Everything below concerns MC1R. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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-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.
| 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 II is a synthetic cyclic heptapeptide analog derived from the core sequence of alpha-melanocyte-stimulating hormone. Researchers at the University of Arizona synthesized it during the 1980s while studying pigmentation and appetite signaling. The compound is not an approved medicine in any major jurisdiction and appears mainly in laboratory and research-chemical settings. Its structure incorporates a lactam bridge between side chains, which constrains the ring and slows enzymatic breakdown relative to the natural hormone.
Melanotan II binds several melanocortin receptor subtypes rather than a single target. MC1R on melanocytes drives melanin synthesis, while MC3R and MC4R participate in energy balance, appetite, and sexual response pathways. This lack of selectivity explains why reported effects extend beyond skin darkening. Substitutions at positions four and seven, including norleucine and D-phenylalanine, increase potency and resistance to peptidases. Understanding which receptor mediates which effect remains an active area of investigation.
Cell biology is the branch of biology that studies the structure, function, and behaviour of cells. Bioenergetics is a field in biochemistry and cell biology that concerns energy flow through living systems. This is an active area of biological research that includes the study of the transformation of energy in living organisms and the study of thousands of different cellular processes such as cellular respiration and other metabolic and enzymatic processes that enable the use of energy. Genetics is the scientific study of inheritance. Classical genetics, specifically, is the study of how genes and traits are passed on from parents to offspring; its principles are called Mendelian inheritance. A Punnett square can be used to predict the results of a test cross. The chromosome theory of inheritance, which states that genes are found on chromosomes, was supported by Thomas Morgans's experiments with fruit flies, which established the sex linkage between eye color and sex in these insects.
Elucidating the regulatory mechanisms used to govern essential cellular processes is an important branch of research. Cellular regulatory networks can be very complex and often involve the coordination of multiple processes that begin with the modulation of gene expression. The binding of transcription factor molecules to DNA, either alone or in combination with other transcription factors, is used to control gene expression in response to both intra- and extracellular stimuli. Characterizing the binding mechanisms and specificities of transcription factors to specific regions of DNA – and identifying these transcription factors – is a fundamental component of the process of resolving cellular regulatory dynamics. Before the introduction of SMiLE-seq technology, ChIP-seq (chromatin immunoprecipitation sequencing) and HT-SELEX (high throughput systematic evolution of ligands by exponential enrichment) technologies were used to successfully characterize nearly 500 transcription factor-DNA binding interactions.
As in the adult, SEP findings in combination with the clinical assessment and EEG findings can contribute to the determination of prognosis in comatose children. In high risk newborns, tracking SEP findings over time can be helpful for outcome prognostication. Several neurodegenerative disorders have abnormal findings in spinal and cortical SEP components. Moreover, compressive lesions on the spine (e.g. Arnold-Chiari malformation or mucopolysaccharidosis) are associated with abnormal SEPs, which may precede abnormalities on MRI.
Sources: en.wikipedia.org
== Pathophysiology == PMD is an idiopathic, non-inflammatory condition. The thinning of the cornea may approach 20% of normal thickness. There may be an increase in the number of mucopolysaccharides in the corneal stroma. The Bowman's layer of the cornea may be absent, irregular, or have ruptured areas.
The first widely accepted set of classification criteria for research purposes was elaborated in 1990 by the Multicenter Criteria Committee of the American College of Rheumatology. These criteria, which are known informally as "the ACR 1990", defined fibromyalgia according to the presence of the following criteria:
Guanidines are a group of organic compounds sharing a common functional group with the general structure (R1R2N)(R3R4N)C=N−R5. The central bond within this group is that of an imine, and the group is related structurally to amidines and ureas. Examples of guanidines are arginine, triazabicyclodecene, saxitoxin, and creatine. One technique for persubstituted guanidine synthesis converts a urea to the diaminodichloride with phosgene and then uses the product to alkylate another amine. Galegine is an isoamylene guanidine.
Sources: en.wikipedia.org
== History == Peptide amphiphiles were developed in the 1990s. They were first described by the group of Matthew Tirrell in 1995. These first reported PA molecules were composed of two domains: one of lipophilic character and another of hydrophilic properties, which allowed self-assembly into sphere-like supramolecular structures as a result of the association of the lipophilic domains away from the solvent (hydrophobic effect), which resulted in the core of the nanostructure. The hydrophilic residues become exposed to the water, giving rise to a soluble nanostructure. Work in the laboratory of Samuel I. Stupp by Hartgerink et al., in the early 2000s, reported a new type of PA that are able to self-assemble into elongated nanostructures. These novel PAs contain three regions: a hydrophobic tail, a region of beta-sheet-forming amino acids, and a charged peptide epitope designed to allow solubility of the molecule in water. In addition, the PAs may contain a targeting or signaling epitope that allows the formed nanostructures to perform a biological function, either targeting or signaling, by interacting with living systems. The self-assembly mechanism of these PAs is a combination of hydrogen-bonding between beta-sheet forming amino acids and hydrophobic collapse of the tails to yield the formation of cylindrical micelles that present the peptide epitope at extremely high density at the nanofiber surface. By changing pH or adding counterions to screen the charged surfaces of fibers, gels can be formed.
