The short version of melanocortin receptor fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-10-01 and is reviewed periodically as new material appears.
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-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.
| 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, also written Melanotan II, is a synthetic cyclic heptapeptide designed as an analogue of alpha-melanocyte-stimulating hormone. Its sequence is Ac-Nle-cyclo[Asp-His-D-Phe-Arg-Trp-Lys]-NH2, and the lactam bridge between the aspartate and lysine side chains constrains the peptide into a ring. This structural change increases receptor affinity and metabolic stability relative to the native hormone. The compound was created in the 1980s as a research tool for studying pigmentation biology.
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.
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.
Receptor-binding studies classify melanotan II as a non-selective melanocortin agonist. It interacts with MC1R, MC3R, MC4R and MC5R, with reported affinities in the low nanomolar range and no strong subtype preference. Activation of MC1R on dermal melanocytes shifts pigment synthesis toward eumelanin, the dark polymer deposited in melanosomes and transferred to keratinocytes. Because the same peptide engages MC4R in the hypothalamus, it also appears in animal work on food intake and erectile response, which is why it is discussed in both pigment and metabolic research. Which receptor populations dominate after systemic exposure in humans is not fully established.
Published pharmacokinetic information is limited and comes mainly from small studies rather than registrational trials. Plasma half-life is usually described as short, on the order of tens of minutes, followed by rapid tissue distribution and clearance of the intact peptide. Metabolites and low concentrations of parent compound have been reported in urine, a detail relevant to anti-doping and forensic testing. Whether repeated exposure changes receptor sensitivity or clearance over time remains an open question. Values differ noticeably between analytical assays, so published numbers should be read as approximate rather than definitive.
In July 2012, the government made a review of the mandatory death penalty applied to certain drug trafficking or murder offences. In the midst of this review, a moratorium was imposed on all the 35 pending executions in Singapore at that time (7 for murder and 28 for drug trafficking). During that period of the review of the mandatory death penalty, one convicted murderer, Pathip Selvan s/o Sugumaran, who made headlines for the violent murder of his girlfriend in 2008, won his appeal in October 2012 and was re-sentenced to 20 years' imprisonment for culpable homicide. Wang Zhijian, a Chinese national who committed the 2008 Yishun triple murders, was sentenced to death for a conviction of murder under Section 300(a) of the Penal Code in November 2012, and another unnamed death row convict died of natural causes while in prison. In November 2012, capital punishment laws in Singapore were revised such that the mandatory death penalty for those convicted of drug trafficking or murder was lifted under certain specific conditions. Judges were empowered with the discretion to sentence such offenders to life imprisonment with the possibility of parole after 20 years. These changes were approved by Parliament and set to take effect in January of the following year. In January 2013, the law was again amended to make the death penalty no longer mandatory for certain capital offences.
Bisphosphonate Bisphosphonates are either administered orally or intravenously. They reduce bone resorption. Mechanism of action: Bisphosphonate binds to the mineral component of the bone and inhibits enzymes (i.e. farnesyl-pyrophosphate synthase) responsible for bone formation, osteoclast recruitment and osteoclast function. This type of drug has a high affinity for hydroxyapatite and stays in bone tissue for a long period of time, with alendronate, it has a half-life of approximately ten years. The risk of a patient having MRONJ after discontinuing this medication is unknown. There are suggestions that bisphosphonate may inhibit the proliferation of soft tissue cells and increases apoptosis. This may result in delayed soft tissue healing. Examples of bisphosphonates: : Zoledronic acid (Reclast, Zometa), Risedronate (Actonel), Alendronate (Fosamax), Etidronate (Didronel), Ibandronate (Boniva), Pamidronate (Aredia), Tiludronate (Skelid). Denosumab Denosumab is a monoclonal antibody which is administrated subcutaneously. It inhibits osteoclast differentiation and activation, reduces bone resorption, improves bone density and lessens skeletal-related events associated with metastasis. Mechanism of action: The drug binds to receptor activator nuclear factor κB ligand (RANKL), preventing the interaction with RANK. It does not bind to bone and its effect on bone diminishes in 9 months. Osteoanabolic drugs
=== Relationship of deficit and debt === Intuitively, the annual budget deficit should represent the amount added to the national debt. However, there are certain types of spending ("supplemental appropriations") outside the budget process which are not captured in the deficit computation, which also add to the national debt. Prior to 2009, spending for the wars in Iraq and Afghanistan was often funded through special appropriations excluded from the budget deficit calculation. In FY2010 and prior, the budget deficit and annual change in the national debt were significantly different. For example, the U.S. added $1 trillion to the national debt in FY2008 but reported a deficit of $455 billion. Due to rules changes implemented under President Obama in 2009, the two figures have moved closer together and were nearly identical in 2013 (a CBO-reported deficit of $680 billion versus change in debt of $672 billion). For FY2014, the difference widened again, with the CBO reporting a deficit of $483 billion compared to a change in total debt outstanding of $1,086 billion.
