The short version of MC1R fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-03-24 and is reviewed periodically as new material appears.
Activity is attributed to agonism at melanocortin receptors, particularly MC1R and MC4R. Activation of MC1R on melanocytes increases melanin synthesis, which underlies the reported tanning effect. MC4R engagement in the central nervous system is linked to appetite suppression and to effects on sexual arousal reported in early clinical studies. Those studies were small and were not designed to establish efficacy or long-term safety. Receptor selectivity among the melanocortin subtypes is not absolute, which complicates attribution of any effect to a single pathway.
Regulatory treatment varies between countries. Several national medicines agencies have classified the peptide as unapproved, and customs authorities in some jurisdictions seize shipments on that basis. A few jurisdictions channel supply through prescription-only frameworks that do not list the substance by name. Because the material circulates mainly through online vendors, composition and purity are rarely verified before sale. Surveys of unapproved peptide products have reported labels that did not match measured content in a substantial fraction of samples.
Melanotan II is a synthetic cyclic heptapeptide analogue of alpha-melanocyte-stimulating hormone, a naturally occurring peptide involved in pigmentation signalling. Its structure substitutes a lactam bridge between side chains to increase stability relative to the native hormone. The compound is also known by the shorthand MT-II and by several non-proprietary synonyms used in research catalogues. It is not an approved therapeutic product in any major jurisdiction; material sold under this name is typically offered as a laboratory reagent rather than as a medicine.
Melanotan-2 is handled in the laboratory as a lyophilised powder that dissolves readily in water, dimethyl sulfoxide and dimethylformamide, with limited solubility in ethanol. Stock solutions prepared in an organic solvent often precipitate when diluted into aqueous buffer, so gradual dilution with mixing is standard practice. The peptide carries a tryptophan residue and a histidine residue, both sensitive to oxidation and to alkaline conditions. Working solutions are therefore kept near neutral to slightly acidic pH, protected from light, and consumed within the same working session whenever that is practical.
Solid peptide kept dry at minus twenty degrees Celsius, shielded from light and moisture, is generally considered stable for extended periods. Solutions are divided into single-use aliquots and held at minus twenty or minus eighty degrees Celsius, because repeated freeze-thaw cycles promote aggregation and loss of material to container surfaces. Hydrolysis of the backbone and oxidation of tryptophan are the principal degradation routes in aqueous solution, and both accelerate at ambient temperature. Hygroscopic uptake after a vial is opened can also shift the actual mass weighed, which affects any concentration calculated from it.
Routine characterisation relies on reversed-phase high-performance liquid chromatography with ultraviolet detection near 214 nanometres, using a C18 column and a water-acetonitrile gradient containing trifluoroacetic acid. Electrospray ionisation mass spectrometry confirms the expected molecular mass and can reveal truncated or oxidised by-products that co-elute poorly. Sequence and stereochemistry require additional work, such as peptide mapping or amino acid analysis, because a chromatographic purity figure alone does not distinguish a diastereomer from the target peptide. Independent testing of research-grade material frequently shows measured content below the stated label, so a certificate of analysis is best read together with the method that produced it.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic cyclic heptapeptide | Analogue of alpha-melanocyte-stimulating hormone |
| Common synonyms | MT-II; melanotan 2 | No internationally accepted non-proprietary name |
| Typical presentation | Lyophilised powder in a sealed vial | Often supplied alongside a separate diluent |
| Regulatory status | Unapproved therapeutic substance | Customs seizure reported in several jurisdictions |
| Reported route in use | Subcutaneous injection | Self-administered outside clinical settings |
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.
Pharmacologically, melanotan-2 behaves as a non-selective agonist across the melanocortin receptor family. Binding at MC1R on dermal melanocytes promotes eumelanin synthesis, which underlies the tanning response described in early human work. Activity at the centrally expressed MC4R receptor is associated with reported effects on appetite and erectile function. Because the peptide does not discriminate strongly among receptor subtypes, attributing any single observed effect to one receptor pathway is generally not possible without selective antagonists or receptor knockout models.
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.
Scientific discussion of Melanotan-2 spans pharmacology, dermatology, and public-health literature. Laboratory studies examine its receptor binding and cellular effects, while clinical reports describe outcomes observed after unregulated use. These two bodies of work differ in rigour and intent. Peer-reviewed trials of the compound as a medicine are limited, so much of the available information comes from case reports and surveillance data. Authors frequently note the gap between experimental findings and real-world use.
Reported observations after unregulated use include shifts in skin pigmentation and, in some accounts, unintended changes to moles and other lesions. Whether these outcomes are causally linked to the compound, and how often they occur, remain open questions because controlled data are scarce. The absence of standardised dosing and verified product purity complicates interpretation. Researchers have called for better surveillance and analytical characterisation of samples obtained outside regulated channels. Conclusions drawn from anecdotal evidence should be treated as provisional.
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.
