The short version of alpha-MSH fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-03-08. Anything still debated is marked as such rather than presented as settled.
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.
The compound emerged from research programs in the 1980s that examined analogues of alpha-melanocyte-stimulating hormone for pigmentation and photoprotection. Investigators modified the native sequence to extend activity duration and potency. A related analogue, afamelanotide, was developed within the same broad line of inquiry and eventually gained approval in certain jurisdictions for a rare light-sensitivity condition. Melanotan-2 itself did not progress through the same regulatory route and has no approved therapeutic indication.
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.
The peptide was developed during the 1980s by researchers investigating melanocortin signalling and skin pigmentation pathways. Early work focused on analogues of alpha-melanocyte-stimulating hormone that would resist enzymatic breakdown more effectively than the parent molecule. Melanotan-2 emerged from that programme as a shortened, cyclised variant. Reports describing its synthesis and receptor activity later appeared in the scientific literature. Commercial availability grew through unregulated channels rather than through pharmaceutical approval.
Structurally, Melanotan-2 retains the core recognition motif of alpha-melanocyte-stimulating hormone while adding a lactam bridge that links two side chains and constrains the molecule into a ring. This modification lowers susceptibility to enzymatic degradation. The compound acts as an agonist at melanocortin receptors, particularly subtypes associated with melanin production. Because the same receptor family influences several physiological processes, researchers note that its activity is not confined to pigmentation alone. Receptor selectivity continues to be examined in published studies.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C50H69N15O9 | Free base; salt forms differ |
| Molecular weight | Approximately 1024 g/mol | Calculated for the free base |
| Appearance | White to off-white powder | Typically supplied as a lyophilised solid |
| Solubility | Soluble in water and polar solvents | Poorly soluble in non-polar solvents |
| Typical storage | -20 degrees Celsius, dry, protected from light | Refers to the solid form |
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.
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.
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.
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.
== Plot == Maia Marten is a prosecutor and mother to her diabetic son Noah, living in London. On the day she is scheduled to appear in court for the trial of crime boss Tommy Boyd, she drops Noah off at school, then goes for a run. While on her run, she receives a call coming from Noah's phone from an unnamed man in Boyd's employ. The Caller informs Maia that he has kidnapped Noah and orders her to follow his instructions to ensure Noah’s safe release. He also reveals that he has hacked her phone and is tracking her, leaving her unable to call others for help. The Caller guides Maia to a dumpster, where she finds Noah's backpack containing a gun that was used by Boyd. The Caller tells Maia he has placed Noah in a diabetic coma using his insulin pump. He instructs her to run to the Excelsus Hotel, where key witness Radian Tafa is being kept under police guard, and use the gun to kill him, telling her that if she does not succeed within one hour, Noah will die. Maia begins to run, still on the phone with the Caller, who taunts her with private information he has learned from hacking her, as well as her colleague and romantic interest Ted. She attempts to steal a phone from passersby to send a text to Ted but is unable to do so. As the Caller interrogates Maia about her father's murder, allegedly committed by her abused mother, she is struck by a car and awakens several minutes later in an ambulance. Leaping out, Maia enters the London Underground to make up time, against the Caller's orders.
4,114 parish registers dating before 1792, with 81 indexes 47 registers of banns publications 15 registers for Protestant civil records 7,300 civil registers (1792–1859) stored in 1,002 boxes The total losses exceeded eight million documents. The memory of the Parisian population, preserved since the 16th century, was thus almost entirely obliterated—both that of the "people of Paris" and of the greatest moments in French history, including the births, baptisms, marriages, deaths, and burials of eminent figures. Historian Count de Chastellux wrote: "The destruction of the civil registers stored at the Paris archives (Avenue Victoria) and the registry of the Seine Civil Court is not only a profound disruption for families but also infinitely distressing from a historical perspective. It was the most complete collection of its kind in France, dating back to the reign of Francis I. Within more than 150,000 registers lay solutions to countless questions: historians, biographers, genealogists, topographers, and autograph enthusiasts found a rich and precious mine there." In the second edition of Critical Dictionary of Biography and History (1872), archivist Auguste Jal similarly lamented: "The Civil Archives of Paris were annihilated by fire, both at the Palais de Justice and the depot on Avenue Victoria, during those bloody days of furious hatred, criminal enterprises, and wild and savage acts that marked the few days in mid-May 1871.
