This is a working overview of MC1R, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-03-25. Anything still debated is marked as such rather than presented as settled.
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 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.
| 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-2 is a synthetic cyclic heptapeptide designed as a structural analogue of alpha-melanocyte-stimulating hormone, the endogenous tridecapeptide that regulates pigment production. Two modifications distinguish it from the natural hormone: norleucine replaces methionine at the N-terminus, which limits oxidation, and a D-phenylalanine substitution raises receptor affinity. The ring is closed through an aspartate-lysine lactam bridge, giving the molecule a constrained conformation. The free base has a molecular mass near 1024 daltons, and commercial material is usually supplied as an acetate salt. It appears in the literature as a research peptide rather than an approved therapeutic agent.
Receptor studies place melanotan-2 among non-selective melanocortin agonists, binding MC1R, MC3R, MC4R and MC5R rather than a single subtype. Activation of MC1R on cutaneous melanocytes raises tyrosinase activity and shifts pigment synthesis toward eumelanin, which is darker and more photostable than pheomelanin. Central receptors, particularly MC4R, are associated with appetite suppression and with reported effects on sexual function. Because subtype selectivity is low, the same molecule engages pigment, metabolic and vascular pathways at once, and this breadth is a common explanation offered for the range of adverse events described in user reports.
No regulatory authority has approved melanotan-2 for human use, and several countries classify it as a prescription-only or controlled substance, which restricts lawful supply. Material sold online is generally labelled as a research chemical and is not required to meet pharmaceutical standards of identity or purity. Published human data consist mainly of small uncontrolled studies, case reports and adverse-event notifications, so the evidence base is descriptive rather than confirmatory. Whether repeated melanocyte stimulation alters long-term naevus behaviour remains an open question that no completed trial has resolved.
Melanotan II is a synthetic cyclic heptapeptide that acts as an agonist at melanocortin receptors. It was designed as a structural analogue of alpha-melanocyte-stimulating hormone, the endogenous peptide involved in pigment production. The analogue carries a lactam bridge that constrains the ring and slows enzymatic breakdown relative to the native hormone. In research literature it appears under several abbreviations, and naming conventions are not fully standardized. Published descriptions usually place it within the broader melanocortin agonist family.
Receptor binding at MC1R on melanocytes raises intracellular cyclic AMP and increases expression of tyrosinase and related enzymes. The downstream result is greater synthesis of eumelanin, the dark pigment, without ultraviolet exposure acting as the trigger. The compound is not selective, however, and also engages MC3R, MC4R and MC5R, which are expressed in the central nervous system and elsewhere. That lack of selectivity is the explanation usually offered for effects reported outside pigmentation, including appetite suppression and nausea. Selectivity remains a central theme in comparative studies of related peptides.
=== University entrance examination === In March 2004, Paetongtarn Shinawatra passed Thailand's national university entrance exam and enrolled at Chulalongkorn University, one of the top universities in Thailand. However, questions arose over her admission, as her cumulative high school GPA was reportedly below 2.75 and her second-round entrance exam scores were significantly higher than her first-round results. Three months later, Adisai Bodharamik, then-Minister of Education, issued a statement claiming no conclusive evidence of exam leaks. However, he ordered disciplinary action and reprimands against Professor Police Colonel Dr. Woradej Chandrasorn, Secretary-General of the Office of the Higher Education Commission, and Sasithorn Ahingsako, Director of the Central Testing Bureau, for their roles in opening exam envelopes prematurely. Following the Ministry of Education's review of the investigation, Woradej resigned from his position. In August 2005, he was later appointed as an Assistant Minister of Education.
== Symptoms == Prodromal symptoms are typically fever, cough, and rhinorrhea. BACM symptoms that follow are most frequently calf pain, gait complaints, and inability to walk. The condition is self-limited and full restitution can be expected. In very rare cases, however, rhabdomyolysis may develop. Affected are preschool and school-age children with a male predominance. In one study, the median age was 6 years (range 2–13.2 years). It has been estimated that BACM has an incidence of 2.69 cases per 100,000 children (<18 years) during epidemic seasons and 0.23 cases during non-epidemic seasons.