== In fiction == In the episode "eps2.3_logic-b0mb.hc" (ep. 5 of season 2) of the drama–thriller television series, Mr. Robot, the protagonist, Elliot, is supposed to be repairing a Tor hidden site which turns out to be a darknet market called "Midland City" styled after the Silk Road for the sale of guns, sex trafficked women, rocket launchers, drugs and hitmen for hire. In the 2016 movie Nerve starring Emma Roberts and Dave Franco, the dark web plays a major role. In Grand Theft Auto Online, players who purchase warehouses and garages for illicit cargo and stolen cars can buy/steal and sell them through trade on the "SecuroServ" syndicate website. After the Biker DLC, players can now purchase buildings for illegal drugs and counterfeit products manufacture, and distribute them through a darknet website called "The Open Road" where law enforcement cannot be notified of the player's trade. In the first arc of the anime series Lupin the 3rd Part V, Lupin III steals digital currency from the "Marco Polo" darknet market.
Using the microemulsion technique, metallic cobalt, cobalt/platinum alloys, and gold-coated cobalt/platinum nanoparticles have been synthesized in reverse micelles of cetyltrimethlyammonium bromide, using 1-butanol as the cosurfactant and octane as the oil phase.,
A 2011 review found that caffeine during pregnancy does not appear to increase the risk of congenital malformations, miscarriage or growth retardation even when consumed in moderate to high amounts. Other reviews concluded that there is some evidence that higher caffeine intake by pregnant women may be associated with a higher risk of giving birth to a low birth weight baby, and may be associated with a higher risk of pregnancy loss. A meta-analysis found a correlation between childhood obesity and maternal caffeine intake during pregnancy. A systematic review analyzed the results of observational studies, and found that women who consumed large amounts of caffeine (greater than 300 mg/day) prior to becoming pregnant may have had a higher risk of experiencing pregnancy loss.
Sources: en.wikipedia.org
=== Kniest dysplasia === Most mutations responsible for Kniest dysplasia result in abnormally short pro-alpha1(II) collagen chains that combine with normal-length chains, producing shorter-than-normal collagen molecules. This results in the characteristic features of Kniest dysplasia.
== Overview == FACIT collagens have interruptions in their triple helical structure. They are involved in assembling fibrillar collagens and other ECM components. Interruptions in the triple helical structure of FACIT collagens occur due to the presence of non-triple helical domains within the collagen molecule. These collagens are typically found alongside fibrillar collagens in various tissues and organs. Fibril-associated collagens with interrupted triple helices (FACIT collagens) are a subset of collagens that contribute to the organization and stabilization of the extracellular matrix (ECM). These collagens are typically found alongside fibrillar collagens in various tissues and organs. These domains vary in length and composition and provide flexibility and additional binding sites for other components of the extracellular matrix. There are eight known types of FACIT collagens: collagens IX, XII, XIV, XVI, XIX, XXI, and XXII. The general FACIT collagen structure contains short triple helical COL domains (COL1, COL2, COL3) interrupted by NC domains with an N-terminal NC domain facing toward the interfibrillar space. FACIT collagen is found in various tissue areas to modulate the surface properties of collagen fibrils and generate tissue-specific three-dimensional patterns in the extracellular matrix. For example, collagen XIV connects the fibrillar networks of the cartilage and skin, and XII is found in connective tissues, particularly at the tendons, ligaments, and periodontium.
=== Pre-discovery === In the late 1940s to early 1960s, the early days of making heavier and heavier transuranic elements, it was predicted that since such elements did not occur naturally, they would have shorter and shorter spontaneous fission half-lives, until they stopped existing altogether around element 108 (now called hassium). Initial work in synthesizing the heavier actinides seemed to confirm this. But the nuclear shell model, introduced in 1949 and extensively developed in the late 1960s by William Myers and Władysław Świątecki, stated that protons and neutrons form shells within a nucleus, analogous to electron shells. Noble gases are unreactive due to a full electron shell; similarly, it was theorized that elements with full nuclear shells – those having "magic" numbers of protons or neutrons – would be stabilized against decay. A doubly magic isotope, with magic numbers of both protons and neutrons, would be especially stabilized. Heiner Meldner calculated in 1965 that the next doubly magic isotope after 208Pb was 298Fl with 114 protons and 184 neutrons, which would be the centre of an "island of stability". This island of stability, supposedly from copernicium (Z = 112) to oganesson (Z = 118), would come after a long "sea of instability" from mendelevium (Z = 101) to roentgenium (Z = 111), and the flerovium isotopes in it were speculated in 1966 to have half-lives over 108 years. These early predictions fascinated researchers, and led to the first attempt to make flerovium, in 1968 with the reaction 248Cm(40Ar,xn).
Sources: en.wikipedia.org
No. No major regulatory agency has granted a marketing authorisation for melanotan II as a medicine. Products sold under this name are generally presented as laboratory reagents and are not subject to the batch-release testing applied to approved drugs.
It was developed in the 1980s by researchers investigating analogues of alpha-melanocyte-stimulating hormone for pigmentation and related endpoints. Early work included small human studies during the 1990s. Development did not progress to licensing, and the compound remained a research and grey-market item.
Peptides are prone to truncation, oxidation and aggregation during synthesis and handling. Without independent testing, a buyer cannot confirm the identity or the content of a vial. Analytical surveys of unapproved peptide products have repeatedly found discrepancies between label claims and measured composition.
Purity is normally stated as an area percentage from high-performance liquid chromatography, for example ninety-five or ninety-eight percent. That figure describes the proportion of ultraviolet-absorbing material eluting as the main peak. It says nothing about water content, counterions, residual solvents or mass fraction of the peptide itself.