alpha-MSH 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 2026-03-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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-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.
| 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 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.
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.
== History == IMS was first developed primarily by Earl W. McDaniel of Georgia Institute of Technology in the 1950s and 1960s when he used drift cells with low applied electric fields to study gas phase ion mobilities and reactions. In the following decades, he integrated the recently developed technology he had been working on with a magnetic-sector mass spectrometer. During this period, others also utilized his techniques in novel and original ways. Since then, IMS cells have been included in various configurations of mass spectrometers, gas chromatographs, and high-performance liquid chromatography instruments. IMS is a method used in multiple contexts, and the breadth of applications that it can support, in addition to its capabilities, is continually being expanded.
=== 20th century === In 1924 Pacific Power installed a turbine where the canal meets the river to generate electricity. In 1984 the city bought the water system from Pacific Power, and shut down the plant in 1991. By 2003 the city had approved a plan to restart the four megawatt-hour hydroelectric plant and in February 2009 the plant opened again. Albany was the headquarters for the Mountain States Power Company from its establishment in 1918 until its merger into Pacific Power & Light (now PacifiCorp) in 1954. In the 1940s, the city started the Albany World Championship Timber Carnival, which drew competitors from all over the world to participate in logging skills contests. The event took place over the four days of the Fourth of July weekend. Men and women would compete in climbing, chopping, bucking, and burling contests. In 2001 the carnival was cancelled because of smaller crowds and the state's declining timber economy.
== External links == The Bülow case at www.crimelibrary.com Clarendon Court Mansion, Bülow's former home Obituary in the Star Gazette National Center for Victims of Crime (formerly the Sunny Von Bulow National Victim Advocacy Center)
Sources: en.wikipedia.org
A cold seep (sometimes called a cold vent) is an area of the ocean floor where seepage of fluids rich in hydrogen sulfide, methane, and other hydrocarbons occurs, often in the form of a brine pool. Cold does not mean that the temperature of the seepage is lower than that of the surrounding sea water; on the contrary, its temperature is often slightly higher. The "cold" is relative to the very warm (at least 60 °C or 140 °F) conditions of a hydrothermal vent. Cold seeps constitute a biome supporting several endemic species. Cold seeps develop unique topography over time, where reactions between methane and seawater create carbonate rock formations and reefs. These reactions may also be dependent on bacterial activity. Ikaite, a hydrous calcium carbonate, can be associated with oxidizing methane at cold seeps.
== Donor payment == Most sperm donors who donate their sperm through a sperm bank receive some payment, though this is rarely a significant amount. A 2012 review of 29 studies from nine countries found that the amount of money donors received varied from $10 to €70 per donation.
===== MeSH D08.811.520.224 – carbon-carbon lyases (EC 4.1) ===== MeSH D08.811.520.224.062 – aldehyde lyases MeSH D08.811.520.224.062.250 – 2-dehydro-3-deoxyphosphoheptonate aldolase MeSH D08.811.520.224.062.400 – fructose-bisphosphate aldolase MeSH D08.811.520.224.125 – carboxy-lyases MeSH D08.811.520.224.125.050 – adenosylmethionine decarboxylase MeSH D08.811.520.224.125.100 – aromatic-L-amino-acid decarboxylase MeSH D08.811.520.224.125.100.500 – dopa decarboxylase MeSH D08.811.520.224.125.250 – glutamate decarboxylase MeSH D08.811.520.224.125.300 – histidine decarboxylase MeSH D08.811.520.224.125.350 – indole-3-glycerol-phosphate synthase MeSH D08.811.520.224.125.387 – methylmalonyl-coa decarboxylase MeSH D08.811.520.224.125.425 – ornithine decarboxylase MeSH D08.811.520.224.125.450 – orotidine-5'-phosphate decarboxylase MeSH D08.811.520.224.125.500 – phosphoenolpyruvate carboxykinase (atp) MeSH D08.811.520.224.125.550 – phosphoenolpyruvate carboxykinase (gtp) MeSH D08.811.520.224.125.650 – phosphoenolpyruvate carboxylase MeSH D08.811.520.224.125.750 – pyruvate decarboxylase MeSH D08.811.520.224.125.800 – ribulose-bisphosphate carboxylase MeSH D08.811.520.224.125.875 – tyrosine decarboxylase MeSH D08.811.520.224.125.900 – uroporphyrinogen decarboxylase MeSH D08.811.520.224.187 – deoxyribodipyrimidine photo-lyase MeSH D08.811.520.224.600 – oxo-acid-lyases MeSH D08.811.520.224.600.200 – anthranilate synthase MeSH D08.811.520.224.600.700 – isocitrate lyase MeSH D08.811.520.224.800 – tryptophanase MeSH D08.811.520.224.900 – tyrosine phenol-lyase
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 laboratory-made peptide, while the natural hormone is alpha-melanocyte-stimulating hormone, a longer peptide produced by the pituitary gland and by skin cells. Melanotan-2 mimics only a short active region of that hormone and contains non-natural residues such as D-phenylalanine.