic and carries three further substitutions. The two are distinct molecules and are not interchangeable in analytical testing.
Binding to the four melanocortin receptor subtypes is well documented in vitro. The relative contribution of each subtype to whole-body effects in humans is far less certain.
No regulatory agency has authorised melanotan-2 as a medicine for any indication. It circulates mainly as a research chemical or through unregulated channels. As a result, identity, purity and content are not independently guaranteed.