melanocortin receptor 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.
Last reviewed on 2026-06-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
2 AgNO3 → 2 Ag + O2 + 2 NO2 Most metal nitrates thermally decompose to the respective oxides. This may be the case for silver nitrate. Unlike most metal oxides, however, silver oxide readily degrades to the elemental silver.
Plant development is the process by which structures originate and mature as a plant grows. It is a subject studied in plant anatomy and plant physiology as well as plant morphology. The process of development in plants is fundamentally different from that seen in vertebrate animals. When an animal embryo begins to develop, it will very early produce all of the body parts that it will ever have in its life. When the animal is born (or hatches from its egg), it has all its body parts and from that point will only grow larger and more mature. By contrast, plants constantly produce new tissues and structures throughout their life from meristems located at the tips of organs, or between mature tissues. Thus, a living plant always has embryonic tissues. The properties of organisation seen in a plant are emergent properties which are more than the sum of the individual parts. "The assembly of these tissues and functions into an integrated multicellular organism yields not only the characteristics of the separate parts and processes but also quite a new set of characteristics which would not have been predictable on the basis of examination of the separate parts." In other words, knowing everything about the molecules in a plant are not enough to predict characteristics of the cells; and knowing all the properties of the cells will not predict all the properties of a plant's structure.
=== Mechanism of action === Clindamycin phosphate is a water-soluble ester of the semi-synthetic antibiotic clindamycin, which is synthesized from lincomycin. Like the macrolide antibiotics, it acts as a bacteriostatic agent by interfering with the 50S subunit of the ribosome of Cutibacterium acnes, inhibiting bacterial protein synthesis and preventing bacteria from replicating. C. acnes plays a role in the development of acne. Benzoyl peroxide also kills C. acnes, but by releasing free radical oxygen species, thus oxidizing bacterial proteins. Also, it dries out the area by reducing sebum production, prevents clogged pores, and is a keratolytic agent. Since benzoyl peroxide is an oxidizer, not an antibiotic, it is not subject to C. acnes resistance unlike clindamycin. Both ingredients have been shown to reduce the number of acne lesions with statistical significance.
=== Labour Party organiser === Galloway joined the Labour Party Young Socialists aged 13, having falsely claimed to have been 15, and was still a teenager when he became secretary of the Dundee Labour Party. Galloway became vice-chairman of the Labour Party in the City of Dundee and a member of the Scottish Executive Committee in 1975. On 5 May 1977, he contested his first election campaign in the Scottish district elections, but failed to hold the safe Labour Gillburn ward in Dundee, being defeated by the independent Bunty Turley. He became the secretary organiser of the Dundee Labour Party in 1977, and at 26, was the youngest ever chairman of the Scottish Labour Party in March 1981, a post he held for a year, after holding the vice-chairman post over the previous year. After a trip to Beirut, Lebanon, during 1977, Galloway became a supporter of Palestine, stating during his libel case against The Daily Telegraph in 2004 that "barely a week after my return I made a pledge, in the Tavern Bar in Dundee's Hawkhill District, to devote the rest of my life to the Palestinian and Arab cause." He supported Dundee City Council when it flew the Palestinian flag over the City Chambers building, and was involved in the twinning of Dundee with the Palestinian West Bank town of Nablus in 1980. In late 1981, in an interview for the Scottish Marxist, Galloway supported the affiliation of the Communist Party of Great Britain (CPGB) to the Labour Party, in the same way as the Fabian Society does.
