The short version of alpha-MSH analogue fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
Melanotan-2 is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone. Its sequence incorporates a lactam bridge that constrains the peptide into a ring, which increases resistance to enzymatic breakdown relative to the natural hormone. Researchers at the University of Arizona synthesised the compound in the late 1980s and early 1990s while studying pigmentation pathways. It has never received marketing approval from any national medicines regulator. In the scientific literature it is usually described as a laboratory research reagent rather than a therapeutic product.
The peptide acts as a non-selective agonist at melanocortin receptors, showing affinity for MC1R, MC3R, MC4R and MC5R. Activation of MC1R on melanocytes drives the conversion of tyrosine into melanin and shifts production toward the darker eumelanin form. MC4R signalling in the central nervous system is linked to appetite and energy balance, which helps explain why reduced food intake appeared in early human studies. Effects on MC4R and on vascular tone also account for the erectile responses recorded as unexpected findings in those same trials.
Melanotan-2 is frequently confused with afamelanotide, a linear analogue authorised in the European Union for erythropoietic protoporphyria. The two compounds differ in chain length, ring structure and receptor selectivity, so findings for one cannot be transferred directly to the other. Published controlled human data on melanotan-2 remain sparse, and much of what circulates online derives from small studies or unpublished reports. Questions about effect size, dose-response behaviour and long-term safety therefore remain unresolved.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic cyclic heptapeptide | Alpha-MSH analogue with a lactam ring |
| Molecular formula | C50H69N15O9 | Commonly cited value for the neutral peptide |
| Molecular weight | 1024.18 g/mol | Calculated for the free molecule |
| Appearance | White to off-white powder | Typically supplied as a lyophilised solid |
| Solubility | Soluble in water, DMSO and ethanol | Dissolution in pure water is often slow |
The compound was developed in the late 1980s and early 1990s by academic researchers investigating melanocortin signaling and pigmentation. Early work explored whether synthetic analogs could reproduce effects of the natural hormone under controlled conditions. The molecule never advanced through the full regulatory pathway required for approval as a medicine. From the mid-2000s onward it appeared in unregulated consumer markets, often distributed through informal channels. That gap between research origins and commercial availability shapes how the compound is discussed today.
Melanotan-2 is a synthetic peptide designed as an analog of alpha-melanocyte-stimulating hormone, a signaling molecule produced in the pituitary and skin. Its structure is a linear chain of seven amino acids that folds into a ring through an internal lactam bridge joining two side chains. The compound is sometimes written as MT-II or MEL-2 in informal and commercial contexts. It belongs to the melanocortin peptide family, a group of short signaling molecules that share a conserved core sequence recognized by melanocortin receptors.
Two structural changes distinguish the synthetic peptide from the natural hormone. A norleucine residue replaces methionine at one position, and a D-configured phenylalanine replaces the natural L-form at another. Both substitutions slow enzymatic breakdown, which extends the molecule's persistence relative to the parent hormone. The lactam bridge further constrains the backbone into a stable conformation. These features are standard design strategies in peptide chemistry and are not unique to this compound; they appear across many research peptides built for improved stability.
Melanocortin receptors comprise five subtypes with distinct tissue distributions and functions. Melanotan-2 is described in the literature as a non-selective agonist that engages several of these subtypes, including MC1R, MC3R, MC4R, and MC5R. MC1R is the subtype most directly linked to melanin production in skin cells. Because the compound is not subtype-selective, its observed effects in experimental settings are generally attributed to activity across multiple receptor pathways rather than to a single target.
Melanotan-2 is a synthetic linear peptide built from seven amino acids arranged in a short chain. Its sequence is commonly written as Ac-Nle-Asp-His-D-Phe-Arg-Trp-Lys-NH2, which includes a modified N-terminus and an amidated C-terminus. The molecule belongs to the melanocortin family and acts as a receptor agonist. Structural features such as the D-phenylalanine residue and the Nle substitution are associated with increased stability against enzymatic degradation relative to the natural parent peptide.
== Winners == The BAFTA ceremonies are typically held in March or April of each year. In some years, BAFTA has given out additional awards just prior to the Electronic Entertainment Expo event, which happens in May or June of the year.
