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 2026-03-22. Where a claim depends on a specific study, the study is described rather than over-claimed.
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 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.
Published human data come mostly from small, short studies rather than large controlled trials. Reported outcomes include increased skin pigmentation and, in some reports, effects on appetite and libido, but sample sizes are small and follow-up is limited. Whether long-term use produces durable pigment changes or adverse effects is not established. Because products sold outside pharmacies are not standardized, the actual content of any given vial is often unknown. Independent testing of such material is uncommon.
| 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 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.
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.
RBR and HBR were defined in the initial release of the DisplayPort standard, version 1.0 HBR2 was introduced in version 1.2 HBR3 was introduced in version 1.3 UHBR10, UHBR13.5, and UHBR20 were introduced in version 2.0 However, transmission mode support is not necessarily dictated by a device's claimed "DisplayPort version number". For example, older versions of the DisplayPort Marketing Guidelines allowed a device to be labeled as "DisplayPort 1.2" if it supported the MST feature, even if it didn't support the HBR2 transmission mode. Newer versions of the guidelines have removed this clause, and currently (as of the June 2018 revision) there are no guidelines on the usage of DisplayPort version numbers in products. DisplayPort "version numbers" are therefore not a reliable indication of what transmission speeds a device can support. In addition, individual devices may have their own arbitrary limitations beyond transmission speed. For example, NVIDIA Kepler GK104 GPUs (such as the GeForce GTX 680 and 770) support "DisplayPort 1.2" with the HBR2 transmission mode, but are limited to 540 Mpx/s, only 3⁄4 of the maximum possible with HBR2. Consequently, certain devices may have limitations that differ from those listed in the following tables. To support a particular format, the source and display devices must both support the required transmission mode, and the DisplayPort cable must also be capable of handling the required bandwidth of that transmission mode. (See: Cables and connectors)
== Concepts and complications == Compounds precipitate from a solution when its concentration exceeds its solubility, i.e. the solution is supersaturated. Supersaturation can arise from temperature changes, solvent evaporation, or by mixing solvents. Precipitation occurs more rapidly from a strongly supersaturated solution.
=== Congenital adrenal hyperplasia === Congenital adrenal hyperplasia (CAH) describes a group of autosomal recessive disorders that cause a lack of an enzyme necessary for the production of cortisol and/or aldosterone, steroid hormones produced by the adrenal cortex. Most cases of CAH are due to 21-hydroxylase deficiencies. The heightened androgen levels seen in congenital adrenal hyperplasia affect the hypothalamic–pituitary–gonadal axis. Heightened androgen levels can also affect the ovaries, which can lead to infertility as well as chronic anovulation. Since CAH consists of multiple disorders, the signs, symptoms and severity of hyperandrogenism may stem from a variety of specific mutations. Genotyping is therefore critical to verify diagnoses and to establish prognostic factors for individuals. Genotyping is also crucial for people seeking to use genetic counselling as an aid to family planning. In women, CAH causes ambiguous genitals at birth and excessive pubic hair, enlargement of the clitoris, and hirsutism in adolescence. Although CAH causes rapid growth in childhood, adult women with CAH are shorter than average due to early puberty and closure of the growth plates in the long bones. Symptoms in males include early showings of pubic hair, enlargement of the penis, and rapid musculoskeletal growth.
Sources: en.wikipedia.org
Neutrophils display highly directional amoeboid motility in infected footpad and phalanges. Intravital imaging was performed in the footpad path of LysM-eGFP mice 20 minutes after infection with Listeria monocytogenes.
=== Murder of Spadafora and aftermath === Hugo Spadafora was a physician and political activist who had first clashed with Noriega when they were both members of Torrijos's government. Though an ally of Torrijos, he and Noriega had been personal enemies for a long time. Despite not being a member of the opposition, he became a vocal critic of Noriega after returning to Panama from Guatemala in 1981. Spadafora amassed evidence of corruption within the government by using his position as an ally of Torrijos to question Noriega's allies, including Rodriguez and Carlton. This included a lengthy conversation with Carlton in mid-1985 after his drug operations had collapsed due to conflicts over a missing shipment, and he had received negative publicity in the Panamanian press. In September 1985 he accused Noriega of having connections to drug trafficking and announced his intent to expose him. The drug trafficking charges threatened Noriega's support among his own constituency of middle class individuals who had benefited under his and Torrijos's government. According to writers R. M. Koster and Guillermo Sánchez, on an occasion when Spadafora was traveling by bus from Costa Rica to Panama, witnesses saw him being detained by the PDF after crossing the border. His decapitated body was later found wrapped in a United States Postal Service mail bag showing signs of brutal torture. Noriega was widely believed to be responsible for the murder, and according to Koster and Sánchez, the U.S. had intelligence implicating Noriega. On the day of Spadafora's arrest, the U.S.
== Symptoms and signs == Classically, patients with chronic granulomatous disease will have recurrent bouts of infection due to the decreased capacity of their immune system to fight off disease-causing organisms. The recurrent infections they acquire are specific and are, in decreasing order of frequency:
Sources: en.wikipedia.org
== Summary table for numbers of each class of nuclides == This is a summary table from List of nuclides. Numbers are not exact and may change slightly in the future, as nuclides are observed to be radioactive, or new half-lives are determined to some precision.
=== A10AB Insulins and analogues for injection, fast-acting === A10AB01 Insulin (human) A10AB02 Insulin (beef) A10AB03 Insulin (pork) A10AB04 Insulin lispro A10AB05 Insulin aspart A10AB06 Insulin glulisine A10AB30 Combinations
baiH (7-β dehydratase): Downstream of baiG, the baiH gene encodes a 7-β dehydratase that has NADH:flavin oxidoreductase activity. This enzyme removes the carbon-carbon double bond introduced by baiCD. The connection between 7-β dehydratase and NADH was illuminated in a study that introduced a purified version of this protein into C. scindens, resulting in a decrease in the ratio of oxidized to reduced bile acid intermediates in the 7ɑ-dehydroxylation pathway. Since NAD+/NADH are electron carriers, these researchers assumed that this change in oxidized:reduced intermediate ratio indicated that 7-β dehydratase affected NADH levels. baiI (Δ-ketosteroid isomerase/7-β dehydratase): baiI, the furthest downstream gene of the bai operon, encodes for a protein that does not appear to be required for 7ɑ-dehydroxylation despite being highly conserved among different strains of Clostridium scindens. The classification of this protein is also under scrutiny, as some researchers believe it to have Δ-ketosteroid isomerase functionality while others believe it is a 7-β dehydratase like baiH.
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 regulator in a major market has approved it for human use. It appears in research settings and in products marketed outside pharmacy channels. Legal status for personal possession varies by country.