==== U.S. regulatory restrictions ==== The US Food and Drug Administration (FDA) position is that red yeast rice products that contain monacolin K are identical to a prescription drug and, thus, subject to regulation as a drug. In 1998, the FDA initiated action to ban a product (Cholestin) containing red yeast rice extract. The U.S. District Court in Utah ruled in favor of allowing the product to be sold without restriction. This decision was reversed on appeal to the U.S. Court of Appeals in 2001. In 2007, the FDA sent warning letters to two dietary supplement companies. One was making a monacolin content claim about its RYR product and the other was not, but the FDA noted that both products contained monacolins. Both products were withdrawn. In a press release the FDA "...is warning consumers to not buy or eat red yeast rice products... may contain an unauthorized drug that could be harmful to health." The rationale for "harmful to health" was that consumers might not understand that the dangers of monacolin-containing red yeast rice are the same as those of prescription statin drugs. A products analysis report from 2010 tested 12 products commercially available in the U.S. and reported that per 600 mg capsule, total monacolins content ranged from 0.31 to 11.15 mg. A 2017 study tested 28 brands of red yeast rice supplements purchased from U.S. retailers, stating "the quantity of monacolin K varied from none to prescription strength". Many of these avoid FDA regulation by not having any appreciable monacolin content.
Sources: en.wikipedia.org
== Education == Smith obtained his B.S. in chemistry in 1971 from Lowell Technological Institute (currently the University of Massachusetts Lowell). He then received his PhD in the field of Physical Chemistry from the University of Utah in 1975.
The term "base" appears to have been first used in 1717 by the French chemist, Louis Lémery, as a synonym for the older Paracelsian term "matrix." In keeping with 16th-century animism, Paracelsus had postulated that naturally occurring salts grew within the earth as a result of a universal acid or seminal principle having impregnated an earthy matrix or womb. ... Its modern meaning and general introduction into the chemical vocabulary, however, is usually attributed to the French chemist, Guillaume-François Rouelle. ... In 1754 Rouelle explicitly defined a neutral salt as the product formed by the union of an acid with any substance, be it a water-soluble alkali, a volatile alkali, an absorbent earth, a metal, or an oil, capable of serving as "a base" for the salt "by giving it a concrete or solid form." Most acids known in the 18th century were volatile liquids or "spirits" capable of distillation, whereas salts, by their very nature, were crystalline solids. Hence it was the substance that neutralized the acid which supposedly destroyed the volatility or spirit of the acid and which imparted the property of solidity (i.e., gave a concrete base) to the resulting salt.
==== The phenethylamine psychedelic mescaline ==== Mescaline is sometimes described as the "first psychedelic", as it was the first to be discovered and characterized by the Western world. American physician John Raleigh Briggs, living in Texas, learned of peyote from Native Americans and Mexicans, who told him that it produced "beautiful visions" and made them journey into the "spirit world". He obtained mescal buttons from Mexico and published a journal article about trying a very low dose of them in May 1887. This article is said to have brought peyote into North American pharmacology. Briggs described the physiological symptoms of his experience, such as dramatically increased heart rate and of experiencing "intoxication". However, a modern interpretation is that Briggs simply had a severe panic attack in response to the drug. In any case, his article was read by George Davis, of Parke, Davis and Company, who then obtained the buttons from Briggs in June 1887. Parke-Davis attempted to market peyote as a cardiac stimulant and for other uses, but met with little success. The German pharmacologist Louis Lewin obtained mescal buttons from Parke-Davis during a trip to the United States in 1887 and began studying them and sharing his findings. James Mooney, the first Westerner known to have participated in a Native American peyote ceremony in 1892, distributed peyote to a number of authorities in 1894. Using these specimens, the hallucinogenic effects of peyote were first properly described by Daniel W. Prentiss and F. P. Morgan in 1895.
The now elderly McCormick reunites with the also elderly Helen and asks her to marry him; she happily accepts, proving that true love does indeed last forever. McCormick introduces Nat to Helen, and the film ends with the three joining hands and going for a seaside stroll together.