Mast cells use a variety of cell surface receptors to detect pathogens. The best known pathway involves FcεRI, a high-affinity receptor for the Fc region of IgE antibodies, involved in allergies. As a molecular target, FcεRI initiates various outcomes in mast cells (MCs) in response to antigens (Ags). Ags bind to immunoglobulin E (IgE) that is bound to FcεRI to cause the crosslinking of IgE–FcεRI complexes and trigger mast cell activation. Activation leads within minutes to degranulation of mast cells and the release of mediators such as histamine, serotonin, and leukotrienes, followed over a period of hours by the secretion of cytokines, chemokines, and growth factors. FcεRI regulates the Ag–IgE interaction, driving allergic responses. FcεRI clustering controls signal transduction and the quality of MC responses. Under resting conditions in the cell membrane, the IgE–FcεRI complex diffuses freely. Multivalent Ag binding to IgE reorganizes FcεRI within seconds to minutes, forming large aggregates on the cell surface, and causing a transition in the receptor from a diffuse to an immobile state. Small aggregates remain mobile on the cell surface, whereas large aggregates abruptly become immobile. Changes in the mobility, kinetics, and size of FcεRI clusters may govern signal initiation and termination. In addition to IgE-dependent MC activation, forms of IgE-independent MC activation have been studied. One of these involves MRGPRX2, a G protein-coupled receptor (GPCR).
Glyceroneogenesis is a metabolic pathway which synthesizes glycerol 3-phosphate (used to form triglycerides) from precursors other than glucose. Usually, glycerol 3-phosphate is generated from glucose by glycolysis, in the liquid of the cell's cytoplasm (the cytosol). Glyceroneogenesis is used when the concentrations of glucose in the cytosol are low, and typically uses pyruvate as the precursor, but can also use alanine, glutamine, or any substances from the TCA cycle. The main regulator enzyme for this pathway is an enzyme called phosphoenolpyruvate carboxykinase (PEPC-K), which catalyzes the decarboxylation of oxaloacetate to phosphoenolpyruvate. Glyceroneogenesis is observed mainly in adipose tissue, and in the liver. A significant biochemical pathway regulates cytosolic lipid levels. Intense suppression of glyceroneogenesis may lead to metabolic disorders such as type 2 diabetes.
=== UK relaunch === In 2018, 40 years after the founding of SOLAR Records, the label was relaunched in the UK by the family of the late Dick Griffey, according to issue 77 of UK Publication 'Soul Survivors Magazine' which featured an interview with both Carrie Lucas and new CEO Jessie Tsang. At the helm of the relaunched label is Griffey's widow Carrie Lucas, his daughter Carolyn Griffey and British Chinese music promoter and IP paralegal consultant Jessie Tsang. Solar Records incorporates the Soul Train Records and Soul Train Club brands. Jessie Tsang is CEO with Sonia Damney as Vice President. In 2022 Carrie Lucas, Carolyn Griffey, Dina Andrews, Virgil Roberts participated with US Cable channel TV One for a special episode of the UNSUNG TV series on Dick Griffey and Solar Records. The episode premiered on November 6, 2022.
Sources: en.wikipedia.org
=== RNA polymerase is purified === The biochemical purification and characterization of RNA polymerase from the bacterium Escherichia coli (E. coli) enabled the understanding of the mechanisms through which RNA polymerase initiates and terminates transcription, and how those processes are regulated to regulate gene expression (i.e. turning genes on and off). Following the isolation of E. coli RNA polymerase, the three RNA polymerases of the eukaryotic nucleus were identified, as well as those associated with viruses and organelles. Studies of transcription also led to the identification of many protein factors that influence transcription, including repressors, activators and enhancers. The availability of purified preparations of RNA polymerase permitted investigators to develop a wide range of novel methods for studying RNA in the test tube, and led directly to many of the subsequent key discoveries in RNA biology.
== Nearly defunct former casual restaurant chains == This list contains chains that were much larger in the past, with some having several hundred locations at their peak, which have since been reduced to a single location.