Sources: en.wikipedia.org
These were not ready until 1901, the year after the system first opened, and Guimard varied the "Métropolitain" lettering somewhat between stations and twice revised the design, which reached its final form in 1902.
The NADP+ structural site is located greater than 20Å away from the substrate binding site and the catalytic coenzyme NADP+ binding site. Its purpose in the enzyme catalyzed reaction has been unclear for many years. For some time, it was thought that NADP+ binding to the structural site was necessary for dimerization of the enzyme monomers. However, this was shown to be incorrect. On the other hand, it was shown that the presence of NADP+ at the structural site promotes the dimerization of dimers to form enzyme tetramers. It was also thought that the tetramer state was necessary for catalytic activity; however, this too was shown to be false. The NADP+ structural site is quite different from the NADP+ catalytic coenzyme binding site, and contains the nucleotide-binding fingerprint. The structural site bound to NADP+ possesses favorable interactions that keep it tightly bound. In particular, there is a strong network of hydrogen bonding with electrostatic charges being diffused across multiple atoms through hydrogen bonding with four water molecules (see figure). Moreover, there is an extremely strong set of hydrophobic stacking interactions that result in overlapping π systems.
However, the importer of the wheat gluten, ChemNutra, claims that they received from Xuzhou Anying results of analyses showing "no impurities or contamination." It has not yet been determined whether Xuzhou Anying products other than wheat gluten have been shipped to North America. The second Chinese supplier involved in shipping melamine-contaminated food ingredients, Binzhou Futian Biology Technology, has been working with importer Wilbur-Ellis since July 2006. Binzhou Futian supplies soy, corn and other proteins to the United States, Europe and Southeast Asia. Binzhou typically ships rice protein concentrate in white bags but on 11 April one bag was pink and had the word "melamine" stenciled on it. Binzhou explained to Wilbur-Ellis that the original bag had broken and a mislabeled, but new, bag had been used. The company only supplies food and feed ingredients. Stephen Sundlof, director of the FDA's Center for Veterinary Medicine, said that melamine turning up in exported Chinese wheat gluten, rice protein concentrate and corn gluten supports theories of intentional adulteration. "That will be one of the theories we will pursue when we get into the plants in China." On 29 April 2007 and 30 April 2007, the International Herald Tribune and The New York Times reported that some animal feed manufacturers in China admit to having used melamine scrap in animal feed for years. Said Ji Denghui, general manager of the Fujian Sanming Dinghui Chemical Company: “Many companies buy melamine scrap to make animal feed, such as fish feed. I don't know if there’s a regulation on it.
Sources: en.wikipedia.org
== Mode of action == Kurtoxin inhibits ion calcium channels by modifying channel gating. The effect of the toxin is voltage-dependent. In a voltage-clamp experiment, it was found that calcium channels are more strongly inhibited by minor depolarization than by a strong depolarization of the cell. The peptide toxin binds close to the channel voltage sensor, and thereby produces complex gating modifications specific for each channel type. In rats, kurtoxin inhibited T-type, L-type, and N-type Ca channels and facilitated P-type channels. Deactivation was accelerated in T-type and L-type channels, slowed down in P-type channels, and not affected in N-type calcium channels. Kurtoxin also has an effect on sodium channels. It slows down both activation and inactivation of the channel.
The lifespan of a lithium-ion battery is typically defined as the number of full charge-discharge cycles to reach a failure threshold in terms of capacity loss or impedance rise. Manufacturers typically specify cycle life as the number of cycles until capacity falls to 80% of its rated value. Simply storing lithium-ion batteries in the charged state also reduces their capacity and increases the cell resistance (primarily due to the continuous growth of the solid electrolyte interface on the anode). Calendar life describes degradation during storage as well as cycling. Battery cycle life is affected by many different stress factors including temperature, discharge current, charge current, and state of charge ranges (depth of discharge). Because batteries in practical applications are usually only partially charged and discharged, researchers sometimes use cumulative discharge or equivalent full cycles, which sum partial cycles into an equivalent number of full charge–discharge cycles. Batteries stored at a high temperature or a high state of charge often lose their capacities more quickly. Over their lifespan, batteries degrade gradually leading to reduced cyclable charge (a.k.a. Ah capacity) and increased resistance (the latter translates into a lower operating cell voltage).
== See also == Blast injury, an injury that may present similar dangers to a gunshot wound. Bullet hit squib, a special effect used in the film industry to portray a gunshot wound. Stab wound, an equivalent penetrating injury caused by a bladed weapon or any other sharp objects.
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 analogue of alpha-melanocyte-stimulating hormone, containing seven amino acids with a lactam ring and a D-configured phenylalanine residue. It is supplied as a lyophilised powder for laboratory research.