=== Setting === Opposing Force is set in the same location and timeframe as that of Half-Life, taking place at a remote New Mexico laboratory called the Black Mesa Research Facility. In Half-Life, the player takes on the role of Gordon Freeman, a scientist involved in an accident that opens an interdimensional portal to the borderworld of Xen, allowing the alien creatures of Xen to attack the facility. The player controls Freeman in an attempt to escape the facility and close the portal, ultimately traveling to Xen to do so. Opposing Force, however, shows the events of Half-Life from the perspective of a different protagonist. The player assumes the role of Adrian Shephard, a U.S. Marine Corps Corporal assigned to the Hazardous Environment Combat Unit, a specialized unit sent in to Black Mesa by the government to quell the alien threat and silence all witnesses. However, after Shephard becomes isolated from his fellow Marines, he must ally with the Black Mesa personnel and attempt to escape the base.
Sources: en.wikipedia.org
Enantiomers of a chiral drug often interact in an enantioselective way in a chiral environment. This may be offered by different biotic substances (viz. proteins, nucleic acids, phospholipids and oligosaccharides). They are made up of chiral building blocks that are put together in space in handed conformations. These biological targets function as receptors for the drug enantiomers. So, at the binding sites of these receptors, enantiomers will be seen as different chemical species. The three point attachment model (Easson & Stedman model) can be used to see how chiral discrimination works. Figure depicts how the enantiomers of a drug interact with receptors in a way that depends on the drug's shape. This model was made for chiral drugs with a single stereogenic center. It says that there are three binding sites in the receptor (B', C' and D') that match the drug's pharmacophoric groups (B, C, D). A three-point fit (good fit) is possible for the eutomer at BB', CC' and DD'(Fig. A). Even though the distomer is the wrong enantiomer, it can fit either a one-point interaction (bad fit), or a two-point attachment (CC' and DD') with the same receptor site as shown in (Fig. B). Eutomer is the version that works the way you want it to, and distomer is the version that doesn't work or works in a way you don't want it to. Most of the time, the mirror-image versions have different binding affinities. In the eutomer, the ligands or moiety around a stereogenic element have more binding energy than in the distomer.
=== Port Adelaide (2015–2019) === At the end of the 2014 season, Ryder left Essendon following the supplements saga. Ryder and his wife Jess were concerned for the health of their unborn child after he was allegedly told of the potential risks of the supplements program when interviewed by ASADA. Of the concern, Ryder stated that "At first we were really scared (about Harlan). What has panned out over a long period of time is that we felt badly let down by the club and lost trust and faith.” He nominated Port Adelaide as his preferred club of destination. Essendon were unwilling to trade Ryder initially, with Ryder and his management suggesting they would take Essendon to the AFL Grievance Tribunal because of the club's breach of its duty of care to players during the scandal. Ryder's manager also suggested that Ryder would consider retirement over returning to Essendon if a trade was blocked by the club. On 16 October, he was traded to the Power. Being Port Adelaide's big name recruit for season 2015, Ryder was unable to take part in the pre-season trial matches and was only cleared from his provisional suspension a few days prior to the round one game against Fremantle due to the ASADA drugs investigation. He played in 18 games for the Power, which included games where he kicked three goals in both showdowns and a four goals against his former club Essendon.
Jung was introduced to Freud's work by Bleuler whilst working at Burghölzli Hospital. Bleuler asked him to write a review of The Interpretation of Dreams (1899), which he read in 1900. In the early 1900s, psychology as a science was still in its early stages, but Jung became a qualified practitioner of Freud's new "psycho-analysis". Freud needed collaborators and pupils to validate and spread his ideas. Burghölzli was a renowned psychiatric clinic in Zurich, and Jung's research had already gained him international recognition. Jung sent Freud a copy of his Studies in Word Association in 1906. The same year, he published Diagnostic Association Studies, a copy of which he later sent to Freud, who had already purchased a copy. Preceded by a lively correspondence, Jung met Freud for the first time in Vienna on 3 March 1907.Jung recalled the discussion between himself and Freud as interminable and unceasing for 13 hours. Six months later, the then 50-year-old Freud sent a collection of his latest published essays to Jung in Zurich. This began an intense correspondence and collaboration that lasted six years. In 1908, Jung became an editor of the newly founded Yearbook for Psychoanalytical and Psychopathological Research. In the late summer of 1909, Jung sailed with Freud and Hungarian psychoanalyst Sándor Ferenczi to the United States. From 7–11 September, they took part in the twentieth-anniversary celebration of the founding of Clark University in Worcester, Massachusetts, the Vicennial Conference on Psychology and Pedagogy.
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. 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.