Flay opened a second Mesa Grill at Caesars Palace in Las Vegas in 2004, and in 2005 he opened Bar Americain, an American Brasserie, in Midtown Manhattan. He continued to expand his restaurants by opening Bobby Flay Steak in the Borgata Hotel Casino & Spa in Atlantic City, New Jersey. This was followed by a third Mesa Grill in the Bahamas, located in The Cove at Atlantis Paradise Island, which opened on March 28, 2007. The Las Vegas Mesa Grill earned Flay his only Michelin Star in 2008, which was taken away in the 2009 edition. Michelin did not publish a 2010 or 2011 Las Vegas edition, so the star could not be re-earned. Bolo Bar & Restaurant closed its doors on December 31, 2007, to make way for a condominium. Aside from his restaurants and television shows, Flay has been a master instructor and visiting chef at the French Culinary Institute. Although he is not currently teaching classes, he occasionally visits when his schedule permits. Flay established the Bobby Flay Scholarship in 2003. This full scholarship to the French Culinary Institute is awarded annually to a student in the Long Island City Culinary Arts Program. Flay personally helps select the awardee each year. Flay opened his first Bobby's Burger Palace (BBP) at the Smith Haven Mall in Lake Grove, Long Island, on July 15, 2008. At its peak, BBP had nineteen locations in eleven states and the District of Columbia. The original Mesa Grill in New York closed in September 2013 following a proposed rent increase by the landlord.
The biotechnical company Defymed, based in France, is developing an implantable bio-artificial device called MailPan which features a bio-compatible membrane with selective permeability to encapsulate different cell types, including pancreatic beta cells. The implantation of the device does not require conjunctive immuno-suppressive therapy because the membrane prevents antibodies of the patient from entering the device and damaging the encapsulated cells. After being surgically implanted, the membrane sheet will be viable for years. The cells that the device holds can be produced from stem cells rather than human donors, and may also be replaced over time using input and output connections without surgery. Defymed is partially funded by JDRF, formerly known as the Juvenile Diabetes Research Foundation, but is now defined as an organization for all ages and all stages of type 1 diabetes. In November 2018, it was announced that Defymed would partner with the Israel-based Kadimastem, a bio-pharmaceutical company developing stem-cell based regenerative therapies, to receive a two-year grant worth approximately $1.47 million for the development of a bio-artificial pancreas that would treat type 1 diabetes. Kadimastem's stem cell technology uses differentiation of human embryonic stem cells to obtain pancreatic endocrine cells. These include insulin-producing beta cells, as well as alpha cells, which produce glucagon. Both cells arrange in islet-like clusters, mimicking the structure of the pancreas.
== Treatment == Copper deficiency is a very rare disease and is often misdiagnosed several times by physicians before concluding the deficiency of copper through differential diagnosis (copper serum test and bone marrow biopsy are usually conclusive in diagnosing copper deficiency). On average, patients are diagnosed with copper deficiency around 1.1 years after their first symptoms are reported to a physician. Copper deficiency can be treated with either oral copper supplementation or intravenous copper. If zinc intoxication is present, discontinuation of zinc may be sufficient to restore copper levels to normal, but this usually is a very slow process. People with zinc intoxication will usually have to take copper supplements in addition to ceasing zinc consumption. Hematological manifestations are often quickly restored to normal. The progression of the neurological symptoms will be stopped and sometimes improved with appropriate treatment, but residual neurological disability is common.
Sources: en.wikipedia.org
== Immunity and autoimmunity == The human body has many defense mechanisms against pathogens, one of which is humoral immunity. This defence mechanism produces antibodies (large glycoproteins) in response to an immune stimulus. Many cells of the immune system are required for this process, including lymphocytes (T-cells and B-cells) and antigen presenting cells. These cells coordinate an immune response upon the detection of foreign proteins (antigens), producing antibodies that bind to these antigens. In normal physiology, lymphocytes that recognise human proteins (autoantigens) either undergo programmed cell death (apoptosis) or become non-functional. This self-tolerance means that lymphocytes should not incite an immune response against human cellular antigens. Sometimes, however, this process malfunctions and antibodies are produced against human antigens, which may lead to autoimmune disease.