Sarcoidosis Granulomatous lung diseases Tuberculosis Fungal infections (e.g., histoplasmosis) Granulomatosis with polyangiitis Idiopathic pulmonary fibrosis Hypersensitivity pneumonitis Asthma Diagnosis of berylliosis is based on history of beryllium exposures, documented beryllium sensitivity, and granulomatous inflammation on lung biopsy. Given the invasive nature of a lung biopsy, diagnosis can also be based on clinical history consistent with berylliosis, abnormal chest x-ray or CT scan findings, and abnormalities in pulmonary function tests. The radiologic and pathologic features of berylliosis are very similar to sarcoidosis. Due to the strong clinical and histopathological resemblance of sarcoidosis and berylliosis, patients are sometimes misdiagnosed with sarcoidosis until the history of exposure to beryllium is elicited and beryllium hypersensitivity demonstrated with specific testing. Some studies suggest that up to 6% of all cases of sarcoidosis are actually berylliosis. The beryllium lymphocyte proliferation test (BeLPT) is the standard way of determining sensitivity to beryllium. The test is performed by acquiring either peripheral blood or fluid from a bronchial alveolar lavage, and lymphocytes are cultured with beryllium sulfate. Cells are then counted and those with elevated number of cells are considered abnormal. Those exposed persons with two abnormal BeLPT tested with peripheral blood, or one abnormal and one borderline result, are considered beryllium sensitized.
In most of the world, a "hot dog" is recognized as a sausage in a bun, but the type varies considerably. The name is often applied to something that would not be described as a hot dog in North America. For example, in New Zealand a "hot dog" is a battered sausage, often on a stick, which is known as a corn dog in North America; an "American hot dog" is the version in a bun.
Sources: en.wikipedia.org
== Mechanism == The reaction catalyzed by this enzyme proceeds via a ping-pong mechanism by using 2 equivalents of NAD(P)H to reduce one equivalent of the azo compound substrate (for example methyl red where Ar = p-dimethylaniline and Ar' = o-benzoic acid) into two equivalents of aniline product:
=== Government response === Following the suspension of operations at three out of four BPI plants, members of the media and leaders were invited by Iowa Governor Terry Branstad to tour the BPI facility that remained open in South Sioux City, Nebraska. The founders of BPI gave campaign contributions to Branstad in 2010, and to other candidates' campaigns. Branstad stated to ABC News that the contributions were not a factor in his decision regarding having the event. Texas Governor Rick Perry, Nebraska Lieutenant Governor Rick Sheehy, Kansas Governor Sam Brownback, and South Dakota Lieutenant Governor Matt Michels, toured the South Sioux City, Nebraska, plant in an attempt to allay "inaccurate information" that they stated as having caused "an unnecessary panic among consumers". The publicity tour emerged with the promotional slogan, "Dude, it's beef!" News reporters were not allowed to ask employees at BPI any questions during the tour. BPI asserts that social media and ABC News "grossly misrepresented" their product. BPI eventually sued ABC News for defamation. On March 28, 2012, Branstad stated, "The problem is, we take this off the market, then we end up with a fatter product that's going to cost more and it's going to increase the obesity problem in this country". Safeway and other retailers that have removed the product from their shelves or product lines have stated they will not raise the price of their beef.
The substrates of the enzyme are α-ketoisovaleric acid, coenzyme A (CoA), and oxidised nicotinamide adenine dinucleotide (NAD+). Its products are isobutyryl-CoA, carbon dioxide, reduced NADH and a proton.
Pacinian corpuscles are rapidly adapting phasic receptors that detect gross pressure changes and vibrations in the skin. Pacinian corpuscles have a large receptive field on the skin's surface with an especially sensitive center. The corpuscles are especially sensitive to vibrations, which they can sense even centimeters away. Their optimal sensitivity is 250 Hz, and this is the frequency range generated upon fingertips by textures made of features smaller than 1 μm. Pacinian corpuscles respond when the skin is rapidly indented but not when the pressure is steady (due to the capsule). It is thought that they respond to high-velocity changes in joint position. They have also been implicated in detecting the location of touch sensations on handheld tools.
== History == The sinoatrial node was first discovered by a young medical student, Martin Flack, in the heart of a mole, whilst his mentor, Sir Arthur Keith, was on a bicycle ride with his wife. They made the discovery in a makeshift laboratory set up in a farmhouse in Kent, England, called Mann's Place. Their discovery was published in 1907.
