Everything below concerns cyclic heptapeptide. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2025-09-16. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| 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 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.
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.
Melanocytes are the pigment-producing cells of the skin, and they carry melanocortin-1 receptors on their surface. When the receptor is activated, cyclic adenosine monophosphate rises inside the cell and raises the activity of enzymes such as tyrosinase, which increases melanin output. Melanotan-2 binds melanocortin-1 receptors in vitro and in animal models, and this binding is generally described as the basis for the tanning effect. Other receptors account for different effects: melanocortin-4 receptors contribute to appetite and erectile signalling, while melanocortin-3 and melanocortin-5 receptors contribute to energy balance and exocrine function.
Early published reports described melanotan-2 as a tanning agent without sun protection, which means darkening is not the same as protection against ultraviolet radiation. Later studies explored the peptide in erectile dysfunction, hemorrhagic shock, and some skin conditions. No regulator in the United States or Europe has approved it for clinical use. Many products labelled melanotan-2 are sold without approval and their identity and purity are unverified. Its long-term safety in humans remains an open question.
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.
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.
The French censor cut some violent scenes and made the director change the end of his movie which was seen as "too pessimistic". Léo Joannon's film Fort du Fou (Fort of the Mad) /Outpost in Indochina was released in 1963. Another film was The 317th Platoon (La 317ème Section) was released in 1964, it was directed by Indochina War (and siege of Dien Bien Phu) veteran Pierre Schoendoerffer. Schoendoerffer has since become a media specialist about the Indochina War and has focused his production on realistic war movies. He was cameraman for the army ("Cinematographic Service of the Armies", SCA) during his duty time; moreover, as he had covered the Vietnam War he released The Anderson Platoon, which won the Academy Award for Documentary Feature. Graham Greene's novel The Quiet American takes place during this war. In 2011, Vietnamese software developer Emobi Games released a first-person-shooter called 7554. Named after the date 07-05-54 (7 May 1954) which marks the end of the decisive Battle of Dien Bien Phu, it commemorates the First Indochina War from the Vietnamese point of view. The 2017 film by Olivier Lorelle, Ciel Rouge, starring Cyril Descours and Audrey Giacomini, is set during the early part of the First Indochina War.
== Sticky-end ligation == Restriction enzymes can generate a wide variety of ends in the DNA they digest, but in cloning experiments most commonly used restriction enzymes generate a 4-base single-stranded overhang called the sticky or cohesive end (exceptions include NdeI which generates a 2-base overhang, and those that generate blunt ends). These sticky ends can anneal to other compatible ends and become ligated in a sticky-end (or cohesive end) ligation. EcoRI for example generates an AATT end, and since A and T have lower melting temperature than C and G, its melting temperature Tm is low at around 6°C. For most restriction enzymes, the overhangs generated have a Tm that is around 15°C. For practical purposes, sticky end ligations are performed at 12-16°C, or at room temperature, or alternatively at 4°C for a longer period. For the insertion of a DNA fragment into a plasmid vector, it is preferable to use two different restriction enzymes to digest the DNA so that different ends are generated. The two different ends can prevent the religation of the vector without any insert, and it also allows the fragment to be inserted in a directional manner. When it is not possible to use two different sites, then the vector DNA may need to be dephosphorylated to avoid a high background of recircularized vector DNA with no insert. Without a phosphate group at the ends the vector cannot ligate to itself, but can be ligated to an insert with a phosphate group.
Carminic acid (C22H20O13) is a red glucosidal hydroxyanthrapurin that occurs naturally in some scale insects, such as the cochineal, Armenian cochineal, and Polish cochineal. The insects produce the acid as a deterrent to predators. An aluminum salt of carminic acid is the coloring agent in carmine, a pigment. Natives of Peru had been producing cochineal dyes for textiles since at least 700 CE. Synonyms are C.I. 75470 and C.I. Natural Red 4. The chemical structure of carminic acid consists of a core anthraquinone structure linked to a glucose sugar unit. Carminic acid was first synthesized in the laboratory by organic chemists in 1991. In 2018, researchers genetically engineered the microbe Aspergillus nidulans to produce carminic acid. It was previously thought that it contains α-D-glucopyranosyl residue, which was later redetermined to be the β-D-glucopyranosyl anomer.