Acrokeratoelastoidosis of Costa (keratoelastoidosis marginalis) Aquagenic keratoderma (acquired aquagenic palmoplantar keratoderma, aquagenic syringeal acrokeratoderma, aquagenic wrinkling of the palms, transient reactive papulotranslucent acrokeratoderma) Bart–Pumphrey syndrome (palmoplantar keratoderma with knuckle pads and leukonychia and deafness) Camisa disease Carvajal syndrome (striate palmoplantar keratoderma with woolly hair and cardiomyopathy, striate palmoplantar keratoderma with woolly hair and left ventricular dilated cardiomyopathy) Corneodermatoosseous syndrome (CDO syndrome) Diffuse epidermolytic palmoplantar keratoderma (palmoplantar keratoderma cum degeneratione granulosa Vörner, Vörner's epidermolytic palmoplantar keratoderma, Vörner keratoderma) Diffuse nonepidermolytic palmoplantar keratoderma (diffuse orthohyperkeratotic keratoderma, hereditary palmoplantar keratoderma, keratosis extremitatum progrediens, keratosis palmoplantaris diffusa circumscripta, tylosis, Unna–Thost disease, Unna–Thost keratoderma) Erythrokeratodermia variabilis (erythrokeratodermia figurata variabilis, keratosis extremitatum progrediens, keratosis palmoplantaris transgrediens et progrediens, Mendes da Costa syndrome, Mendes da Costa type erythrokeratodermia, progressive symmetric erythrokeratoderma) Focal acral hyperkeratosis (acrokeratoelastoidosis lichenoides, degenerative collagenous plaques of the hand) Focal palmoplantar and gingival keratosis Focal palmoplantar keratoderma with oral mucosal hyperkeratosis (focal epidermolytic palmoplantar keratoderma, hereditary painful callosities, hereditary painful callosity syndrome, keratosis follicularis, keratosis palmoplantaris nummularis, nummular epidermolytic palmoplantar keratoderma) Haim–Munk syndrome (palmoplantar keratoderma with periodontitis and arachnodactyly and acro-osteolysis) Hidrotic ectodermal dysplasia (alopecia congenita with keratosis palmoplantaris, Clouston syndrome, Clouston's hidrotic ectodermal dysplasia, Fischer–Jacobsen–Clouston syndrome, keratosis palmaris with drumstick fingers, palmoplantar keratoderma and clubbing) Howel–Evans syndrome (familial keratoderma with carcinoma of the esophagus, focal non-epidermolytic palmoplantar keratoderma with carcinoma of the esophagus, palmoplantar ectodermal dysplasia type III, palmoplantar keratoderma associated with esophageal cancer, tylosis, tylosis–esophageal carcinoma) Hystrix-like ichthyosis–deafness syndrome (HID syndrome) Keratoderma climactericum (acquired plantar keratoderma, climacteric keratoderma, Haxthausen's disease) Keratosis punctata palmaris et plantaris (Buschke–Fischer–Brauer disease, Davis Colley disease, keratoderma disseminatum palmaris et plantaris, keratosis papulosa, keratoderma punctatum, keratodermia punctata, keratoma hereditarium dissipatum palmare et plantare, palmar and plantar seed dermatoses, palmar keratoses, papulotranslucent acrokeratoderma, punctate keratoderma, punctate keratoses of the palms and soles, maculosa disseminata) Keratitis–ichthyosis–deafness syndrome (erythrokeratodermia progressiva Burns, ichthyosiform erythroderma with corneal involvement and deafness, KID syndrome) Mal de Meleda (acral keratoderma, Gamborg–Nielsen keratoderma, mutilating palmoplantar keratoderma of the Gamborg–Nielsen type, palmoplantar ectodermal dysplasia type VIII, palmoplantar keratoderma of the Norrbotten type) Naxos syndrome (diffuse non-epidermolytic palmoplantar keratoderma with woolly hair and cardiomyopathy, diffuse palmoplantar keratoderma with woolly hair and arrythmogenic right ventricular cardiomyopathy of Naxos, Naxos disease) Olmsted syndrome (mutilating palmoplantar keratoderma with periorificial keratotic plaques, mutilating palmoplantar keratoderma with periorificial plaques, polykeratosis of Touraine) Pachyonychia congenita type I (Jadassohn–Lewandowsky syndrome) Pachyonychia congenita type II (Jackson–Lawler pachyonychia congenita, Jackson–Sertoli syndrome) Palmoplantar keratoderma and spastic paraplegia (Charcot–Marie–Tooth disease with palmoplantar keratoderma and nail dystrophy) Palmoplantar keratoderma of Sybert (Greither palmoplantar keratoderma, Greither syndrome, keratosis extremitatum hereditaria progrediens, keratosis palmoplantaris transgrediens et progrediens, Sybert keratoderma, transgrediens and progrediens palmoplantar