== Role in development and regulation == Tyrosine-protein kinase CSK is involved in the following developmental, metabolic, and signal transduction cascades: Adherens junction organization, blood coagulation, brain development, cell differentiation, cell migration, cellular response to peptide hormone stimulus, central nervous system development, epidermal growth factor receptor signaling pathway, innate immune response, epithelium morphogenesis, regulation of bone resorption, negative regulation of cell proliferation, negative regulation of ERK1 and ERK2 cascade, negative regulation of Golgi to plasma membrane protein transport, negative regulation of interleukin-6 production, negative regulation of kinase activity, negative regulation of low-density lipoprotein particle clearance, negative regulation of phagocytosis, dendrocyte differentiation, peptidyl-tyrosine autophosphorylation, platelet activation, positive regulation of MAP kinase activity, regulation of cell proliferation, regulation of cytokine production, regulation of Fc receptor mediated stimulatory signaling pathway, T cell costimulation, T cell receptor signaling pathway.
Glucokinase has a lower affinity for glucose than the other hexokinases. Glucokinase changes conformation and/or function in parallel with rising glucose concentrations in the physiologically important range of 4–10 mM (72–180 mg/dL). It is half-saturated at a glucose concentration of about 8 mM (144 mg/dL). Glucokinase is not inhibited by physiological concentrations of its product, glucose-6-phosphate. This allows continued signal output (e.g., to trigger insulin release) amid significant amounts of its product. Another distinctive property of glucokinase is its moderate cooperativity with glucose, with a Hill coefficient (h) of about 1.7. These features allow it to regulate a "supply-driven" metabolic pathway. That is, the rate of reaction is driven by the supply of glucose, not by the demand for end products. Because of the cooperativity, the kinetic interaction of glucokinase with glucose does not follow classical Michaelis-Menten kinetics. Rather than a Km for glucose, it is more accurate to describe a half-saturation level S0.5, the concentration at which the enzyme is 50% saturated and active. The S0.5 and h result in an inflection of the curve enzyme activity as a function of glucose concentration at about 4 mM. In other words, at a glucose concentration of about 72 mg/dL, which is near the low end of the normal range, glucokinase activity is most sensitive to small changes in glucose concentration.
The oxygenase reaction of RuBisCO may prevent CO2 depletion near its active sites and contributes to the regulation of CO2 concentration in the atmosphere The photorespiratory pathway is a major source of hydrogen peroxide (H2O2) in photosynthetic cells. Through H2O2 production and pyrimidine nucleotide interactions, photorespiration makes a key contribution to cellular redox homeostasis. In so doing, it influences multiple signalling pathways, in particular, those that govern plant hormonal responses controlling growth, environmental and defense responses, and programmed cell death. It has been postulated that photorespiration may function as a "safety valve", preventing the excess of reductive potential coming from an overreduced NADPH-pool from reacting with oxygen and producing free radicals (oxidants), as these can damage the metabolic functions of the cell by subsequent oxidation of membrane lipids, proteins or nucleotides. The mutants deficient in photorespiratory enzymes are characterized by a high redox level in the cell, impaired stomatal regulation, and accumulation of formate.
=== Complete === Complete tears of the plantar fascia are often due to sudden trauma or injury. Often, the rupture will be accompanied by a popping sound and painful snapping sensation. The bottom of the foot often bruises and swells. Former NFL athlete Peyton Manning suffered a complete rupture in 2015. The surgical procedure known as a plantar fascia release actually involves the purposeful infliction of a complete tear of the plantar fascia. This is intended to relieve plantar fasciitis symptoms when the tissue recovers by building more tissue, elongating the previously tight plantar fascia.
Sources: en.wikipedia.org
It is a synthetic cyclic heptapeptide modelled on alpha-melanocyte-stimulating hormone. A lactam bridge links two side chains, forming a ring that stabilises the molecule against proteolysis. It belongs to the broader melanocortin peptide family.
No national medicines agency has approved melanotan-2 for clinical use. Afamelanotide, a related but distinct peptide, holds a marketing authorisation in the European Union for a rare photosensitivity disorder. Melanotan-2 itself is handled as a laboratory chemical.
Its broad activity across melanocortin receptors makes it a tool for probing pigmentation, appetite and vascular signalling. Early trials recorded skin darkening and other effects that were not the original focus of the work. Those observations generated hypotheses that later studies have examined.
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.