Sources: en.wikipedia.org
The secretin-cholecystokinin test (aka Secretin-CCK test, Secretin-Pancreozymin test) is a combination of the secretin test and the cholecystokinin test and is used to assess the function of both the pancreas and gall bladder.
18 February 1919: In spite of the ceasefire, there is fighting near Rynarzewo. The Poles capture the armoured train. 9 February 1919: A volunteer company of Great Polish soldiers moves to Lesser Poland to fight against the Ukrainians. 20 March 1919: The Ostmarkenzulage, a special allowance for German officials working in the eastern provinces to stimulate the German colonization of the Prussian Partition, is canceled. 23 March 1919: The Poles win a landslide in elections to the city council of Poznań. 24 March 1919: The Commission of the NRL asks the Polish government in Warsaw to create separate administration of the former Prussian Partition, as it is far more developed than the rest of the country. Ignacy Paderewski forces the government to leave all power in hands of the NRL until the final recognition of Polish-German border, with later autonomy there (only Upper Silesia would obtain it). The NRL mobilises men born in 1891, 1892, 1893, 1894 and 1901. 5 April 1919: The Sejm Ustawodawczy announces byelections in the former Province of Posen for next 42 MPs. 9 April 1919: The Commission of the NRL decrees an eight-hour workday in industry and trade. 10 April 1919: The Commission of the NRL decrees the removal of signs in German language from offices and train stations the changing of all streets names into Polish. The punishment for breaking the law is two years of prison and a fine of Mp. 10,000. 16 April 1919: The NRL decides that 3 May is the national holiday. 7 May 1919: The Wszechnica Piastowska is opened. 15 May 1919: Polish becomes the only official language.
Computer simulations indicated energy barriers of 0.61–0.75 eV for hydroxyl-terminated atomic defects that participate in a Grotthuss-type relay, while pyrylium-like ether terminations did not. Recently, Paul and co-workers at IISER Bhopal demonstrated solid state proton conduction for oxygen functionalized few-layer graphene (8.7 × 10−3 S/cm) with a low activation barrier (0.25 eV).
Sources: en.wikipedia.org
Myostatin (also known as growth differentiation factor 8, abbreviated GDF8) is a protein that in humans is encoded by the MSTN gene. Myostatin is a myokine that is produced and released by myocytes and acts on muscle cells to inhibit muscle growth. Myostatin is a secreted growth differentiation factor that is a member of the TGF beta protein family. Myostatin is assembled and produced in skeletal muscle before it is released into the blood stream. Most of the data regarding the effects of myostatin comes from studies performed on mice. Animals either lacking myostatin or treated with substances that block the activity of myostatin have significantly more muscle mass. Furthermore, individuals who have mutations in both copies of the myostatin gene (popularly called the "Hercules gene") have significantly more muscle mass and are stronger than normal. There is hope that studies into myostatin may have therapeutic application in treating muscle wasting diseases such as muscular dystrophy.
Committee on Armed Services Subcommittee on Cybersecurity Subcommittee on Emerging Threats and Capabilities Subcommittee on Seapower Committee on Commerce, Science, and Transportation Subcommittee on Space and Science (Ranking Member) Subcommittee on Communications, Media, and Broadband Subcommittee on Surface Transportation, Maritime, Freight, and Ports
Instead the bottler may identify only the general geographical area of the source, or simply market the product using their own brand name without identifying their source. This may, in some cases, give the independent bottling company the flexibility to purchase from multiple distillers without changing their labels.
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.
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.