keratoderma) Papillon–Lefèvre syndrome (palmoplantar keratoderma with periodontitis) Porokeratosis plantaris discreta Punctate palmoplantar keratoderma Schöpf–Schulz–Passarge syndrome (eyelid cysts with palmoplantar keratoderma and hypodontia and hypotrichosis) Scleroatrophic syndrome of Huriez (Huriez syndrome, palmoplantar keratoderma with scleroatrophy, palmoplantar keratoderma with sclerodactyly, scleroatrophic and keratotic dermatosis of the limbs, sclerotylosis) Striate palmoplantar keratoderma (acral keratoderma, Brünauer–Fuhs–Siemens type of palmoplantar keratoderma, focal non-epidermolytic palmoplantar keratoderma, keratosis palmoplantaris varians, palmoplantar keratoderma areata, palmoplantar keratoderma striata, Wachter keratoderma, Wachters palmoplantar keratoderma) Spiny keratoderma (porokeratosis punctata palmaris et plantaris, punctate keratoderma, punctate porokeratosis of the palms and soles) Tyrosinemia type II (oculocutaneous tyrosinemia, Richner–Hanhart syndrome) Vohwinkel syndrome (keratoderma hereditaria mutilans, keratoma hereditaria mutilans, mutilating keratoderma of Vohwinkel, mutilating palmoplantar keratoderma)
(R)-MDMA is more potent and efficacious as a serotonin 5-HT2A and 5-HT2B receptor agonist than (S)-MDMA, whereas (S)-MDMA is somewhat more potent as an agonist of the serotonin 5-HT2C receptor. Due to it being a more potent serotonin 5-HT2A receptor agonist than (S)-MDMA, (R)-MDMA has been hypothesized to have greater psychedelic effects than (S)-MDMA or racemic MDMA. However, this proved not to be the case in a direct clinical comparison of (R)-MDMA, (S)-MDMA, and racemic MDMA, with equivalent hallucinogen-like effects instead found between the three interventions. MDMA produces MDA as a minor active metabolite. Peak levels of MDA are about 5 to 10% of those of MDMA and total exposure to MDA is almost 10% of that of MDMA with oral MDMA administration. As a result, MDA may contribute to some extent to the effects of MDMA. MDA is an entactogen, stimulant, and weak psychedelic similarly to MDMA. Like MDMA, it acts as a potent and well-balanced SNDRA and as a weak serotonin 5-HT2 receptor agonist. However, MDA shows much more potent and efficacious serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptor agonism than MDMA. Accordingly, MDA produces greater psychedelic effects than MDMA in humans and might particularly contribute to the mild psychedelic-like effects of MDMA. On the other hand, MDA may also be importantly involved in toxicity of MDMA, such as cardiac valvulopathy. The duration of action of MDMA (3–6 hours) is much shorter than its elimination half-life (8–9 hours) would imply.
In August 2012, the viral advertising site "Dredd Report" was launched, satirising the Drudge Report. The site featured a video condemning the use of Slo-Mo, and links to news about the film. A tie-in comic book was published; its plot serves as a prequel to the film's narrative and follows Ma-Ma's life as a prostitute, controlled by her pimp Lester Grimes. Ma-Ma forms a relationship with Eric—the creator of Slo-Mo. Lester kills Eric for interfering with his business, Ma-Ma castrates Lester with her teeth in retaliation and Ma-Ma takes over the Slo-Mo operation. The comic was written by Judge Dredd Megazine editor Matt Smith, drawn by 2000 AD artist Henry Flint and was released on 5 September 2012. An exclusive film poster featuring artwork by Jock was released by Mondo to promote the film's appearance at the 2012 Fantastic Fest in September 2012. Dredd's marketing campaign won a Golden Trailer Award for Best Thriller TV Spot for the trailer "Big Addicted", and received nominations for: Best Action TV Spot, Most Original TV Spot, Best Graphics in a TV Spot, Best Music TV Spot, and Best Action Poster and Most Original Poster for the Dredd motion poster. Reports indicate that Lionsgate contributed $25 million to advertising and print costs. Dredd premiered at San Diego Comic-Con on 11 July 2012. It was also screened at the Toronto International Film Festival on 6 September, and at the Fantastic Fest in late September. The film was first theatrically released on 7 September in the UK and on 21 September worldwide. A South African release followed on 28 September.
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.
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.