Sources: en.wikipedia.org
In March 2018 Sara Rojas and her team published their research on drug incorporation and delivery with various biocompatible MOFs other than CD-MOF-1 through simulated cutaneous administration. The group studied the loading and release of ibuprofen (hydrophobic) and aspirin (hydrophilic) in three biocompatible MOFs (MIL-100(Fe), UiO-66(Zr), and MIL-127(Fe)). Under simulated cutaneous conditions (aqueous media at 37 °C) the six different combinations of drug-loaded MOFs fulfilled "the requirements to be used as topical drug delivery systems, such as released payload between 1 and 7 days" and delivering a therapeutic concentration of the drug of choice without causing unwanted side effects. The group discovered that the drug uptake is "governed by the hydrophilic/hydrophobic balance between cargo and matrix" and "the accessibility of the drug through the framework". The "controlled release under cutaneous conditions follows different kinetics profiles depending on: (i) the structure of the framework, with either a fast delivery from the open structure MIL-100 or a slower drug release from the narrow 1D pore system of MIL-127 or (ii) the hydrophobic/hydrophilic nature of the cargo, with a fast (Aspirin) and slow (Ibuprofen) release from the UiO-66 matrix." Moreover, a simple ball milling technique is used to efficiently encapsulate the model drugs 5-fluorouracil, caffeine, para-aminobenzoic acid, and benzocaine. Both computational and experimental studies confirm the suitability of [Zn4O(dmcapz)3] to incorporate high loadings of the studied bioactive molecules.
The building, at the cross sections of those streets that were once called Belascoaín, Carlos III, Fraternidad, and Pocito, is at 508 Avenida de Carlos III (English: Carlos III Avenue). To level the ground beneath the Temple, loads of soil and sand were brought in from each of the Six Provinces of Cuba and many of their major rivers; Camagüey Province, Havana Province, Las Villas Province, Matanzas Province, Oriente Province, and Pinar del Río Province.The building's cornerstone was laid on March 25, 1951, by Grand Master Carlos M. Piñero y del Cueto and the building's architect, Emilio Vasconcelos Frayde. Costs for the construction were made possible by voluntary donations donations from the Grand Lodge and Supreme Council of Cuba, and the Daughters of Acacia. A delegate from the Grand Lodge of Pennsylvania, upon seeing the Temple, wrote: "The cost of the temple was approximately US$4,000,000, and when we realize that there are but 31,700 Masons in Cuba, one can fully realize what a magnificent undertaking was brought to completion." On February 27, 1955, the National Masonic Temple of Cuba was officially inaugurated during the Third Inter-American Conference of Symbolic Freemasonry. At the consecration ceremony, Grand Master Carlos M. Piñeiro del Cueto said: "The consecration of the National Masonic Temple stands as a bulwark in the struggle for the freedom of all peoples and the dignity of mankind." At a height of eleven floors, it was at one time the second-tallest building on the entire island of Cuba.
====== Allergology ====== To train in the add-on specialty of allergology a physician must first be a specialist in general practice, occupational and environmental medicine, pediatric allergology, endocrinology and diabetology, geriatrics, hematology, dermatology and venerology, internal medicine, cardiology, clinical immunology and transfusion medicine, pulmonology, medical gastroenterology and hepatology, nephrology or otorhinolaryngology.
The isotopic substitution changes the vibrational frequencies of various bonds in the molecule, which can have observable effects on the chemical reactivity via the kinetic isotope effect, and even by extension the biological activity in some cases.
Sources: en.wikipedia.org
No. Melanotan-2 is manufactured synthetically. The naturally occurring peptide in the same family is alpha-melanocyte-stimulating hormone, which the body produces as part of normal endocrine and neural signalling.
Both are synthetic analogues derived from the same parent hormone. Reference descriptions usually characterise afamelanotide as more selective for the MC1R subtype, whereas melanotan-2 is reported to interact with a wider range of melanocortin receptors.
Early studies explored melanocortin signalling and pigmentation, which later led to informal use of the label tanning peptide. That label is not a regulatory category and does not imply approved status for any purpose.
It is a synthetic cyclic heptapeptide and an analogue of alpha-melanocyte-stimulating hormone. The molecule is produced by chemical synthesis rather than extracted from a biological source.