Sources: en.wikipedia.org
=== Ben Cousins === Ben Cousins played for the West Coast Eagles and Richmond Football Club in his 12 years of playing AFL. On 16 October 2007, Cousins was arrested in Northbridge, Perth, after police had pulled his vehicle over "due to the manner of his driving". Police searched his car and found quantities of prohibited drugs. Cousins was then sacked by West Coast after serious breaches of his contract with them. In 2009, Cousins joined Richmond to continue his AFL career, but on 12 April Cousins and three other Richmond players were suspended by the club after a drunken altercation in a Sydney hotel. Although Cousins was not intoxicated it was ruled that he had not acted responsibly leading to his suspension for 1 week. A few months later in July, Cousins was admitted to hospital after a severe reaction to the prescribed sleeping pills he had taken. This incident led to the debate of whether legal stimulants (such as caffeine) and legal sedatives (such as sleeping pills) could be used by athletes. The Premier of Victoria, John Brumby, disapproved of their use within sporting events.
== Mechanism == AGRP has been demonstrated to be a competitive antagonist of melanocortin receptors, specifically MC3-R and MC4-R. The melanocortin receptors, MC3-R and MC4-R, are directly linked to metabolism and body weight control. These receptors are activated by the peptide hormone α-MSH (melanocyte-stimulating hormone) and antagonized by the agouti-related protein. Whereas α-MSH acts broadly on most members of the MCR family (with the exception of MC2-R), AGRP is highly specific for only MC3-R and MC4-R. This inverse agonism not only antagonizes the action of melanocortin agonists such as α-MSH but also further decreases the cAMP produced by the affected cells. The exact mechanism by which AgRP inhibits melanocortin-receptor signalling is not completely clear. It has been suggested that Agouti-related protein binds MSH receptors and acts as a competitive antagonist of ligand binding. Studies of Agouti protein in B16 melanoma cells supported this logic. The expression of AgRP in the adrenal gland is regulated by glucocorticoids. The protein blocks α-MSH-induced secretion of corticosterone.
=== Norwegian === According to Guinness Book of Records (2001), the longest meaningful word used in Norwegian is minoritetsladningsbærerdiffusjonskoeffisientmålingsapparatur (63 letters), meaning devices for measuring coefficients of diffusion of carriers of minority charges. Nouns, and also verbs and adjectives, can be prefixed as qualifiers to other words quite freely, e.g. to make an unlikely, but understandable and grammatically correct, compound word like damplokomotivfyrbøteraspirantluemerkeprodusentdatterkinoavtaletidspunkt, an agreed meeting time for a cinema date with a daughter of a producer of hat badges for trainees aiming to become firemen on steam locomotives.
In 1974, Rudolf Jaenisch created a transgenic mouse by introducing foreign DNA into its embryo, making it the world's first transgenic animal. However it took another eight years before transgenic mice were developed that passed the transgene to their offspring. Genetically modified mice were created in 1984 that carried cloned oncogenes, predisposing them to developing cancer. Mice with genes removed (termed a knockout mouse) were created in 1989. The first transgenic livestock were produced in 1985 and the first animal to synthesize transgenic proteins in their milk were mice in 1987. The mice were engineered to produce human tissue plasminogen activator, a protein involved in breaking down blood clots. In 1983, the first genetically engineered plant was developed by Michael W. Bevan, Richard B. Flavell and Mary-Dell Chilton. They infected tobacco with Agrobacterium transformed with an antibiotic resistance gene and through tissue culture techniques were able to grow a new plant containing the resistance gene. The gene gun was invented in 1987, allowing transformation of plants not susceptible to Agrobacterium infection. In 2000, Vitamin A-enriched golden rice was the first plant developed with increased nutrient value. In 1976, Genentech, the first genetic engineering company was founded by Herbert Boyer and Robert Swanson; a year later, the company produced a human protein (somatostatin) in E. coli. Genentech announced the production of genetically engineered human insulin in 1978.
== Gene == Alternative splicing results in two transcript variants encoding the same protein. This gene and the gene that encodes ribonuclease, RNase A family, 4 share promoters and 5' exons. Each gene splices to a unique downstream exon that contains its complete coding region.
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.